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The principal intestinal Entozoa to describe are roundworms, threadworms, whipworms and tapeworms; the chief visceral larval form is the hydatid. “In this country” refers to the British setting of the paper. It is not a claim that all human helminths were common or acquired locally. A contemporary account already distinguished Nematoda, Cestoda and Trematoda, and recognised that an adult worm and a larval cyst could be different phases of one life cycle.^[ref] The life cycles below use present knowledge to explain transmission; their inclusion does not imply that every migratory stage or intermediate host was established in 1865.

Ascaris lumbricoides lives as a large, cylindrical, unsegmented, tapering roundworm in the small intestine; adults are cream-coloured or pinkish and roughly 15–35 cm long, with the male generally smaller and its tail curved. Eggs leave in faeces and become infective after development in the environment. After ingestion, larvae cross the intestinal wall, pass through the liver and lungs, ascend the airway, are swallowed and mature in the small intestine. Adults can wander into the bile ducts. The pulmonary migration belongs to the larval history, not to the usual location of the adult.^[ref]

Enterobius vermicularis, the threadworm, is a small white nematode of the caecal and adjacent colonic region. The female is about 8–13 mm long and has a conspicuous pointed tail; the male is shorter. The gravid female migrates to the perianal skin and deposits eggs, often at night, so itching and transfer by contaminated fingers favour renewed infection. Eggs become infective rapidly; a pulmonary migration is not part of its usual life cycle. This explains why a perianal adhesive sample can be more useful than an ordinary stool examination.^[ref]

Trichuris trichiura, historically Trichocephalus dispar, inhabits the caecum and colon. The adult is about 3–5 cm long, with a very slender anterior portion embedded in the mucous membrane and a thicker posterior portion projecting into the lumen: the outline resembles a whip. Eggs pass in faeces, mature in soil and infect after ingestion. The adult shape and the characteristic eggs with polar plugs distinguish it from the preceding worms.^[ref]

Adult Taenia are flat, ribbon-like tapeworms, several metres long, with a small attachment head or scolex, a narrow neck and a chain of proglottids. Taenia solium has four suckers and a hooked rostellum; Taenia saginata, also called Taenia mediocanellata in period literature, has four suckers but lacks that crown of hooks. Their larval cysticerci occur in pig and cattle tissues respectively; ingestion of inadequately cooked infected meat permits an adult to develop in the human small intestine. Eggs and segments pass in faeces. Egg appearance alone does not reliably distinguish these two species.^[ref]

For Taenia solium, swallowing eggs is a different event from swallowing pork cysticerci: eggs can establish tissue cysticercosis in humans, including abdominal tissues, whereas pork larvae cause intestinal taeniasis. A cysticercus is a small fluid-filled bladder with an invaginated scolex, not a miniature chain of segments.^[ref]

The hydatid of Echinococcus granulosus is particularly important in the liver. Humans acquire eggs from contamination associated with infected dogs and act as intermediate hosts. Larvae reach viscera and form a fluid-filled cyst with a laminated wall and an inner germinal layer; brood capsules, protoscolices and sometimes daughter cysts develop inside. The tiny adult tapeworm belongs in the dog's intestine, not as the normal human liver worm. Dogs complete the cycle by eating infected viscera from an intermediate host.^[ref]

Less usual examples deserve proportionate mention. Diphyllobothrium latum is a broad, segmented fish tapeworm with two longitudinal attachment grooves rather than four suckers; aquatic intermediate hosts and infected fish link it to humans. It should not be presented as a uniformly common British infection.^[ref] Fasciola hepatica, a leaf-shaped fluke roughly 2–3 cm long with oral and ventral suckers, can inhabit the bile ducts; its cycle requires a freshwater snail and infective stages on aquatic vegetation. Human disease was an unusual counterpart of an important infection of grazing animals.^[ref] Trichinella spiralis has minute intestinal adults after ingestion of infected meat, but its enduring encysted larvae occupy skeletal muscle; those muscle cysts should not be misdescribed as the typical abdominal hydatid.^[ref]

Gross form and location guide identification, but microscopy of eggs, larvae or segments and knowledge of the life cycle supply the confirmation.

The signs depend on the obstructed site: a stone in the cystic duct, the common bile duct and the outlet shared with the pancreatic duct can produce different syndromes. “An impacted gallstone” is not enough anatomical information to choose a treatment.

A typical pain pattern is severe upper abdominal pain, often in the right upper quadrant or epigastrium, sometimes radiating to the back or shoulder, with nausea and vomiting. Despite the term “colic”, the pain can remain steady during an attack. Persistent focal tenderness with fever suggests acute cholecystitis rather than an uncomplicated transient obstruction. Cystic-duct obstruction does not necessarily obstruct hepatic bile flow and therefore need not produce jaundice.

A stone obstructing the common bile duct can produce jaundice, dark urine and pale stools. Fever or rigors with jaundice and biliary pain raises concern for acute cholangitis, while shock or altered awareness indicates serious illness. Obstruction at the distal outflow can precipitate acute pancreatitis, often with prominent pain radiating to the back and vomiting. These are patterns to investigate, not findings supplied by the examination; absence of a full classical combination does not exclude dangerous obstruction.^[ref]

An 1866 clinician would try to establish the pain's origin, look for jaundice, observe the urine and stools, relieve severe pain, support fluid intake and watch for persistent obstruction or inflammation. Warm external applications and an opiate were among the symptomatic measures of the period. Passage of a recovered stone could strengthen the diagnosis, but failure to find one in the stool did not disprove it, and temporary relief did not demonstrate duct clearance. Neither a purgative nor an asserted stone-dissolving mixture could be assumed to free an impacted duct. These are reconstructions of the diagnostic and palliative aims available before modern duct imaging and endoscopic treatment, not a current management recipe.

Modern correction: investigate promptly and relieve consequential obstruction, rather than treating the pain alone. Obtain appropriate examination, liver function tests and ultrasonography. If suspicion of common-duct stones remains because of abnormal tests or duct dilatation despite no stone being shown, magnetic resonance cholangiopancreatography can clarify the ducts; endoscopic ultrasonography is an additional option when needed. Evaluate for acute pancreatitis and other causes of an acute abdomen. Relief of pain, fluid support and treatment of associated illness proceed alongside investigation.^[ref]

Symptomatic gallbladder stones generally lead to consideration of laparoscopic cholecystectomy; early surgery is recommended for suitable acute cholecystitis. Common-duct stones require duct clearance, endoscopically or surgically as appropriate.^[ref] Acute cholangitis requires urgent treatment of infection and biliary decompression. Antibiotics and resuscitation do not remove an obstructing stone. Endoscopic drainage is generally preferred when feasible; stone removal may accompany it if the person's condition permits, while an unstable person may need decompression before a more extensive procedure.^[ref] This is why prolonged pain with jaundice or fever cannot safely be managed merely by repeating historical analgesic mixtures.

The liver is both a metabolic processing organ and the producer of bile. These functions must be distinguished: much of what the liver contributes to the body enters the blood, whereas bile is its secretion into the digestive system.

Portal venous blood brings absorbed materials from the alimentary organs to the liver, while the hepatic artery supplies oxygenated blood. Within the hepatic sinusoids, the incoming blood encounters hepatocytes and scavenging Kupffer cells. Hepatocytes take up, transform, store and release substances; their bile canaliculi conduct bile towards the bile ducts. The organ's position therefore makes it a useful regulator between absorption from a meal and supply to the rest of the body.

Its main non-biliary functions include the following:

This modern list extends beyond the knowledge and biochemical vocabulary of 1867. It is consistent with the organ's combined metabolic, storage and clearance roles, rather than treating bile production as the whole explanation.^[ref]

Bile contains water, electrolytes, bile salts, phospholipids, cholesterol and bilirubin conjugates. Hepatocytes form the primary secretion; ductal epithelium modifies it. The gallbladder stores and concentrates bile between meals and releases it into the duodenum. Production of bile must therefore be distinguished from its intermittent delivery to a meal.

Its two central functions are assistance with lipid digestion and nutrient absorption, and excretion of selected waste substances. Amphipathic bile salts help disperse dietary fat and form mixed micelles carrying products of lipid digestion to the absorptive surface of the small intestine. They thereby promote uptake of fatty acids, monoglycerides, cholesterol and fat-soluble vitamins. Bile is not itself a source of pancreatic lipase, nor does emulsification chemically hydrolyse triglycerides. Biliary bilirubin, produced through haem breakdown, provides an excretory route; cholesterol and selected other substances also leave in bile. Most secreted bile salts are recovered, especially in the terminal ileum, and return through the portal vein: the enterohepatic circulation conserves the useful detergent.^[ref]

Two comparisons reveal why both sorts of function matter. First, compare a fresh liver extract with an extract prepared after an appropriate controlled interval: testing for reducing sugar and isolating glycogen distinguishes a stored precursor from newly liberated glucose. A reliable interpretation needs prompt sampling and controls because post-mortem glycogenolysis can change the result after the animal has died; detecting sugar in an organ alone does not prove where all of it was made. Secondly, in classical biliary fistula observations, diverting bile away from the intestine while collecting it separately allowed its output to be measured and the loss of normal fat assimilation to be examined. Comparing faecal fat with and without delivery of bile distinguishes a digestive contribution from a merely excretory one. The modern explanation is that loss of intestinal bile salts impairs mixed micelle formation, while jaundice from retained biliary pigment is a separate consequence of failed pigment elimination.