Paragonimus spp. are parasitic flatworms known as lung flukes. A fluke is a type of trematode, which is a flat, leaf-shaped worm that infects humans through food. These parasites most often enter the body when someone eats raw or undercooked freshwater crabs or crayfish that contain the infectious larval stage. Once swallowed, the larvae pass through the stomach and intestine before migrating through the abdominal cavity and eventually into the lungs, where they mature.
The biology of Paragonimus involves several stages of tissue invasion. After ingestion, the larvae penetrate the intestinal wall. Penetration means the larvae physically break through the gut lining to travel deeper into the body. That movement can cause abdominal pain, diarrhea, and eosinophilia, which is a rise in a specific white blood cell type involved in allergic responses and parasitic infections. This early gut phase explains why some patients initially experience gastrointestinal symptoms rather than the coughing and chest pain more typical of lung disease.
Once the parasite reaches the lungs, the adult flukes create cyst-like cavities that can lead to chronic cough, blood in sputum, and chest discomfort. Because these symptoms overlap with tuberculosis and lung cancer, misdiagnosis is common. Some species can stray from the lungs and form ectopic infections in the brain, skin, or abdomen, creating a wide range of possible symptoms.
Paragonimus infection also provides a window into the gut–lung axis, which is the two-way communication system between the gastrointestinal tract and the lungs. Research in respiratory infections shows that inflammation in the lungs can alter gut microbiome composition. While direct studies of Paragonimus and the microbiome are limited, lung infections in general can decrease microbial diversity and shift key microbial families. These shifts can weaken immune regulation and may worsen disease severity. That said, no studies yet demonstrate a consistent microbiome signature specific to Paragonimus.
High parasite burden can intensify both lung and gut symptoms, while mild infections may go unnoticed for years. Low parasite load may still trigger changes in immune signaling pathways, including cytokines, which are chemical messengers that coordinate inflammation. These immune shifts can contribute to symptoms even when imaging or stool tests are negative. Conversely, a patient may have symptoms without an active infection if inflammation persists after the parasite has died. Because stool testing often misses Paragonimus eggs early in infection, clinicians may need serology or imaging to confirm the diagnosis.