Jane Austen (18 page)

In 1964 an article appeared in the
British Medical Journal
entitled ‘Jane Austen’s Illness’ by Sir Vincent Zachary Cope, Consulting Surgeon to St Mary’s Hospital, Paddington, London. Jane died, said Cope,

By perusing Jane’s letters and those of her family, Cope set about attempting to identify the illness that prematurely terminated Jane’s life. Of the symptoms suffered by Jane, Cope concludes that whereas many of them might be accounted for by a number of disease conditions, there are very few disease conditions which could account for them all.

Cope describes how he read Jane’s letter to Fanny Knight of 23/25 March 1817, many times before it struck him that in her use of the words, ‘recovering my looks a little, which have been bad enough, black and white and every wrong colour’, she was describing ‘that symptom which is almost pathognomonic of
Addison’s disease’. Cope goes on to explain that this appearance is due to pigmented areas of the skin mingling with non-pigmented areas. There is no disease other than Addison’s disease, he says, that could produce a face that was ‘black and white’ and at the same time give rise to the other symptoms described in her letters.
1

Addison’s disease is named after the person who first described it: English physician Dr Thomas Addison (1793–1860) of Guy’s Hospital who, in 1855, published an important work on
The Constitutional and Local Effects of Diseases of the Suprarenal
Capsules
(now commonly known as the adrenal glands). He summarised the main features of the disease as follows:

It should also be noted that this is a rare disease; the onset of which is insidious. From time to time there may be severe attacks of nausea, vomiting or diarrhoea. Pigmentation of the skin only occurs late on in the disease and gradually increases – its colour ranging from a bronzy yellow to brown, or even occasionally black. This shows itself, particularly, over exposed parts of the body, such as the face and hands, and wherever prolonged pressure is applied to the skin, such as beneath a waist belt and, occasionally, on mucous membranes as in the mouth. The patient’s temperature is usually, somewhat subnormal.
2

Although Addison’s disease was not described until after Jane Austen’s time, it is now known to be caused by a malfunction of the adrenal glands (one of which is situated above each kidney) which normally produce the so-called corticosteroid
hormones – hydrocortisone and aldosterone. A deficiency of the above hormones, which is found in Addison’s disease, causes the pituitary gland to react by secreting excessive amounts of adrenocorticotrophic hormone (ACTH), and also of melanocyte stimulating hormone (MSH). It is the latter which causes the skin to increase its production of melanin pigments – hence the excessive pigmentation.

Another feature of Addison’s disease is the occurrence, at intervals, of so-called Addisonian crises which occur due to the failure of the adrenal glands to produce corticosteroid hormones, which normally help the body to cope with stress. In the Addisonian crisis, the patient develops extreme muscle-wasting, becomes dehydrated, confused and comatose. He or she also suffers from hypotension (low blood pressure) and often hypoglycaemia (a deficiency of sugar in the blood). As Addison’s disease progresses to the chronic stage, the patient becomes tired, weak and suffers with vague abdominal pains and weight loss.
3
This begs the question, what causes the adrenal glands to fail?

Samuel Wilks, a pupil of Addison’s and also his co-worker, declared that Addison’s disease was always caused by the suprarenal capsules (adrenal glands) becoming infected with tuberculosis – an infectious disease caused by the bacterium Mycobacterium tuberculosis. Tuberculosis is passed from person to person in airborne droplets, by coughs and sneezes, and it can also be contracted by drinking the milk of tuberculous cattle. The disease, in this latter case, is caused by a similar organism, Mycobacterium bovis.

Tuberculosis commonly begins with the infection of one organ of the body at a so-called primary site. Following this, the infected person will either go on to develop immunity, or the disease will spread to other secondary sites. Any organ of the body may be infected: the commonest being lungs, intestines,
bones and glands. (Incidentally, Jane’s great-grandfather John Austen died of ‘consumption’ in 1704 – consumption being an early name for tuberculosis, a disease which appears to consume the body).

In 1911 (when the incidence of tuberculosis among the population was probably little different from what it had been in Jane Austen’s time), an article on Addison’s disease in the
Encyclopaedia Britannica
read as follows:

(Note that this figure of 80% is somewhat lower than Wilks’s 100%.)

