150 Typhomalarial Fever

Typhomalarial fever as a specific disease is not recog­nized by medical authorities today, but for the last half of the nineteenth century it was a frequently useful diagnostic category of diverse and often impre­cise meaning.

Distribution and Incidence

William Osler once wrote that typhomalarial fever existed “in the minds of doctors but not in the bodies of patients.” If so, it existed in the minds of many American doctors in the South, Midwest, and western regions of the country as well as in the minds of military and other European physicians practicing in the unsanitary, malarious regions of the globe, par­ticularly the Mediterranean, British India, and some areas of China. It was primarily an Anglo-American phenomenon, although there are a few reports from southern Europe, which indicate that the possibility of the diagnosis was at least considered.

Etiology and Epidemiology

Typhomalarial fever was generally regarded as a noncontagious, infectious disease that resulted from exposure to the atmospheric or environmental in­fections or toxins that caused malarial fevers and typhoid fevers. Most commonly, patients were previ­ously debilitated, or their vital powers were de­pressed in some way. In Woodward’s classic formula­tion, this was the result of the depression produced by army camp life and malnutrition — particularly in­cipient scurvy. The disease required an area of en­demic malarial fever, frequently a marsh, into which the animal causes of typhoid fever — crowding and improper sanitation - intruded.

Clinical Manifestations and Pathology

The clinical course of the disease was extremely var­ied, depending on whether the malarial or typhoid elements predominated. When the malarial element was dominant, the symptoms were those of periodic fever - usually of the remittent rather than the inter­mittent variety. It was frequently quotidian but could be tertian, quartan, or irregularly remittent. How­ever, the patient was more than usually depressed; there were frequent central nervous system symp­toms, commonly stupor or coma, as well as gastroin­testinal complaints, most commonly diarrhea. The disease was of more rapid onset than classic typhoid fever, but if the typhoid elements dominated, the dis­ease would clinically resemble typhoid fever except for a definite periodicity, frequent hepatic tender­ness, and a greater degree of splenomegaly, often with pain on palpitation. The convalescence would be more rapid than typical typhoid fever.

At postmortem there was a “greater tendency to the deposit of black pigment in the enlarged folli­cles” of the small bowel in typhomalarial than in typhoid fever. Furthermore, there were, in Wood­ward’s (1863) formulation, some differences in the enlargement of the intestinal glands, the glands ris­ing more gradually from the Sturounding tissue in typhomalarial fever cases than in typhoid. By 1876, however, Woodward denied the significance of this supposed difference.

History and Geography

Woodward’s concept was bom of the frustrations of mid-nineteenth-century medicine, particularly in America.

1800-50

At the beginning of the nineteenth century, diagno­sis was based almost entirely upon patient descrip­tions of their complaints - that is, the perceived func­tional derangements that resulted in a consultation with the physician. The physicians placed these com­plaints in the context of their own experience and knowledge, made a diagnosis, and offered the pa­tient their professional advice.

The two main categories were periodic and contin­ued fever, but they were also categorized by such terms as malignant, pernicious, epidemic, putrid, spotted, and bilious, based upon the understandings of the physician observing a particular case. Periodic fevers - intermittent and remittent fevers, which had a classic periodicity — were believed to be caused by the atmospheric contamination of vegetable de­composition associated with marshes and other well- recognized areas of periodic-fever endemicity. Dur­ing the nineteenth century, this poison came to be called “malaria,” and the fevers it caused were “ma­larial” fevers. The continued fevers were more vari­able: Some were of short duration and only an incon­venience to the patient, whereas others were long and grave of prognosis. Those continued fevers with coma or stupor and of severe aspect were frequently called typhus by the Anglo-American medical world of the late eighteenth century. The adjective “ty­phoid” was applied to fevers that were typhus-like but not true typhus.

During the first half of the nineteenth century, a group of research-oriented, urban hospital-based physicians began to define disease on the basis of the postmortem findings as correlated with the clinical course. This hospital-based medicine was most strongly associated with the hospitals and patholo­gists of Paris, particularly Rene Laennec, Jean Corvisart, and Pierre Louis. In Great Britain, the Irish clinicians William Stokes and Robert Graves and the London hospital physicians Richard Bright, Thomas Addison, and Thomas Hodgkins were part of the same movement. This approach to medicine spread through the world but did not fully replace the purely clinical approach, particularly among those whose chief interests were in medical practice. In 1829 Louis described a specific fever with lesions of Peyer’s patches of the small bowel and named it “typhoid” because he thought it was the disease Brit­ish authorities of the previous generation had called “typhus.” This is, of course, the disease known today as typhoid fever.

All of this nosographic confusion was reflected in the American medical literature. Daniel Drake, the great medical geographer of the interior valley of North America, wrote about the typhoid stage of autumnal fever, by which he probably meant what we might call pernicious malaria. Louis’s American students brought his view of typhoid to America, and one of them, James Jackson, Jr., demonstrated that what was commonly called autumnal fever in New England was the same disease Louis called typhoid. Another student of Louis, William Gerhard of Philadelphia, proved that the disease his mentor had termed typhoid was distinct from the disease usually called autumnal fever in Philadelphia.

Based largely on his New England practice and experience, Elisha Bartlett described typhoid fever as the most common disease in the United States. By 1847, however, he realized that malarial fevers were the dominant concern of physicians in the South and Midwest, but not enough people learned of the revised opinion.

1850s-1870s

In the 1850s, as the American South became increas­ingly isolated culturally, there arose a campaign for a distinctively southern medicine. In part, this de­sire reflected real geographic differences in disease, but in part it was a result of the increasingly stri­dent southern nationalism that led to the Civil War. As a result of this campaign and the preexisting nosological confusion, there was, by 1860, a belief in a southern typhoid fever that was occasionally peri­odic and frequently cured by quinine therapy.

