Scurvy, as a disease entity, has an impressionable
and indelible history in the annals of medicine. The review of recorded history suggests scurvy to be an ancient disease. Medical writings from
antiquity to the Middle Ages describe the classic signs and symptoms of
scurvy. Critical appraisal of such literature raises the question of
whether other diseases were mistaken for scurvy.1 The
Renaissance witnessed an unprecedented sense of adventurism and
exploration by sea. The early sea voyages were often prolonged and
lacked adequate supplies of fresh fruits, vegetables, or animal foods.
Such dietary deprivations led to explosive outbreaks of scurvy among
the sailors and to the eventual failure of many expeditions.
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EARLY HISTORY OF SCURVY |
One of the earliest outbreaks of scurvy at sea was sustained by
the crew of Vasco da Gama during his 1497 expedition to
India.2 Da Gama began his expedition from Lisbon on July
9, 1497, with a fleet of 4 ships and a crew of 140 men. It took them 6 months to round the Cape of Good Hope. By the time da Gama's crew
landed on the southeast coast of Africa, most of them were afflicted with scurvy. Da Gama recorded: "Many of our men fell ill here, their
feet and hands swelling, and their gums growing over their teeth so
that they could not eat."2 As they sailed farther up the
east coast of Africa, they met local traders, who traded them fresh
oranges. Within 6 days of eating the oranges, da Gama's crew recovered
fully and he noted, "It pleased God in his mercy that ... all our
sick recovered their health for the air of the place is very
good."2
From India, da Gama returned across the Arabian Sea. Within 12 weeks of
sailing, his crew was again afflicted and weakened by scurvy. Da Gama
commented: "We addressed vows and petitions to the Saints ... it
pleased God in his mercy to send us a wind which in the course of six
days, carried us within sight of land ... at this we rejoiced
as ... we hoped to recover our health there as we had done
before ... the Captain-Major sent a man on shore to bring off a
supply of oranges which were much desired by our sick."2 Da Gama lost more than half of his crew by the end of his journey. His
crew sustained scurvy when they had been at sea for 10 weeks or more.
They recognized oranges to be an effective antiscorbutic by the second
outbreak. The experience of da Gama in dealing with scurvy did not
become common knowledge, and over the next several centuries, scurvy
remained as the scourge of the sea explorers.
James Lind's experiment to test the potency of various antiscorbutic
remedies is an important milestone in the history of scurvy.3 Lind performed his famous experiment in 1747 while a naval surgeon aboard the British naval ship
Salisbury.4 He chose 12 patients with severe
scurvy and housed them in a sick bay. The basic diet was similar for
all the patients. The 12 men were divided into 6 groups and each group
was given a different remedy. The antiscorbutic remedies tested were
cider, elixir of vitriol, vinegar, seawater, 2 oranges and 1 lemon for
6 days, and a medicinal paste made of nutmeg and a variety of other
ingredients. The patients receiving the oranges and lemons made a
remarkable recovery and were well in 6 days and were appointed to nurse
the rest of the sick. Lind was able to conclude that citrus fruits had
the most effective antiscorbutic potency. It took another 50 years
before the British navy made the provision of lemon juice routine
onboard.2,3 Such a measure resulted in a sharp decline of
scurvy among the British naval sailors.
As scurvy was becoming rare at sea during the 19th century, an
"epidemic" of land scurvy was witnessed.1,2,5 The
populations of the Great Potato Famine, the armies of the Crimean war
and American civil war, the Arctic explorers, and the California gold
rush communities were all prominent victims of scurvy on
land.2,6 It was indeed unfortunate that the knowledge
gained in conquering "sea scurvy" did not translate in the
avoidance of land scurvy. Toward the end of the 19th century, on the
heels of land scurvy arrived "infantile scurvy," as a new disease,
often affecting the affluent infant subsisting on a diet of proprietary
foods and heated milk.