It seems more than likely, therefore, that Jane was suffering from tuberculosis, and that this is what had destroyed her adrenal glands. This would explain her night fevers – a typical symptom of tuberculosis (but not of Addison’s disease). Also, if tuberculosis was present in her spinal column which, from the above statement, seems likely, then this could account for the backache of which she complained – this symptom again being atypical of Addison’s disease. How, therefore, did Jane contract tuberculosis?

In early nineteenth-century England, it is estimated that a quarter of all deaths were due to tuberculosis, and the following examples, which were known to Jane, reveal just how prevalent it was. In November 1798 Jane described how Anna Lefroy had seen ‘a great deal of the Mapletons while she was in Bath’, David Mapleton being a surgeon-apothecary in that city. The Mapletons had a 17-year-old son, of whom Jane remarked: ‘Christian is still in a very bad state of health, consumptive [tubercular] and not likely to recover’.
4
In fact, Christian lived on until 1839. On 12–13 May 1801, Jane declared, in respect of 22-year-old Marianne Mapleton, sister of Christian, ‘I am always told that she is better … Her complaint is billious fever’.
5
However, shortly afterwards, Jane recorded that Marianne’s disorder had ‘ended fatally’.
6
So had Marianne also contracted tuberculosis?

Further evidence that the disease was rife in the community in which Jane lived is born out by Mrs Lefroy, who in June 1801, described how her husband had recently visited one James Corbett, who was ‘in a deep consumption’.
7

Jane herself may have contracted tuberculosis from infected milk or other dairy produce, or she may have contracted it via droplet infection through a chance encounter with an infected stranger. However, it is more likely that she caught it from another member of her family, namely her brother Henry.

As long ago as 29 October 1801, Henry’s wife Eliza had written to her cousin Phylly expressing concern about her husband

On 3 November 1813 Jane wrote to Cassandra about Henry, who had not been well. She wrote that Henry’s

Three days later, Jane wrote again to Cassandra: ‘Dearest Henry! What a turn he has for being ill! & what a thing Bile is!’
10
In other words, Henry’s symptoms and Jane’s were similar in this respect.

Henry’s health did not improve, for Jane’s niece Caroline described how, in the autumn of 1815, when Jane was visiting him at his house, now Hans Place, London, ‘He was seized with a low fever and became so ill that his life was despaired of’.
11
He survived, however, and was nursed for some weeks by Jane. On 17 October of that year Jane herself stated that Henry was ‘not quite well’ and suffering from ‘a bilious attack with fever’.
12
This fever was still present when Jane wrote to Cassandra again the following month. In his
Memoir
, James E. Austen-Leigh describes Henry’s fever as ‘dangerous’ and his convalescence from it as, ‘slow’.
13
As already mentioned, fever, especially at night, is a symptom of tuberculosis, as are ‘bilious attacks’.

It seems likely, therefore, that Henry was suffering from tuberculosis and that Jane contracted it from him. After all, she had nursed her brother for several weeks and it is known that the longer a person is exposed to someone with tuberculosis, the more likely he or she is to become infected. Jane had been in close and prolonged contact with Henry since the autumn of 1815. Her own symptoms had commenced at the beginning of the following year 1816. This correlates with the average incubation period for tuberculosis being twenty weeks, though it can be as short as two weeks.
14

If Henry did indeed have tuberculosis, why did he not succumb to the disease? The answer is that the body reacts to an attack of tuberculosis by enclosing the infected area in fibrous tissue, which has the effect of preventing the spread of the infection. (If the bacteria leak out then the infection may spread). Whatever the truth of the matter may be, Henry survived and lived to the age of 78.

Jane’s brother Edward, was another member of the family who suffered poor health, and on 24/25 December 1798, Jane wrote to Cassandra about him thus:

In other words, Jane believed that it was necessary for Edward to endure the above symptoms, prior to him recovering.

On 2 June 1799 Jane wrote to Cassandra from Bath, indicating that Edward’s health was still not good: