Post-Infectious Autonomic Neuropathy?
AI-generated by EvidenceHunt:
Key Findings
Dumping syndrome has been reported in an adult patient following meningitis, suggesting a potential link between post-infectious sequelae affecting the autonomic nervous system and the development of dumping syndrome [1].
While primarily associated with gastric surgery, dumping syndrome can also result from vagus nerve damage, which may occur as a consequence of central nervous system infections [2].
A comprehensive understanding and management of autonomic symptoms in patients with central nervous system infections are needed due to potential post-infectious or immunological mechanisms leading to conditions like dumping syndrome [1].
Observational Studies and Case Reports
A case report describes an adult patient who developed dumping syndrome after meningitis without any prior gastric or small bowel surgical procedures [1]. This suggests that dysfunction of the autonomic nervous system, possibly due to post-infectious sequelae or an immunological mechanism, can lead to dumping syndrome. The study emphasizes the need for comprehensive assessment and management of autonomic symptoms in patients with central nervous system infections [1].
A literature review notes that dumping syndrome, while frequently observed after bariatric surgery, can also arise from vagus nerve damage [2]. This aligns with the idea that central nervous system infections, such as meningitis, could indirectly cause dumping syndrome by affecting autonomic nerve function [1] [2].
Summary
Dumping syndrome is primarily recognized as a complication of gastric surgery, particularly bariatric procedures, with prevalence rates reaching up to 50% in partial gastrectomy patients and up to 40% after Roux-en-Y gastric bypass (RYGB) [2] [3]. However, there is evidence suggesting that dumping syndrome can also occur in the absence of gastric surgery, potentially linked to post-infectious autonomic neuropathy. A case report highlights an adult patient who developed dumping syndrome following meningitis, indicating that autonomic nervous system dysfunction due to post-infectious or immunological mechanisms could be a cause [1]. This is further supported by literature indicating that damage to the vagus nerve, which can be a consequence of central nervous system infections, may also lead to dumping syndrome [2]. Therefore, while not a common cause, post-infectious autonomic neuropathy is a recognized, albeit less frequent, potential cause of dumping syndrome.
References:
1) JH Park et al. [Post-meningitis Dumping Syndrome: A Case Report and Literature Review]. The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi (2020). https://pubmed.ncbi.nlm.nih.gov/32581206/
2) YD Chaves et al. PATHOPHYSIOLOGY, DIAGNOSIS AND TREATMENTOF DUMPING SYNDROME AND ITS RELATION TO BARIATRIC SURGERY. Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery (2016). https://pubmed.ncbi.nlm.nih.gov/27683791/
3) M Nofal et al. Dumping Syndrome after Bariatric Surgery. Annali italiani di chirurgia (2024). https://pubmed.ncbi.nlm.nih.gov/39186345/
AI-generated by EvidenceHunt:
Key Findings
Inflammation and immune dysregulation are significant factors contributing to bone loss and altered bone turnover in various conditions, including HIV infection, hemophilia, rheumatoid arthritis, and systemic mastocytosis [1] [2] [3] [4].
Systemic inflammatory markers, such as C-reactive protein (CRP) and Systemic Immune-Inflammation Index (SII), are associated with lower bone mineral density (BMD) and increased fracture risk [5].
Specific conditions show localized or generalized bone density changes and altered bone turnover markers, though the direct correlation between localized DEXA differences and a high bone turnover specifically due to infection/inflammation/immune-driven reactions is not consistently detailed across all provided studies [2] [6] [3].
Inflammation, Infection, and Bone Turnover
Inflammation and immune-driven reactions play a crucial role in bone health. For instance, HIV infection and antiretroviral therapy (ART) are recognized as independent risk factors for osteoporosis, with inflammation and immune dysregulation impacting bone turnover [1]. In a study involving 10 healthy men, human endotoxemia (an experimental model of systemic infection and inflammation) led to a transient fall in parathyroid hormone (PTH) and a nearly two-fold increase in osteopontin (OPN) levels after 6 hours (155+/-19 pg/ml in LPS vs. 85+/-13 pg/ml in placebo, p<0.001). This also reduced C-terminal telopeptide of type I collagen (CTX) levels (0.44+/-0.4 pg/ml in LPS vs. 0.59+/-0.06 pg/ml in placebo, p=0.003) and increased N-terminal propeptide of type I collagen (P1NP) levels [6].
