What are the causes of myositis and muscular abscess?

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Causes of Myositis and Muscular Abscess

Primary Etiologic Categories

Myositis and muscular abscesses arise from four major categories: infectious agents (viral, bacterial, fungal, parasitic), drug-induced mechanisms (particularly immune checkpoint inhibitors and statins), autoimmune/idiopathic inflammatory processes, and malignancy-associated disease. 1, 2, 3


Infectious Causes

Viral Myositis

  • Viral pathogens cause acute, self-limited myositis with diffuse myalgias, typically resolving within 3-7 days 4, 5
  • Common viral agents include influenza, HIV, and SARS-CoV-2 1
  • Viruses may also cause acute rhabdomyolysis and have been isolated in inclusion body myositis cases 5
  • Characterized by normal to mildly elevated CK levels that normalize rapidly, distinguishing it from autoimmune myositis 4

Bacterial Myositis and Pyomyositis

  • Bacterial infections typically cause localized myositis or muscular abscesses (pyomyositis) rather than diffuse disease 2, 3
  • More common in immunocompromised patients and at sites compromised by trauma or surgery 2
  • Specific bacterial syndromes include:
    • Pyomyositis: localized collections within muscles 2
    • Gas gangrene: clostridial myonecrosis 2
    • Group A streptococcal myonecrosis 2
    • Non-clostridial myonecrosis 2
  • These conditions are life-threatening and require urgent recognition and treatment 2

Fungal and Parasitic Myositis

  • Fungal pathogens cause myositis, particularly in immunocompromised hosts 2, 3
  • Parasitic organisms including Toxoplasma have been implicated in myositis 5, 3

Drug-Induced Myositis

Immune Checkpoint Inhibitor-Associated Myositis

  • PD-1/PD-L1 inhibitors cause myositis more commonly than ipilimumab, with median exposure of 4 weeks 6
  • Presents as de novo myositis or reactivation of preexisting paraneoplastic polymyositis/dermatomyositis 6
  • Can be severe and fatal, with fulminant necrotizing course, rhabdomyolysis, and myocardial involvement requiring urgent treatment 6
  • Characterized by markedly elevated CK levels, proximal weakness (difficulty standing, lifting arms, climbing stairs), and myalgia in severe cases 6

Statin-Induced Myopathy

  • Statins are much more likely than antipsychotics to cause drug-induced muscle disorders 7
  • Persistent and marked CK elevation (>10x normal) suggests necrotizing myopathy rather than simple drug effect 7

Autoimmune/Idiopathic Inflammatory Myopathies

Polymyositis

  • Characterized by symmetric proximal muscle weakness with CD8+ cytotoxic T cells invading nonnecrotic muscle fibers 6
  • Develops subacutely over weeks to months with persistently elevated CK 4
  • Distinguished by true proximal weakness (difficulty rising from seated position, climbing stairs, lifting arms overhead) rather than just pain 7, 4

Dermatomyositis

  • Presents with characteristic rash: erythematous photosensitive rash, Gottron papules, heliotrope rash, periorbital edema, periungual telangiectasias 6
  • Juvenile dermatomyositis affects children <18 years with calcinosis cutis, cutaneous vasculitis, and gastrointestinal vasculopathy 6
  • Symmetric proximal muscle weakness develops over weeks to months with elevated muscle enzymes 6

Immune-Mediated Necrotizing Myopathy (IMNM)

  • Severe myopathy with minimal inflammatory infiltrate on biopsy 6
  • Triggered by viral infections, statins, and malignant neoplasms 6

Inclusion Body Myositis

  • Pathologic features suggest degenerative neuromuscular disease with muscle fiber vacuolization 6
  • Abnormal accumulation of amyloid-β and phosphorylated tau proteins 6

Malignancy-Associated Myositis

  • Myositis may be paraneoplastic, associated with underlying malignancy 6, 1
  • Requires specific evaluation and treatment beyond standard immunomodulatory therapy 1

Overlap Syndromes and Other Causes

Myositis with Connective Tissue Diseases

  • Myositis occurs with associated rheumatologic diseases, suggesting different pathogenetic mechanisms 5
  • Immunological and pathological differences exist between isolated myositis and overlap syndromes 5

Distinctive Myositis Subtypes

  • Eosinophilic myositis and granulomatous myositis have distinctive clinical and pathological features reflecting different injury mechanisms 5
  • Orbital myositis and localized nodular myositis are confined to single muscles or muscle groups 5

Critical Diagnostic Distinctions

Differentiating Myositis from Myalgia Syndromes

  • Polymyalgia rheumatica-like syndrome presents with severe myalgia and fatigue but no true weakness 6
  • CK levels remain within normal limits in polymyalgia-like syndromes, differentiating from true myositis 6
  • MRI and EMG show no evidence of myopathy or muscle inflammation in pain-only syndromes 6

Key Laboratory Markers

  • Persistently elevated CK (often markedly so) indicates true myositis 6, 4
  • Myositis-specific autoantibodies (anti-Jo-1, anti-Mi-2, anti-MDA5, anti-TIF1-gamma, anti-NXP2) define autoimmune myositis phenotypes and predict outcomes 6, 7, 4
  • Inflammatory markers (ESR, CRP) are highly elevated in immune-mediated myositis 6

References

Research

Secondary Causes of Myositis.

Current treatment options in neurology, 2020

Research

Infection and musculoskeletal conditions: Infectious myositis.

Best practice & research. Clinical rheumatology, 2006

Research

Infective myositis.

Brain pathology (Zurich, Switzerland), 2021

Guideline

Differentiating Viral Myositis from Autoimmune Myositis in Teenagers

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Inflammatory myopathies: Part 1.

Annals of neurology, 1985

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Antipsychotic-Associated Muscle Disorders

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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