Influenza Virus Myopathy

Introduction

Influenza virus myopathy is a viral myopathy associated with influenza virus infection. It typically presents as a self-limiting muscle disorder but can, in rare cases, lead to severe complications such as rhabdomyolysis. It is most common in children, although adults can also be affected.

Pathophysiology

The exact mechanism is not fully understood, but it is thought that direct viral invasion of muscle tissue or immune-mediated muscle injury plays a role. Cytokine release and inflammation during systemic infection can contribute to muscle damage. 

Clinical Manifestations

The onset typically occurs a few days after flu-like symptoms such as fever, cough, and malaise. Common symptoms include diffuse muscle pain (especially in the calves and thighs), tenderness, weakness, and, in children, difficulty walking or refusal to walk.

Diagnosis

• Based on clinical suspicion during an influenza outbreak or confirmed influenza infection
• Elevated CK supports the diagnosis
• Exclusion of other causes of myopathy or rhabdomyolysis 

Treatment

• Rest Adequate hydration
• Antipyretics and analgesics
• Antiviral therapy may be used
• Monitor for complications like rhabdomyolysis (rare but serious)

Prognosis

The prognosis is usually excellent, with most cases resolving spontaneously within a few days to a week. Full recovery is expected without any long-term muscle damage.

Coxsackie Virus Myopathy

Introduction

Coxsackie virus, part of the enterovirus family, is a common cause of viral infections in children and adults. While it typically causes mild symptoms such as fever, sore throat, or hand-foot-mouth disease, it can occasionally lead to muscle involvement in the form of myositis or viral myopathy. Coxsackie virus B is particularly associated with muscle complications.

Pathophysiology

The virus can invade and replicate within skeletal muscle tissue, causing direct muscle cell injury and inflammation. This may lead to muscle fiber necrosis, release of muscle enzymes into the bloodstream, and secondary immune-mediated damage. The infection can also affect cardiac muscle in some cases, leading to myocarditis.

Clinical Manifestation

Symptoms typically appear a few days after the onset of a general viral illness. Patients may experience diffuse muscle pain, tenderness (especially in proximal muscles like the thighs and shoulders), muscle weakness, difficulty walking (or refusal to walk in children), fever, and malaise. In severe cases, rhabdomyolysis may occur, presenting with dark urine and elevated creatine kinase (CK) levels.

Diagnosis

• Diagnosis is based on clinical presentation
• Elevated serum creatine kinase (CK)
• Viral PCR or serology for Coxsackie virus
• Urinalysis (may show myoglobinuria in rhabdomyolysis)
• Electromyography (EMG) in teh case of prolonged muscle weakness 
• Muscle biopsy (rarely needed) shows muscle fiber necrosis and inflammation

Treatment

• Rest and avoidance of strenuous activity
• Adequate hydration
• Pain management (e.g., acetaminophen)
• Monitoring for rhabdomyolysis or renal complications
• Hospitalization in severe cases

Prognosis

The prognosis is generally good. Most patients recover completely within days to weeks without long-term sequelae. Severe complications such as rhabdomyolysis or myocarditis are rare but require prompt medical attention.

HIV-Associated Myopathy

Introduction

Human Immunodeficiency Virus (HIV) can lead to various systemic complications, including muscle involvement. HIV-associated myopathy is a condition where muscle weakness and pain occur as a result of the viral infection itself or as a side effect of treatments. This myopathy can be part of the broader spectrum of HIV-associated muscle disorders, including HIV-associated wasting syndrome. It can be seen in both acute and chronic stages of HIV infection.

Pathophysiology

HIV can cause myopathy through several mechanisms. These include direct invasion of muscle tissue by the virus, immune-mediated inflammation, and side effects of antiretroviral drugs—especially nucleoside reverse transcriptase inhibitors (NRTIs)—which may lead to mitochondrial dysfunction and muscle toxicity. Additionally, HIV-associated cachexia can result in muscle wasting and weakness due to loss of body mass and energy.

Clinical Manifestation

HIV-related myopathy may present with muscle weakness, typically in the proximal muscles such as the shoulders and hips, along with muscle pain and tenderness—especially in the lower extremities. Patients may have difficulty with activities like walking, climbing stairs, or rising from a seated position, and in advanced stages, muscle wasting or significant atrophy can occur. Fatigue and general malaise are common, and in some cases, muscle pain may be present even without detectable weakness.

Diagnosis

The diagnosis of HIV-associated myopathy is based on clinical presentation, a history of HIV infection, and the exclusion of other causes. Elevated creatine kinase (CK) levels typically indicate muscle injury. Electromyography (EMG) and muscle biopsy may be used in severe cases to assess muscle inflammation and damage, while screening for other causes of muscle weakness, such as opportunistic infections or antiretroviral drug side effects, is also important. PCR testing or serology may be performed to confirm HIV infection if it has not been previously diagnosed.

Treatment

• Antiretroviral therapy (ART) to control HIV replication and improve immune function, which may help alleviate muscle-related symptoms over time
• Discontinuation or adjustment of medications causing muscle toxicity, particularly NRTIs, if suspected
• Supportive treatments, including physical therapy to maintain muscle strength, manage pain, and prevent further deterioration
• Pain management (e.g., non-steroidal anti-inflammatory drugs) for muscle discomfort
• Nutritional support and management of HIV-associated cachexia to prevent further muscle wasting

Prognosis

The prognosis for HIV-associated myopathy largely depends on the management of HIV infection and the early identification of potential complications. With effective antiretroviral therapy, many patients experience improvement in muscle symptoms. However, muscle wasting and weakness can be persistent in some cases, particularly in individuals with advanced HIV or those experiencing side effects from long-term ART.

Cytomegalovirus (CMV) Myopathy

Introduction

Cytomegalovirus (CMV) myopathy is a rare but significant complication in patients with CMV infection, particularly in immunocompromised individuals, such as those with HIV, organ transplant recipients, or individuals on immunosuppressive therapy. CMV can cause direct muscle inflammation and damage, leading to myopathy, although it is less common than other manifestations of CMV infection.

Pathophysiology

CMV can affect muscles through direct viral invasion, causing inflammation, muscle fiber necrosis, and myofiber damage. It can also trigger immune-mediated responses that contribute to muscle injury. In immunocompromised patients, CMV may lead to systemic infection with widespread tissue involvement, including the muscles, and can disrupt muscle metabolism and mitochondrial function, further exacerbating muscle damage.

Clinical Manifestation

CMV-associated myopathy typically presents with muscle weakness, especially in the proximal muscles like the hips and shoulders, making it difficult to rise from a seated position or climb stairs. Muscle pain or tenderness may occur, often accompanied by fever and malaise, particularly in immunocompromised individuals. Myalgias can become more pronounced after physical exertion, and significant muscle atrophy and weakness may develop in severe cases. CMV-related myopathy may also present alongside other systemic signs of CMV infection, such as fever, lymphadenopathy, or organ-specific involvement.

Diagnosis

• Elevated creatine kinase (CK) levels, indicating muscle injury or inflammation
• PCR testing for CMV in blood, tissue, or muscle biopsy samples
• Muscle biopsy may reveal viral inclusions, inflammation, and muscle fiber necrosis
• Electromyography (EMG) may show myopathic changes, but it is not specific to CMV
• CMV serology and viral cultures can help confirm the presence of active CMV infection
• Imaging studies may show muscle changes, though muscle biopsy is the gold standard for diagnosis

Treatment

• Antiviral therapy (e.g., ganciclovir, valganciclovir) treats active CMV infection and prevents viral replication.
• Discontinuation of immunosuppressive therapies, if applicable, or adjusting the dosage
• Supportive measures such as physical therapy to improve muscle strength, prevent atrophy, and manage pain
• Pain management with non-steroidal anti-inflammatory drugs (NSAIDs) or other analgesics
• Nutritional support and careful management of any underlying immunocompromised condition to aid recovery

Prognosis

The prognosis for CMV-related myopathy depends on the severity of the infection, the extent of muscle involvement, and the patient's underlying health. In immunocompetent individuals, CMV myopathy is rare and typically self-limited with appropriate antiviral therapy. In immunocompromised patients, especially those with advanced HIV or following organ transplantation, CMV myopathy may be more severe and persistent.

Epstein-Barr Virus (EBV) Myopathy

Introduction

Epstein-Barr Virus (EBV) is a common herpesvirus that primarily causes infectious mononucleosis (IM) but can also lead to various systemic manifestations, including myopathy. EBV myopathy is typically observed in immunocompromised individuals, such as those with HIV, organ transplant recipients, or patients undergoing immunosuppressive treatment. While EBV-related myopathy is rare, it can cause significant muscle weakness and inflammation in affected individuals.

Pathophysiology

EBV myopathy can occur through direct viral invasion of muscle tissue, resulting in inflammation and muscle cell damage. It may also involve immune-mediated mechanisms, where the body's response to the infection leads to muscle inflammation.

Additionally, EBV can cause systemic infection, contributing to muscle injury indirectly through fever, lymphadenopathy, and disturbances in muscle metabolism. The virus may further exacerbate muscle weakness by inducing mitochondrial dysfunction, oxidative stress, and metabolic changes within the muscle. 

Clinical Manifestation

Symptoms of EBV-related myopathy typically include proximal muscle weakness, particularly in the shoulders, hips, and legs, which can make walking, standing, or climbing stairs difficult. Muscle tenderness, pain, or stiffness may occur, often accompanied by fever and general malaise during the acute phase of infection. Fatigue and generalized weakness can persist even after the primary EBV infection has resolved. In more severe cases, patients may experience muscle atrophy and significant difficulty with basic motor functions, often alongside classic EBV symptoms such as fever, sore throat, lymphadenopathy, and splenomegaly.

Diagnosis

• Elevated creatine kinase (CK) levels reflect muscle injury or inflammation.
• Detection of EBV DNA in blood or muscle tissue via PCR.
• EBV serology to confirm current or past infection (e.g., presence of EBV-specific antibodies).
• Muscle biopsy may show viral inclusions, muscle fiber degeneration, and inflammation, although these are not specific to EBV.
• Imaging studies may show muscle edema, though muscle biopsy remains the gold standard for diagnosing EBV myopathy.
• Electromyography (EMG) can help assess muscle involvement, revealing myopathic changes typical of inflammatory myopathies.

Treatment

• Treatment for EBV myopathy generally involves: Antiviral therapy (e.g., acyclovir, valacyclovir) for acute EBV infection to limit viral replication and reduce symptoms.
• Supportive management of muscle weakness, including physical therapy to prevent atrophy, improve strength, and enhance mobility.
• Pain management with analgesics, particularly non-steroidal anti-inflammatory drugs (NSAIDs), to reduce muscle inflammation and discomfort.
• Immunosuppressive therapy may need to be reduced or adjusted if the patient is on such treatment, as it can exacerbate EBV infection and muscle damage.
• Nutritional support to help maintain muscle strength and overall health during recovery.
• Corticosteroids or other immunosuppressive drugs may sometimes be used in severe cases, though their use is typically reserved for cases with significant immune-mediated damage.

Prognosis

The prognosis for EBV-related myopathy depends on the severity of muscle involvement and the patient's overall health. The condition is usually mild and self-limiting in otherwise healthy individuals, improving as the EBV infection resolves. In immunocompromised patients, however, it can be more severe and prolonged, with a risk of long-term muscle weakness or atrophy. Early diagnosis and treatment with antivirals and supportive care can improve outcomes, though some individuals may continue to experience residual muscle fatigue and weakness even after recovery.

Staphylococcus aureus Myopathy

Introduction

Staphylococcus aureus is a common bacterium that can cause various infections, including skin infections, pneumonia, sepsis, and osteomyelitis. It can also lead to myopathy in rare cases, particularly in bacteremia or systemic infection. S. aureus myopathy is often seen in immunocompromised individuals, patients with long-term catheters, or severe infections involving multiple organ systems. The condition is characterized by muscle inflammation, weakness, and pain due to bacterial invasion or toxin production.

Pathophysiology

S. aureus myopathy can result from direct bacterial invasion of muscle tissue, leading to localized damage, inflammation, and necrosis. The bacteria also produce toxins, such as exotoxins, which may contribute to local and systemic muscle injury. In some cases, systemic infection and inflammation can cause rhabdomyolysis and metabolic disturbances, and abscess formation within the muscles may lead to severe pain and swelling.

Clinical Manifestation

Symptoms of S. aureus-related myopathy often include acute muscle pain and tenderness, typically localized to areas like the thighs, calves, or shoulders. Muscle weakness, especially in the proximal muscles, can make activities such as walking, climbing stairs, or daily tasks difficult. Fever, chills, and swelling or redness in the affected muscles are common, particularly if an abscess has formed. In severe cases, rhabdomyolysis may occur, leading to elevated creatine kinase (CK) levels, potential kidney damage, and septic shock if the infection is not managed correctly.

Diagnosis

• Clinical suspicion based on symptoms of muscle weakness, pain, and systemic infection (fever, chills, sepsis).
• Blood cultures detect the presence of S. aureus in the bloodstream, especially if bacteremia or sepsis is suspected.
• Elevated creatine kinase (CK) levels in the blood indicate muscle injury.
• Muscle biopsy may show evidence of bacterial infection, inflammation, or abscess formation in muscle tissue.
• Imaging studies (e.g., ultrasound or MRI) to identify abscesses or signs of muscle damage.
• PCR testing or culture from muscle tissue can confirm the presence of S. aureus in the affected muscle.