Systemic Conditions and Bone Density/Turnover
Various systemic conditions are linked to altered bone density and turnover. In 80 male patients with hemophilia, low bone mineral density (BMD) was found in 27.5%, with higher bone turnover values associated with lower BMD. Cortical deficits at the radius were influenced by low-grade inflammation, and trabecular alterations at the tibia were associated with hepatitis C virus (HCV) status and orthopedic joint score [2]. A retrospective analysis of 40 older patients (20 with hip fractures, 20 controls) showed that those with fractures had significantly elevated C-reactive protein (CRP) (66.2 ± 70.3 mg/L vs. 3.8 ± 4.0 mg/L, p = 0.0008) and Systemic Immune-Inflammation Index (SII) (1399.7 ± 1143.4 vs. 751.4 ± 400.8, p = 0.025). Higher CRP levels correlated with lower BMD at the hip (r ≈ -0.63, p = 0.002), spine (r ≈ -0.60, p = 0.005), and wrist (r ≈ -0.60, p = 0.005) [5].
Rheumatoid arthritis (RA) causes generalized bone loss and periarticular erosions due to pro-inflammatory cytokines. A study of 62 RA patients (49 female, 13 male, aged 40-79 years) showed that biologic anti-inflammatory drugs increased hip BMD by 0.001g/cm2 (0.11%, p<0.001) and lumbar spine BMD by 0.0396g/cm2 (3.96%, p<0.001) in responder patients. CTX levels dropped from 164 pg/ml to 131 pg/ml in responders after 12 weeks [3]. Similarly, guidelines for systemic mastocytosis recommend bisphosphonates for osteoporosis, acknowledging the role of inflammation [4].
Localized Differences in DEXA Scans
While several studies indicate generalized bone loss and altered turnover in inflammatory and immune-driven conditions, the direct association of high bone turnover with localized differences in DEXA scans (e.g., -2.3 hip, -3.1 L4 vertebra) is not explicitly detailed as a distinct pattern across the provided literature. However, some studies hint at site-specific changes. For example, in hemophilia patients, cortical deficits were noted at the radius and trabecular deficits at the tibia [2]. In autosomal dominant hyper IgE syndrome (AD-HIES), 79% of children and adults had osteopenia or osteoporosis, and low radial BMD correlated with fractures, but hip and spine BMD did not [7]. In ankylosing spondylitis (AS), osteopenia at the hip and spine was found in 56% and 41% respectively of patients with disease duration <5 years, with 11% and 15% having osteoporosis [8].
Summary
High bone turnover and localized differences in DEXA scans can be associated with infections, inflammation, and immune-driven reactions. Conditions like HIV, hemophilia, rheumatoid arthritis, and systemic mastocytosis demonstrate how inflammation and immune dysregulation contribute to bone loss and altered bone turnover [1] [2] [3] [4]. Systemic inflammatory markers, such as CRP, are linked to lower BMD and increased fracture risk [5]. While general bone loss and altered turnover are common, some studies indicate site-specific changes in bone density, although a direct, consistent pattern of localized DEXA differences (e.g., -2.3 hip, -3.1 L4 vertebra) specifically linked to high bone turnover due to infection/inflammation/immune reactions is not uniformly elaborated across all provided articles.
