Richard de Grijs
Sydney, Australia

In October 1770, H.M. Bark Endeavour limped into the port of Batavia, capital of the Dutch East Indies (present-day Jakarta, Indonesia), after having almost foundered on the Great Barrier Reef. The hardy crew of Captain James Cook (1728–1779), although renowned for their good health throughout the three-year voyage (1768–1771), soon fell prey to something that was far more insidious than coral reefs or storms: tropical dysentery.

Captain Cook was known to be unusually meticulous about his crew’s diet and cleanliness. He had successfully held off the devastating effects of scurvy for much of their expedition. Yet in Batavia, the Endeavour encountered an enemy against which they were far less prepared. Within weeks, many of Cook’s men were “poisoned by the bacteria that infested [their] supplies.”¹ Despite his best efforts, almost one-third of the Endeavour’s crew succumbed to what had commonly become known as the “bloody flux.”^2,3

Dysentery—resulting in bloody diarrhea, abdominal pain, and dehydration—was a pervasive threat during the Age of Sail. Although its causes remained poorly understood until the nineteenth century, the condition’s symptoms were well-known, feared, and often fatal. In the confined, unsanitary, and nutritionally deficient world of eighteenth-century naval life, dysentery thrived like never before.

Eighteenth-century shipboard conditions were uniquely conducive to disease. Food preservation was rudimentary—salted meats, ship’s biscuit, and dried peas formed the staple diet, and all were vulnerable to rot, mold, and infestation. Fresh produce, if available at all, rarely lasted beyond the first weeks following a port call. Water was stored in casks, often collected from poor sources and tainted with organic material; it grew rank with algae or leaked through the wood. The sailors’ poor diet, deficient in fiber and vital nutrients, upset digestive health and rendered the crew vulnerable to bowel complaints.

Diarrhea—typically three or more loose stools per day—was the mildest of their routine afflictions. Nevertheless, the loss of fluids presented a real danger, particularly in tropical climates where sailors were already prone to dehydration. It was often caused by enteric (intestinal) pathogens—bacteria, viruses, or parasites—spread by improperly handled food or water contaminated by fecal material. Medical treatment was limited: surgeons might prescribe a restricted diet, administer mild sedatives for intestinal spasms, or resort to emetics (vomit-inducing agents) to purge the stomach.⁴ More often than not, they simply waited and hoped for divine intervention.

Yet diarrhea could worsen. Prolonged episodes might develop into “flux,” a more serious and distressing condition. In 1790, naval surgeon Frederick Thomson suggested that fluxes were provoked by “coarse, indigestible food [and] the warm, humid air they breathe in betwixt decks.”⁵ We now know that the principal culprit was bacterial invasion of the large intestine. As one naval surgeon described it in clinical, if disturbing, detail:

… a frequent and plentiful discharge of thin, watery, frothy, greasy or blackish stool, sometimes mixed with the excrements, and sometimes not, but without blood, and without any inflammation or ulcers in the bowels … it is frequently attended with gripings [cramps], but not always … The patient is weak, makes but little water, has a poor appetite and is sometimes feverish.⁶

These symptoms, while alarming, were not yet the full manifestation of dysentery. Flux was painful and debilitating, but it was the progression to dysentery that signaled real danger.

The bloody flux

Dysentery was the most feared of all gastrointestinal complaints. It was distinguished by the passage of blood- and mucus-streaked stools, accompanied by intense abdominal cramping, a constant yet futile urge to defecate, and sometimes even rectal prolapse (protrusion) from repeated straining. In advanced cases, dehydration and systemic inflammation might rapidly result in death.

Naval records are replete with references to dysentery outbreaks. The bloody flux was endemic aboard ships in the tropics, particularly during the rainy season when fresh water was often sourced from swamps or other stagnant supplies. Captain Cook’s experience in Batavia was emblematic: after months at sea, the crew’s immune systems may have become somewhat adapted to their own contaminated food and water environment, but external, shore-bought supplies introduced new pathogens to which they had no resistance.

Dysentery was more likely contracted ashore than at sea, and stopovers meant to replenish provisions often undermined months of shipboard discipline and cleanliness. Tropical fruits (especially coconuts), fresh alcohol, and poor water supplies disrupted digestive health.⁷ In the West Indies, where death from bowel disease was a common occurrence, it was said that “nineteen in twenty” European sailors died from “fevers and fluxes.”⁸

Throughout the eighteenth century, dysentery remained medically enigmatic. Naval surgeons debated whether the condition stemmed from corrupted humors, environmental miasmas (unhealthy smells or vapors), or from moral failings such as “fear and other passions of the mind.”⁹ A consensus of sorts was that dysentery was both contagious and environmental, exacerbated by “intemperate” climates and filth. Yet no clear theory of its pathology emerged until the bacterial and protozoal (single-celled) distinctions were drawn in the late nineteenth century.

Even then, contemporary practitioners struggled to agree on effective treatments. The Royal Navy physician William Cockburn (1669–1739) famously developed an “anti-dysentery electuary” (a sweet medicine in powder form)¹⁰ that became standard issue in the early 1700s. He reportedly cured an entire ship of a severe outbreak in a single day, earning the support of senior naval officers. His remedy—probably a blend of purgatives and astringents (lotions)—was supplied to both navy and army doctors for decades. However, by 1757, its efficacy was questioned. The “Sick and Hurt Board,” the body responsible for naval health, dropped it from standard use for want of proven results.