Treatment

• Antibiotics: Intravenous antibiotics such as vancomycin or clindamycin are commonly used to treat S. aureus infections. The choice of antibiotic may depend on whether the strain is methicillin-resistant (MRSA).
• Drainage of abscesses, if present, using surgical or needle aspiration techniques to remove the infected material from the muscles.
• Supportive care such as hydration, pain management with NSAIDs or opioids, and muscle rest to reduce inflammation and prevent further muscle damage.
• Rhabdomyolysis management: In severe cases, addressing rhabdomyolysis through intravenous fluids, monitoring kidney function, and electrolyte management may be necessary.
• Physical therapy to restore muscle strength and function after infection resolves.

Prognosis

The prognosis for S. aureus myopathy depends on the severity of the infection and the patient's overall health. Most patients recover without long-term muscle damage if treated early with appropriate antibiotics and supportive care. However, severe cases may lead to lasting muscle weakness, atrophy, or permanent damage, especially if kidney function is affected. Early diagnosis and aggressive treatment are essential for improving outcomes, as immunocompromised patients or those with delayed treatment may experience more severe complications.

Streptococcus pyogenes Myopathy

Introduction

Streptococcus pyogenes (Group A Streptococcus, GAS) is a gram-positive bacterium that can cause various diseases, from mild pharyngitis to life-threatening invasive infections. Though rare, S. pyogenes can lead to myopathy through direct muscle invasion (myositis), toxin-mediated damage, or secondary to necrotizing fasciitis. Myopathy caused by S. pyogenes is a medical emergency due to its rapid progression and potential for systemic toxicity.

Pathophysiology

S. pyogenes-related myopathy can arise from direct muscle infection, such as myositis, often following trauma or during bacteremia. In some cases, toxin-mediated injury occurs, particularly in streptococcal toxic shock syndrome (STSS), where superantigens trigger widespread immune activation and tissue damage. The condition may also be necrotizing fasciitis, a rapidly progressing soft tissue infection that invades muscle layers and causes severe systemic illness. Bacterial enzymes like streptolysins and hyaluronidase further drive muscle breakdown and local tissue destruction.

Clinical Manifestation

S. pyogenes myopathy typically presents acutely with severe, localized muscle pain and rapid swelling, tenderness, and redness. Systemic signs such as fever, chills, low blood pressure, and fast heart rate are common. Muscle weakness can develop quickly and may progress to immobility in affected areas. In severe cases, such as necrotizing fasciitis or streptococcal toxic shock syndrome (STSS), symptoms may include skin discoloration or necrosis, rash, multi-organ failure, and altered mental status.

Diagnosis

• Clinical suspicion, especially in patients with rapidly worsening muscle pain, systemic symptoms, or a history of trauma.
• Elevated creatine kinase (CK) indicates muscle damage.
• Leukocytosis and elevated inflammatory markers (CRP, ESR)
• Positive blood cultures for S. pyogenes
• Imaging (MRI or CT) to assess for myositis, abscess, or necrotizing fasciitis.
• Muscle biopsy or surgical exploration, if needed, may show necrotic muscle with neutrophilic infiltration and Gram-positive cocci.
• Rapid antigen detection or PCR for GAS can aid in identification.

Treatment

• High-dose penicillin is the mainstay, often combined with clindamycin (to inhibit toxin production). 
• Surgical debridement is required for cases involving necrotizing fasciitis or abscess formation to remove necrotic tissue. 
• Intensive care monitoring for patients with toxic shock or sepsis IV fluids and vasopressors, if needed 
• Pain control Intravenous immunoglobulin (IVIG) may be considered in severe cases (e.g., STSS) to neutralize superantigens.
• Physical therapy after stabilization to aid in recovery from muscle injury.

Prognosis

Early recognition and treatment are crucial for a favorable prognosis. With timely antibiotics and surgical intervention, recovery is possible, though some patients may have residual muscle weakness or scarring. Delayed treatment, especially in cases of STSS or necrotizing fasciitis, can result in severe complications or death, particularly in immunocompromised or elderly individuals.