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INFANTILE SCURVY: A BRIEF HISTORY |
Francis Glisson, a Cambridge professor, made one of the earliest
recorded descriptions of infantile scurvy. In his famous treatise on
rickets, published in 1650, he referred to scurvy occurring conjointly
with rickets: "Scurvy is sometimes conjoyned with this Affect
(rickets). It is either hereditary, or perhaps in so tender a
Constitution contracted by infection, or lastly, it is produced from
the indiscreet and erroneous regiment (diet) of the Infant, and chiefly
from the inclemency of the Ayr (air) and Climate where the Child is
educated."7
During the next 200 years, the literature is devoid of references to
the occurrence of infantile scurvy. The lack of reporting of infantile
scurvy after the Glisson era probably reflects a true diminished
occurrence of scurvy. The advances in agriculture witnessed during the
18th century had an impact on the occurrence of scurvy. The concept of
"market gardening" close to urban areas increased the supply and
consumption of fresh vegetable produce.8 The adoption of
potato as a staple and as a weaning food for infants during the 18th
century ensured the adequacy of dietary intake of vitamin C. The
practice of prolonged breastfeeding during the 17th and 18th centuries
protected the infants from developing scurvy.9
Incidentally, with the introduction of proprietary foods during the
middle of the 19th century for infant feeding, infantile scurvy emerged
as a "new" disease.
Clinicians failed to recognize infantile scurvy as a separate disease
entity and mislabeled it "acute rickets."9 During the
19th century, rickets was a prevalent chronic morbid condition among
infants. As infantile scurvy was a relatively rare condition and was
often engrafted on to preexisting rickets, it was understandable why it
was misconstrued to be acute rickets. The acute rickets confusion
lasted until Dr Thomas Barlow clarified the true nature of infantile
scurvy in 1883.10
In 1875, Dr Thomas Smith of the Hospital for Sick Children, Great
Ormond Street, London, mistakenly described a case of infantile scurvy
as "hemorrhagic periostitis."10,11 Dr Barlow was a
registrar under Dr Smith and had performed the autopsy on the case
described as hemorrhagic periostitis. According to Barlow, the
diagnosis of infantile scurvy was considered by Dr Smith but dismissed,
as the infant had no gum involvement.10
W. B. Cheadle, a pediatrician at the Hospital for Sick Children,
described 3 cases of scurvy in 1878.10,11 Cheadle's
patients were between 16 months to 3 years in age and all of them had
rickets. Cheadle had accurately analyzed the diets of these children
and wrote, "The diet was, however, more than a rickety diet
it
was a scurvy diet."12 The typical weaning diet of those
days included potatoes and gravy, as meat was expensive. Unlike
patients with just rickets, these 3 cases of scurvy with rickets lacked
potatoes and fresh milk in their diet. Cheadle cured the scurvy of his
patients by feeding them raw meat, fresh milk, and mashed potatoes
mixed with milk.
In 1881, Dr Samuel Gee of St Bartholomew's Hospital, London, mistook 5 cases of infantile scurvy to be cases of "osteal or periosteal
cachexia."10,11 Dr Cheadle was able to relate to the
cases described by Dr Gee and concluded that those were cases of scurvy
supervening on rickets precipitated by a "scurvy
diet."13
Dr Thomas Barlow, an assistant physician at the Hospital for Sick
Children, established the true nature of infantile scurvy. In 1883, Barlow studied 31 cases of acute rickets: 11 were his patients, 19 were
from the published literature, and 1 was a case history communicated to
him.10 By clinical and pathologic analysis he concluded
that the cases described as "acute rickets" were indeed a
combination of scurvy and rickets, but with scurvy as an essential
element and rickets as a variable element. To this day, Barlow's
clinical description of infantile scurvy, with the appropriate
pathologic correlation remains a classic. Barlow stated that the
extreme pain and tenderness seen in the cases of infantile scurvy
reflected bone pathology.10 By postmortem studies, Barlow
established that subperiosteal hemorrhage was the anatomic basis for
limb affection in infantile scurvy. Barlow implicated the diet as an
etiologic factor. His antiscorbutic regimen included raw-meat juice,
fresh milk, orange juice, and access to as much fresh air as possible.
He ventured to state that proprietary "infant foods" could not be
trusted as "sole aliment for any lengthened period, however useful
they may be as adjuncts."10 Soon infantile scurvy became
a recognizable entity and was referred to as "Barlow's disease."
By the end of the 19th century, infantile scurvy was readily recognized
and was being frequently observed in the United States and Great
Britain.