References:
1) I Ofotokun et al. HIV: inflammation and bone. Current HIV/AIDS reports (2011). https://pubmed.ncbi.nlm.nih.gov/22179898/
2) K Holstein et al. The Bone Microarchitecture Deficit in Patients with Hemophilia Is Influenced by Arthropathy, Hepatitis C Infection, and Physical Activity. Thrombosis and haemostasis (2021). https://pubmed.ncbi.nlm.nih.gov/34587640/
3) MM Al-Bogami et al. The clinical assessment of changes in bone density in rheumatoid arthritis patients’: Role of DEXA scan and bone turnover biomarkers. Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine (2024). https://pubmed.ncbi.nlm.nih.gov/38851075/
4) Richtlijnendatabase.nl
5) BA Cedeno-Veloz et al. Systemic Inflammation in Hip Fracture and Osteoarthritis: Insights into Pathways of Immunoporosis. International journal of molecular sciences (2025). https://pubmed.ncbi.nlm.nih.gov/41009701/
6) G Grimm et al. Changes in osteopontin and in biomarkers of bone turnover during human endotoxemia. Bone (2010). https://pubmed.ncbi.nlm.nih.gov/20420943/
7) KJ Sowerwine et al. Bone density and fractures in autosomal dominant hyper IgE syndrome. Journal of clinical immunology (2014). https://pubmed.ncbi.nlm.nih.gov/24402620/
8) K Karberg et al. Bone loss is detected more frequently in patients with ankylosing spondylitis with syndesmophytes. The Journal of rheumatology (2005). https://pubmed.ncbi.nlm.nih.gov/15996067/
Staphyloccus pseudintermedius has zoonotic potential as it has been found in humans that live with companion animals in the same household.[38][30][20] S. pseudintermedius is not a normal commensal bacterium found in humans, however it is capable of adapting to the human microbiota and has become increasingly more common.[20] People at the highest risk for contracting this pathogen are pet owners and veterinarians due to their higher contact with dogs and to a lesser extent cats.[41] The most common colonization site in the human body is within the nasal cavity and from here, the bacteria can cause infections.[42][43] S. pseudintermedius infections in a human host have been known to cause endocarditis, post-surgical infections, inflammation of the nasal cavity (rhinosinusitis) and catheter-related bacteremia.[6] Staphyloccus pseudintermedius becomes established in a human wound, it has the ability to form antibiotic resistance biofilms.[6] Mechanisms of biofilm resistance of S. pseudintermedius are likely multifactorial and may help to establish infections in humans.[6]
AI-generated by EvidenceHunt:
Key Findings
Staphylococcus pseudintermedius (S. pseudintermedius) can cause invasive infections in humans, including serious conditions like aortitis and spinal infections [1] [2].
Methicillin-resistant S. pseudintermedius (MRSP) strains are a significant concern due to their multidrug resistance, complicating treatment in both veterinary and human medicine [3] [4].
Human infections are often linked to close contact with dogs, with 92.1% of cases in one study reporting dog contact [5].
Invasive Infections Beyond the Skin Barrier
S. pseudintermedius has been identified as a cause of severe invasive infections in humans. A case report describes an 83-year-old patient with aortitis and a mycotic aneurysm caused by S. pseudintermedius, successfully treated with flucloxacillin [1]. Another case involved a 60-year-old woman with an invasive spinal infection associated with a spinal fixation device and dog contact, treated effectively with intravenous flucloxacillin followed by oral clindamycin [2]. These cases highlight the potential for S. pseudintermedius to cause serious endovascular and deep abscess-forming infections.
While primarily a canine pathogen, S. pseudintermedius has an expanding host range, including humans, and can cause infections beyond skin and soft tissue, particularly in immunocompromised individuals [6]. Its ability to colonize and adapt to the human body, along with the presence of virulence factors and antibiotic resistance, indicates its potential as an important human pathogen [7] [8].
Antimicrobial Resistance and Identification Challenges
Methicillin-resistant S. pseudintermedius (MRSP) strains are intrinsically multidrug-resistant, posing serious public health consequences and compromising treatment outcomes [3] [4]. In a study of 24 human cases, methicillin resistance was found in 22.2% of isolates, and multidrug resistance was commonly observed [5].