Clostridium spp.-Associated Myopathy

Introduction

Clostridium species are anaerobic, gram-positive, spore-forming bacilli capable of causing severe soft tissue and muscle infections. Myopathy due to Clostridium—particularly Clostridium perfringens and Clostridium septicum—is rare but often life-threatening. These infections are commonly associated with trauma, surgery, injection drug use, or malignancy and may lead to gas gangrene (clostridial myonecrosis), a rapidly progressive necrotizing infection of muscle tissue.

Pathophysiology

Clostridial myopathy results from the direct invasion of muscle tissue by the bacteria and the release of potent exotoxins (e.g., alpha-toxin), which cause extensive tissue necrosis, gas production, and systemic toxicity. The toxins damage cellular membranes, impair blood supply, and trigger massive inflammatory responses. The anaerobic environment of devitalized muscle provides ideal conditions for Clostridium growth.

Clinical Manifestation

Clostridial myopathy typically presents acutely with sudden, severe localized muscle pain, swelling, and crepitus due to gas formation. The overlying skin may show discoloration, tense edema, or bullae. Systemic signs develop rapidly and include fever, tachycardia, hypotension, and altered mental status. Without prompt treatment, progression to septic shock and multiorgan failure is common. In cases involving C. septicum, infection may occur without trauma and is often associated with occult malignancy, particularly of the colon.

Diagnosis

• Clinical suspicion based on rapid progression, tissue gas, and systemic toxicity
• Imaging (X-ray, CT, or MRI): may show gas in soft tissues and muscle planes
• Laboratory findings: leukocytosis, elevated creatine kinase (CK), and metabolic acidosis
• Microbiology: Gram stain and anaerobic culture from wound/tissue; blood cultures often positive
• Surgical exploration may be needed for definitive diagnosis and debridement

Treatment

• High-dose penicillin plus clindamycin (to suppress toxin production)
• Urgent surgical debridement of necrotic tissue is critical and often lifesaving
• Hyperbaric oxygen therapy (HBOT) may be considered as adjunctive treatment in some centers
• Supportive care in ICU: fluids, vasopressors, mechanical ventilation as needed
• Monitoring for and management of complications such as renal failure and DIC

Prognosis

The prognosis depends on the speed of recognition and intervention. Mortality is high—especially without prompt surgical and medical treatment. Early aggressive therapy can significantly improve outcomes. Delayed treatment often results in limb loss, systemic complications, or death. C. septicum infections may also indicate an underlying malignancy and warrant further oncologic evaluation.

Myopathy Due to Trichinella spiralis

Introduction

Trichinella spiralis is a parasitic nematode that causes trichinosis primarily by consuming undercooked or raw meat from infected animals, particularly pork. While trichinosis often presents with gastrointestinal and systemic symptoms, it can also lead to myopathy when the larvae invade skeletal muscle. This myopathy is due to the encystment of the larvae in muscle tissue and the following inflammatory response.

Pathophysiology

After ingesting infected meat, the Trichinella larvae mature and encyst in the muscle tissues. The larvae trigger an immune response in the host, leading to inflammation and muscle damage. The inflammatory process involves eosinophils and other immune cells infiltrating muscle tissue, causing pain, swelling, and dysfunction. Muscle weakness results from the direct effects of the larvae and the inflammatory process surrounding the cysts.

Clinical Manifestation

Myopathy in Trichinella infection typically presents with muscle pain, weakness, and tenderness, especially in the upper arms, legs, and diaphragm. Symptoms usually occur within 1-3 weeks after ingestion and are often associated with fever, gastrointestinal symptoms (diarrhea, nausea, vomiting), and swelling of the eyelids and face. Muscle involvement may progress to more generalized weakness, difficulty with movement, and respiratory complications due to diaphragm involvement.

Diagnosis

• Clinical suspicion based on exposure history (eating undercooked meat, particularly pork)
• Serological tests: detection of Trichinella-specific antibodies
• Muscle biopsy: Identifying Trichinella larvae within muscle tissue 
• Elevated eosinophil count in blood samples PCR-based techniques can be used to detect Trichinella DNA

Treatment

• Anti-parasitic therapy: Mebendazole or Albendazole are commonly used to kill the larvae
• Steroids: To reduce inflammation and muscle damage
• Pain management and anti-inflammatory drugs: For muscle pain and swelling
• Supportive care: Hydration, nutrition, and respiratory support if needed

Prognosis

With early treatment, the prognosis is generally favorable. Most individuals recover with minimal long-term effects, although severe cases can lead to lasting muscle weakness, particularly if treatment is delayed. In some cases, the disease can lead to life-threatening complications, such as respiratory failure or myocarditis.