Still, alternatives were few. Trials of other treatments—including those proposed by Edward Hogben¹¹ (1737–1763) and Gulielmi Pinto¹²—produced disappointing results, with most failing to cure patients. Remedies included bleeding (removing up to eight ounces of blood), emetics, and various mucilaginous (viscous) enemas.¹³ Naval surgeons in the Caribbean experimented with indigenous remedies: pomegranate rinds, guava bark, cassava starch, and even lemon-tree mistletoe teas.¹⁴ These occasionally relieved symptoms, but none were actual cures.

Among the more reliable agents were calomel (mercury chloride) and ipecacuanha (ipecac)—both emetics and purgatives used to clear the bowels.¹⁵ While these concoctions may have alleviated symptoms by removing infected material, they could also exacerbate dehydration, sometimes hastening the patient’s decline.

The epidemic at sea

To the Royal Navy, dysentery was not just a medical concern but a strategic threat. As Surgeon-General Benjamin Moseley (1742–1819) put it during the American War of Independence, “If the cause of humanity were not alone a sufficient motive to induce to this research, we need but turn our eyes on [the] political field; there we may behold the best concerted measures defeated by its influence.”¹⁶ Ships could lose upward of a quarter of their crews without ever engaging the enemy. Fleets in the West Indies or off the African coast often reported mortality not from combat but from bowel disease.

The seasonal character of dysentery also troubled naval commanders. Observations by Robert Robertson (1813–1885) and others revealed that it peaked in the humid months—August and September in the northern hemisphere—and in tropical zones where stagnant air and rotting organic matter bred illness. Yet prevention remained elusive. “Cleanliness is the key to relieve the disease,”¹⁷ Robertson concluded, noting that sick bays in particular needed constant scrubbing.

Captain Cook’s experience supported this view. His insistence on fresh air, dry decks, regular cleaning, and careful provisioning significantly reduced the prevalence of scurvy and fevers. Nonetheless, even he could not prevent dysentery when infected supplies were taken aboard.  

Dysentery’s ambiguous origins—partly environmental, partly microbial—meant that few efforts at prevention or cure were reliably successful. The close shipboard quarters, where men shared food bowls, slept in hammocks inches apart, and relieved themselves near drinking water, made hygienic control nearly impossible.

Only with the emergence of germ theory in the late nineteenth century did the picture begin to clear. Dysentery was identified as two distinct diseases: bacillary dysentery, caused by Shigella bacteria, and amebic dysentery caused by the protozoan Entamoeba histolytica. The former responds well to antibiotics, whereas treatment of the latter remains more elusive. Yet both are still major global health concerns, particularly in regions without clean water supplies.

During the Age of Sail, dysentery was more than a medical inconvenience. It was a persistent scourge that shaped naval life, sapped military strength, and haunted the memories of surgeons and sailors alike. Its bloodied symptoms marked ships as places of suffering, and its resistance to early medical intervention underscored the limits of Enlightenment science when confronted with the realities of the lower decks.

Whereas Captain Cook is rightly praised for his efforts to safeguard his men’s health, the deaths at Batavia remind us that even the most forward-thinking commanders could not always outwit the microbial world. Ironically, Cook’s greatest failure in disease prevention occurred at a port, not at sea. Dysentery—bloody, relentless, and fatal—thus served as a grim constant amid the uncertainties of naval exploration during the long eighteenth century.

References

1. Collingridge, V, Captain Cook: The Life, Death and Legacy of History’s Greatest Explorer (London: Ebury Press, 2003), 243.
2. McDermott, PJ, “Pacific Exploration,” The Brisbane Courier, 6 November 1878, p. 5.
3. Hough, R, Captain James Cook (London: Hodder and Stoughton, 1995).
4. Convertito, C, The Health of British Seamen in the West Indies, 1770–1806. PhD Thesis, (University of Exeter, UK, 2011), 75.
5. Thomson, F, An Essay on the Scurvy: shewing Effectual and Practicable means for its Prevention at Sea. With some Observations on Fevers, and Proposals for the more Effectual Preservation of the Health of Seamen, (London, unpaginated, 1790).
6. Anonymous, The Ship-Master’s Medical Assistant; or Physical Advice to all masters of ships who carry no surgeons; particularly useful to those who trade abroad in hot or cold climates. Containing a brief description of diseases, especially those peculiar to seamen in long voyages. With a concise method of cure, the result of many years practice and experience in all climates, (London, unpaginated, 1777).
7. Convertito, Health of British Seamen, 77.
8. Lind, J, An essay on the diseases incidental to Europeans in hot climates. With the method of preventing their fatal consequences. (London, 1777), 9–10.
9. Lettsom, JC, Of the Dysentery or Flux, (London, unpaginated, ca. 1767).
10. National Maritime Museum, Greenwich. Admiralty record ADM/E/18: Letter from a Mr Latouche to the Admiralty, 21 January 1757; see also Convertito, 121.
11. National Maritime Museum, Greenwich. ADM/F/17: Letter from the Sick and Hurt Board to the Admiralty, 14 April 1758.
12. National Maritime Museum, Greenwich. ADM/E/35: Letter from Gulielmi Pinto to the Admiralty, 26 March 1762.
13. Lettsom, Of the Dysentery.
14. Convertito, Health of British Seamen, 123.
15. Lettsom, Of the Dysentery.
16. Haycock, DB, “Exterminated by the bloody flux,” Journal for Maritime Research 4:1 (2002): 15–39.
17. Robertson, R, Metrological and Physical Observations made in 1769, 1772, 1773 and 1774, on the Coast of Africa and in the West-indies (London: Printed for E. and C. Dilly, J. Rorson, T. Cadwell, and T. Evans, 1769), 170.