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INFANTILE SCURVY IN THE UNITED STATES |
In 1889, Dr Northrup, of New York, had seen a case of infantile
scurvy. His failure to diagnose the condition resulted in the death of
the infant. He realized the true nature of the infant's illness on
postmortem examination. That was the first case of infantile scurvy
recorded in the medical literature of the United States.14
By 1894, Northrup had collected 114 cases of infantile scurvy and
reported them at a meeting of the New York Academy of Medicine. He had
observed that "use of proprietary foods and condensed milk produces
more scurvy than all other causes combined."14
L. Emmett Holt's descriptions of scurvy in his 1897 textbook
illustrate the advances in understanding of the clinical presentations of infantile scurvy.15 Holt classified infantile scurvy into 3 clinical types: a fatal severe form, a severe form culminating in full recovery on identification and treatment, and a mild form without gum involvement or limb swellings. According to Holt, the mild
version of infantile scurvy was perhaps the most common, and was often
not recognized because of lack of classic gum involvement. Holt, in his
discussions on the causes of infantile scurvy, refers to the use of
heated infant formulas and concluded that it was the faulty formula and
not the process of heating, which caused infantile scurvy. Holt
concluded, "proprietary infant-foods are most certain to produce
scurvy, when they form the exclusive diet."15
As infantile scurvy became more prevalent, a collective investigation
of the problem was conducted by the American Pediatric Society in
1898.16 A total of 379 cases were collected and analyzed.
Most of the patients in this series were white and were between the
ages of 7 and 14 months. Most patients were from a well-to-do
background. Dietary history was available for 356 cases. Proprietary
foods were part of the diet of 214 patients. Sterilized, pasteurized,
or condensed milk had been given to 165 cases.
The members of the research committee concluded that most patients had
received proprietary foods and that prolonged usage of unsuitable foods
led to the development of scurvy. Tentative as these conclusions were,
1 of the committee members disagreed and a minority report was added.
In the minority report "chronic ptomaine poisoning" attributable to
absorption of toxins was considered to cause scurvy, and sterilizing,
pasteurizing, or cooking of the milk were not implicated in the
causation of scurvy. These conclusions reflect the confusion regarding
the causation of scurvy in the minds of the American pediatricians of
that era.
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CAUSE OF INFANTILE SCURVY |
Without doubt, the explosive increase of infantile scurvy during
the latter part of 19th century coincided with the advent of usage of
heated milks and proprietary foods.17 Bacterial contamination of raw milk was responsible for significant mortality and
morbidity among infants during that time.2 Usage of heated
milk led to noticeable decline in infant mortality. The advent of
heated milks was heralded as a great advance in infant feeding.
Unfortunately, the process of heating the milk led to loss of vitamin
C. Exclusive usage of heated milks with no other antiscorbutic
supplementation led to the development of scurvy. Proprietary foods
were touted as being comparable to breast milk in infant feeding. Being
farinaceous and of poor nutritional quality, they were a poor
substitute for breast milk. They were extensively adopted by the
well-to-do. Such indiscreet use of wealth led to increased incidence of
scurvy among infants from higher socioeconomic strata.
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CONCLUSION |
The eventual solving of the malady of infantile scurvy can be tied
to the monumental work of Holst and Frolich.18,19 Between
1907 and 1912, they induced and cured scurvy in guinea pigs by dietary
modification. Guinea pigs exposed to a diet of cereal grains developed
scurvy. Addition of fruits, fresh vegetables, or their juices to the
grains prevented the occurrence of scurvy in guinea pigs. Their study
was instrumental for several advances in the understanding of etiology
and treatment of scurvy.20
In 1914, Alfred Hess, a pediatrician at the Hebrew Asylum in New York,
had noted several cases of scurvy among infants fed on pasteurized
milk.21 The increased incidence of infantile scurvy at the
Hebrew Asylum had coincided with the elimination of orange juice from
the diet. The New York Milk Commission was of the opinion that
pasteurized milk heated to 145°F retained its chemical constituents.
On the basis of such an assumption, orange juice was excluded from the
infants' diet. Hess was able to effect a cure for scurvy by providing
raw milk or orange juice or potatoes. His experiments clearly
established that pasteurization resulted in the loss of antiscorbutic
potency of milk. Hess recommended that infants receiving heated
formulas be supplemented with fresh fruit or vegetable juices to
prevent scurvy. Such advances in the understanding of scurvy led to the
eventual eradication of infantile scurvy.
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Abstract
Conclusion