Myopathy Due to Toxoplasma gondii

Introduction

Toxoplasma gondii is a protozoan parasite that infects humans and other warm-blooded animals. In most cases, Toxoplasma infection is asymptomatic or mild, but in immunocompromised individuals, it can cause more severe systemic illness, including myopathy. Toxoplasma can invade skeletal muscle and cause inflammation, leading to muscle pain and weakness.

Pathophysiology

The parasite is transmitted primarily through undercooked meat or contact with cat feces. Once ingested, Toxoplasma forms cysts in various tissues, including muscle. The parasite induces an inflammatory response in infected muscle tissue, causing localized muscle damage and pain. The immune system’s reaction to the cysts can lead to muscle cell death and impaired muscle function.

Clinical Manifestation

Myopathy due to Toxoplasma infection typically presents with muscle pain, weakness, and tenderness. It is often associated with systemic symptoms such as fever, headache, lymphadenopathy, and malaise. In immunocompromised individuals, such as those with HIV/AIDS, myopathy can be more severe and widespread. Symptoms may be subtle or can progress to significant muscle weakness, particularly in the limbs and respiratory muscles.

Diagnosis

• Serological testing: Detection of Toxoplasma antibodies (IgG and IgM)
• PCR testing: Detection of Toxoplasma DNA in blood or muscle tissue
• Muscle biopsy: Demonstration of Toxoplasma cysts in muscle fibers
• Imaging: MRI or CT scans may show muscle inflammation or involvement in severe cases

Treatment

• Antimicrobial therapy: Pyrimethamine and sulfadiazine, often with folinic acid, are the standard treatment regimen for Toxoplasma infection
• Corticosteroids: In severe cases, corticosteroids may be used to reduce inflammation
• Supportive care: Analgesics for muscle pain and management of other systemic symptoms In immunocompromised individuals, prompt treatment is critical to prevent severe complications.

Prognosis

The prognosis of Toxoplasma myopathy depends on the patient's immune status. In immunocompetent individuals, myopathy is typically self-limiting, and full recovery is common. In immunocompromised individuals, the disease can lead to chronic muscle weakness and other systemic complications, requiring more intensive treatment.

Myopathy Due to Sarcocystis spp.

Introduction

Sarcocystis spp. are intracellular protozoan parasites that infect various vertebrates, including humans. Human sarcocystosis is more commonly intestinal and asymptomatic, but in rare cases, it can cause muscular sarcocystosis—a form of myopathy that arises when the parasite invades skeletal muscle. This is usually associated with Sarcocystis nesbitt and occurs sporadically or in outbreaks, particularly in Southeast Asia.

Pathophysiology

Humans may become accidental intermediate hosts by ingesting sporocysts from contaminated water or food. The parasites migrate via the bloodstream, forming sarcocysts (tissue cysts) in skeletal muscle. The host’s immune response to the encysted parasites causes muscle inflammation, damage, and associated symptoms. The process involves infiltration of eosinophils, lymphocytes, and muscle fiber necrosis.

Clinical Manifestation

Myopathy due to Sarcocystis spp typically presents with an acute or subacute onset of muscle pain, tenderness, and weakness, often in the limbs and trunk. Some patients develop facial or orbital swelling and low-grade fever. Eosinophilia is a common laboratory finding. In more severe or prolonged cases, symptoms may include difficulty with ambulation or chewing, depending on which muscles are affected. Unlike other parasitic myopathies, gastrointestinal symptoms are less prominent.

Diagnosis

• Exposure history: Travel to endemic areas (e.g., Malaysia) and possible ingestion of contaminated water
• Blood tests: Eosinophilia, elevated muscle enzymes (e.g., CK)
• Serological testing: No standardized commercial tests are available; experimental assays may be used
• Muscle biopsy: Identification of sarcocystosis within muscle fibers and surrounding inflammatory infiltrates
• PCR: Detection of Sarcocystis DNA in tissue (used in research settings)

Treatment

• Antiparasitic therapy: Albendazole is often used empirically, though efficacy is not well-established
• Steroids: May be used in moderate to severe cases to reduce inflammation and muscle damage
• Supportive care: Analgesics for muscle pain, hydration, and physical therapy as needed

Prognosis

The prognosis is generally favorable in immunocompetent individuals, with most patients recovering over weeks to months. However, prolonged fatigue and residual myalgia may persist. Severe or recurrent cases are rare but may require extended supportive care. In immunocompromised patients, muscle damage may be more extensive.