Accurate identification of S. pseudintermedius is crucial but challenging, as it can be misidentified as Staphylococcus aureus using routine biochemical tests [4] [9]. The increased use of techniques like matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) is improving the specific identification of this organism [2].
Summary
S. pseudintermedius, primarily a canine pathogen, is increasingly recognized as an emerging zoonotic threat capable of causing serious invasive infections in humans when it breaches the skin barrier. Documented cases include severe conditions like aortitis and spinal infections, demonstrating its potential for deep-seated infections [1] [2]. A significant concern is the prevalence of multidrug-resistant strains, particularly methicillin-resistant S. pseudintermedius (MRSP), which complicates treatment [3] [5]. Human infections are frequently linked to close contact with dogs, with 92.1% of patients in one study having confirmed canine contact [5]. Accurate identification of S. pseudintermedius is essential for appropriate treatment due to its resistance patterns and potential for misdiagnosis [4] [2].
References:
1) D Jones et al. A novel case of Staphylococcus pseudintermedius aortitis. Access microbiology (2025). https://pubmed.ncbi.nlm.nih.gov/40160443/
2) CA Darlow et al. A spinal infection with Staphylococcus pseudintermedius. BMJ case reports (2017). https://pubmed.ncbi.nlm.nih.gov/28784907/
3) IB Moses et al. Human Colonization and Infection by Staphylococcus pseudintermedius: An Emerging and Underestimated Zoonotic Pathogen. Microorganisms (2023). https://pubmed.ncbi.nlm.nih.gov/36985155/
4) S Bhooshan et al. Staphylococcus pseudintermedius: an undocumented, emerging pathogen in humans. GMS hygiene and infection control (2021). https://pubmed.ncbi.nlm.nih.gov/33391967/
5) R Somayaji et al. Human infections due to Staphylococcus pseudintermedius, an emerging zoonosis of canine origin: report of 24 cases. Diagnostic microbiology and infectious disease (2016). https://pubmed.ncbi.nlm.nih.gov/27241371/
6) E Roberts et al. Not just in man’s best friend: A review of Staphylococcus pseudintermedius host range and human zoonosis. Research in veterinary science (2024). https://pubmed.ncbi.nlm.nih.gov/38805894/
7) W Kmieciak et al. Are zoonotic Staphylococcus pseudintermedius strains a growing threat for humans?. Folia microbiologica (2018). https://pubmed.ncbi.nlm.nih.gov/29804274/
8) P Glajzner et al. Pathogenic potential and antimicrobial resistance of Staphylococcus pseudintermedius isolated from human and animals. Folia microbiologica (2022). https://pubmed.ncbi.nlm.nih.gov/36221001/
9) L Van Hoovels et al. First case of Staphylococcus pseudintermedius infection in a human. Journal of clinical microbiology (2006). https://pubmed.ncbi.nlm.nih.gov/17050817/
AI-generated by EvidenceHunt:
Key Findings
Pneumonia can lead to long-term consequences on various organ systems, with severity often linked to the acute phase of the disease [1] [2].
High C-reactive protein (CRP) levels, such as CRP > 150 mg/L, are associated with more severe outcomes in pneumonia, including increased hospital stay, intubation rates, and mortality [3].
While an immune-mediated mechanism is associated with acute autonomic and sensory neuropathy, the provided literature does not specifically detail the consequences of untreated pneumonia with high CRP on the development of Post-Infectious Autonomic Neuropathy [4].
General Consequences of Pneumonia
Pneumonia, an acute respiratory infection affecting the lower respiratory tract, is a significant health concern associated with high morbidity and both short-term and long-term mortality across all age groups [5]. The severity of the infection and its outcome are largely determined by the host’s immune response, with pathogen characteristics playing a less prominent role [5] [6]. Extensive lung involvement, consolidations, low body mass index (BMI) ( 150 mg/L), and D-dimer (> 3000 ng/mL FEUs), along with significant tobacco exposure (> 20 pack-year), are independently correlated with complications such as pneumomediastinum in COVID-19 pneumonia [3]. Patients with pneumomediastinum experienced a longer hospital stay (mean 31.2 ± 20.2 days vs. 19.6 ± 14.2 days in controls), higher intubation rates (52.5% vs. 17.6%), and increased in-hospital mortality (48.9% vs. 23.5%) [3].
