AGENT FACTORS:

Capillaria philippinensis

Capillaria hepatica

Capillaria aerophila

Capillaria plica

ENVIRONMENTAL FACTORS:
A. External Environment
Temperate and tropical zones on every continent and infestation rates of wild-caught rats of up to

100% have been reported.

Air and damp soil.

Unsanitary environment

Rainy season

Ambient temperature

B. Internal Environment
Human jejunum: lumen, mucosa and crypts of Lieberkuhn

Mammal, fishes, amphibian

Immunocompromised individuals

Intestines of freshwater and blackish-water fish from lagoons in endemic areas

HOST FACTORS:
Definitive host: Fish eating bird

Intermediate host: fish

Accidental host: human

Children under the age of 5.

People with unsafe eating practices/food preferences: eating raw fish

Poor hygiene: toilet practices

TISSUE AND PHYSIOLOGIC CHANGES

Reduction in the thickness of the intestinal mucosa, flattening or complete destruction of the

intestinal villi, deepening of the crypts of Liberkuhn, and localized inflammation.

Generalized malabsorption, hypoproteinemia, low blood calcium, low potassium, and

hypocholesterolemia.
Crypts were atrophic and contained parasites or cellular debris.

Mucosal gland dilation.

Lamina propria was infiltrated with plasma cells, lymphpcytes, macrophages, eosinophils and
neutrophils.

Loss of adhesion specialization and widespread separation of epithelial cells.

Micro-ulcers in the epithelium.

Chronic inflammation and encapsulation of the dead worms in collagen fibers, and eventually to

septal fibrosis (abnormal connective tissue growth) and cirrhosis of the liver.
Septal fibrosis originates from several portal spaces simultaneously

Fatty metamorphosis: liver

Renal vacuolization: renal proximal tubular lining cells

Vacuolization of the straited muscle.

SIGNS AND SYMPTOMS

Diarrhea (4-5 up to 8-10) watery stools per day. borborygmi, and vague abdominal pain

Weight loss, malaise and vomiting

Abdominal distension, epigastric tenderness, edema, cachexia

Abdominal pain in the liver area, decreased appetite, fever and chills, hepatitis (liver

inflammation), ascites (excess fluid in the peritoneal cavity) and hepatolithiasis (gallstones in the
bile ducts)
Diminished reflexes, distant heart sounds, hypotension, gallop rhythms and pulsus alterans
(cardiomyopathy)

Pronounced eosinophilia

ILLNESS

DISABILITY
Generalized malabsorption

DEFECT
Reduction in the thickness of the intestinal mucosa, flattening or complete destruction of the

intestinal villi, deepening of the crypts of Liberkuhn.

Generalized malabsorption: hypoproteinemia, low blood calcium, low potassium, and
hypocholesterolemia.

CHRONIC STATE

Chronic inflammation and encapsulation of the dead worms in collagen fibers, and eventually to

septal fibrosis (abnormal connective tissue growth) and cirrhosis of the liver.
Generalized malabsorption

Weight loss

Ascites (excess fluid in the peritoneal cavity) and hepatolithiasis (gallstones in the bile ducts).

Septal fibrosis originates from several portal spaces simultaneously.

Fatty metamorphosis: liver

Pronounced eosinophilia

DEATH