Etiologic theories of the mid-nineteenth century also contributed to the confusion. Urban diseases, like typhus and typhoid, were believed to be the result of the unsanitary conditions of life in the early industrial city. Crowding, a general lack of cleanli-

ness, and a combination of animal and human waste, gave rise to a distinct and unpleasant odor in the cities. Where the smell was worst was also fre­quently the area of greatest morbidity, and it was believed that there were animal miasmas that caused urban fevers, much like the marsh miasmas (malaria) that caused rural fevers. If the two causes were simultaneously present, a combined or compos­ite disease state should be expected. In the camps of the Civil War, that is exactly what was experienced, and typhomalarial fever was the name officially sanctioned for the camp disease that was not obvi­ously a malarial or typhoid fever.

During and immediately after the war, an era when disease theory was changing and the diagnostic precision of the profession was limited, physicians found the concept of typhomalarial fever to be very useful and flexible in diagnosis. There were, however, serious doubts on the part of leading medical theo­rists concerning the specific nature of typhomalarial fever. In the 1870s, these doubts increased, but so did the utilization of the diagnosis. By the late 1870s, the specificity, in pathological terms, of typhomalarial fever was an idea of the past, but the clinical reality remained, and the name seemed to explain the etiol­ogy of the symptom complexities so described.

For the same reasons physicians in other parts of the world began seriously to consider the American diagnosis in the 1870s. In the 1860s, British army surgeons stationed on Malta had identified a new disease originally called gastric remittent fever and later Malta fever. We know it today as brucellosis. In 1875 W. C. Maclean, professor of military medicine at the Army Medical School at Netley, suggested that Malta fever might be typhomalarial fever. James Donaldson, on the other hand, suggested the name “faeco-malarial fever” to reflect more accu­rately the current understanding of dual causes. By the 1870s, the special role of human fecal matter in the propagation of typhoid fever was becoming ac­cepted in Great Britain, largely as a result of the work of Charles Murchison and William Budd. Simi­lar new diseases reported by the British doctors in the Indian Medical Service and the Chinese Impe­rial Customs Medical Service were also considered as typhomalarial fever by some authorities.

The primary interest of these physicians was in disease prevention, and the name “typhomalarial” lent force to their campaign for cleanliness. J. Lane Notter explained:

The cause then of this disease is, I maintain, a preventable one. It essentially consists in defective drainage, in having to sleep in houses and breathe air impregnated with faecal organic vapours given off from saturated subsoil or filthy waterclosets, aided by climatic conditions which make en­teric fever in Malta assume a malarial type, and which would, under similar conditions in England, simply pro­duce typhoid fever.

1880s

In the 1880s the miasmatic etiologic speculations began to give way to the new germ theory of disease based in medical microbiology. Alphonse Laveran ob­served the malaria plasmodium; Georg Gaflky iso­lated Salmonella typhi. David Bruce discovered an organism that caused Malta fever; he called it Mi­crococcus melitensis, but the genus was subsequently named Brucella. However, the germ theory and medi­cal microbiology were not immediately accepted by all or even most practitioners. Debate on typho- malaria remained lively, particularly in the Ameri­can medical literature. Leading physicians saw etio­logic research and eventual etiologic definition of disease as the way to resolve the clinical difficulties, but microbiological techniques remained largely in the realm of experimental pathology, not yet overly useful to practitioners. The possibility of specific dis­eases similar to typhoid and malaria yet etiologically unique remained viable, but the profession was di­vided on how prevalent such diseases might be. Peri­odic typhoid and severe malaria were clinically real and needed names. Debate continued, but the terms were changing.

1890s-1900s

In the 1890s, progress in medical microbiology and the development of serum diagnostic tests for ty­phoid and Malta fevers made etiologic definitions of disease more useful to practitioners, and doubts in­creased about the utility of typhomalarial fever as a diagnosis.

When America mobilized volunteers for the war with Spain in 1898, the sanitation in the camps was very bad. Disease was widespread and Army Sur­geon General George Miller Stemberg appointed a commission of experts composed of Walter Reed, Vic­tor Vaughan, and E. O. Shakespeare to investigate. Using modem techniques - blood smear examina­tions and Femand Widal’s Serodiagnostic test — the commission proved that most of the cases diagnosed as typhomalarial fever were typhoid. Because the conditions, particularly in camps in the Deep South, approximated those under which Woodward had originally postulated the existence of typhomalarial fever, these results were particularly significant. By

the early twentieth century, the diagnosis of typho- Hialarial fever was widely regarded as an admission of diagnostic failure, and slowly it vanished from the medical literature.

Dale Smith

Bibliography

Donaldson, J. 1876. On the diagnosis and causation of faecomalarial fever. Report of the Army Medical De­partment for 1876, 238—42.

Drake, Daniel. 1850. A systematic treatise, historical, etio­logical, and practical, on the principal diseases of the interior valley of North America. Cincinnati, Oh.

Maclean, W. C. 1875. On Malta fever: With a suggestion. British Medical Journal ii: 224-5.

Notter, J. L. 1876. On Malta fever. Edinburgh Medical Journal 22: 289-98.

Smith, Dale C. 1982. The rise and fall of typhomalarial fever. Journal of the History of Medicine 37: 182—220, 287-321.

Reed, Walter, Victor C. Vaughan, and Edward C. Shake­speare. 1904. Report on the origin and spread of ty­phoid fever in U.S. military camps during the Spanish War of1898, 2 vols. Washington, D.C.

Woodward, Joseph J. 1863. Outlines of the chief camp dis­eases of the United States armies. Philadelphia.