Immune System Activation and Neuropathy
The immune response to pneumonia involves both innate and adaptive immune systems, coordinating to eliminate microbes and prevent severe lower respiratory infections [6]. High CRP levels are indicative of significant inflammation and are associated with worse outcomes in pneumonia [3] [7]. In critically ill patients with community-acquired pneumonia, biomarker-concordant steroid use (when CRP was ≥150 mg/L) was associated with faster resolution of lung injury and increased ICU- and hospital-free days, highlighting the role of inflammation in disease progression [8]. Acute autonomic and sensory neuropathy, a rare disorder, has been anecdotally reported with antecedent events often being upper respiratory tract or gastrointestinal tract infections. This condition is characterized by profound autonomic failure and sensory impairment, with an immune-mediated mechanism suggested to be involved [4]. However, the provided literature does not specifically address the direct consequences of untreated pneumonia with a CRP over 150 mg/L on the development of Post-Infectious Autonomic Neuropathy.
Summary
Pneumonia is a severe infection with potential long-lasting consequences on multiple physiological systems [2]. High inflammatory markers such as CRP levels exceeding 150 mg/L are associated with more severe disease progression and adverse outcomes, including longer hospital stays, increased intubation rates, and higher mortality [3]. While acute autonomic and sensory neuropathy is linked to immune-mediated mechanisms following infections, the specific impact of untreated pneumonia with a high CRP on the development of Post-Infectious Autonomic Neuropathy is not detailed in the provided articles [4].
References:
1) F Patrucco et al. Long-lasting consequences of coronavirus disease 19 pneumonia: a systematic review. Minerva medica (2021). https://pubmed.ncbi.nlm.nih.gov/34856780/
2) LJ Quinton et al. Integrative Physiology of Pneumonia. Physiological reviews (2018). https://pubmed.ncbi.nlm.nih.gov/29767563/
3) S Negri et al. Pneumomediastinum in COVID-19: Risk factors and outcomes from a multicentre case-control study. Respiratory medicine (2024). https://pubmed.ncbi.nlm.nih.gov/38823564/
4) H Koike et al. Clinicopathological features of acute autonomic and sensory neuropathy. Brain : a journal of neurology (2010). https://pubmed.ncbi.nlm.nih.gov/20736188/
5) A Torres et al. Pneumonia. Nature reviews. Disease primers (2021). https://pubmed.ncbi.nlm.nih.gov/33833230/
6) KE Traber et al. The Integrated Pulmonary Immune Response to Pneumonia. Annual review of immunology (2025). https://pubmed.ncbi.nlm.nih.gov/40036700/
7) L Lu et al. Meningitis patients with pneumonia: correlation between blood parameters and clinical features. Biomarkers in medicine (2023). https://pubmed.ncbi.nlm.nih.gov/36861490/
8) YE Odeyemi et al. Biomarker-Concordant Steroid Use in Critically Ill Patients with Pneumonia. Mayo Clinic proceedings. Innovations, quality & outcomes (2020). https://pubmed.ncbi.nlm.nih.gov/33367210/
Binnen de cardiologische definitie van autonome dysfunctie tonen deze onderzoeken inderdaad geen afwijkingen. Echter, de hypertensieve respons, supratarget tachycardie en PVC’s onder inspanning zijn wél overeenkomend met sympathische hyperreactiviteit en systemische autonome ontregeling, zoals later in het ziekteverloop bevestigd. De cardiologische test sluit dus alleen primaire cardiale dysautonomie uit, niet perifere of postinfectieuze autonome neuropathie.