What Made Helen Keller Blind and Deaf
Abstract
In 1882, at 19 months of age, Helen Keller developed a febrile illness that left her both deaf and blind. Historical biographies attribute the illness to rubella, scarlet fever, encephalitis, or meningitis. This analysis of her illness suggests she likely had bacterial meningitis, caused by Neisseria meningitidis or possibly Haemophilus influenzae.
In the winter of 1882, Helen Keller, a healthy 19 months old, lived with her parents and 2 step-brothers at their homestead in Tuscumbia, Alabama. Suddenly she developed a febrile illness that persisted for an unknown number of days. In her autobiography, she wrote:
"Then, in the dreary month of February, came the illness which closed my eyes and ears and plunged me into the unconsciousness of a new-born baby. They called it acute congestion of the stomach and brain. The doctor thought I could not live. Early one morning, however, the fever left me as suddenly and mysteriously as it had come. There was great rejoicing in the family that morning, but no one, not even the doctor, knew that I should never see or hear again." [1]
Not only did Helen survive this illness, but her intellect remained remarkably intact. Although deaf and blind, she graduated from Radcliffe College and became an internationally recognized author and lecturer. Throughout her life, she remained a dedicated advocate for social reform and the care of the handicapped, serving, until her death in 1968 at age 87, as a powerful public face of the potential for persons with severe disabilities to lead productive, meaningful lives.
WHAT CAUSES DEAFBLINDNESS?
Many deaf and blind persons suffer from a genetic disease, most likely Usher syndrome or the CHARGE syndrome (ie, coloboma of the eye, heart defects, atresia of the choanae, retardation of growth and development, and ear abnormalities and deafness) [2]. Others are either deaf or blind for a variety of reasons and subsequently lose their vision or hearing, respectively, from another cause. In addition, infections may lead to hearing and/or vision loss [3–5].
Although no medical analysis of the illness that left Helen Keller deafblind has previously been undertaken, various historical accounts have attributed it to encephalitis [6], rubella [7, 8], scarlet fever [7, 8], or meningitis [8]. Which was it, or could it have been something else?
THE STATE OF KNOWLEDGE OF INFECTIOUS DISEASES AT THE TIME OF HELEN KELLER'S ILLNESS
By in 1882, the germ theory of disease was replacing the notion of miasmas or bad air as the cause of epidemics, and treatment of infectious diseases consisted of drainage of abscesses and symptomatic relief. Cold baths, quinine, digitalis, and salicylates served as antipyretics [4, 9], chloroform and bromide of potassium as sedatives and analgesics [9], and smallpox vaccination was available [4]. In the face of little effective, specific therapy, quarantine, isolation, disinfectants, and sanitary measures were used to control the spread of infectious diseases [9].
ENCEPHALITIS AS A POSSIBLE CAUSE OF HELEN KELLER'S DEAFBLINDNESS
The ability to distinguish what we now call encephalitis from other neurologic processes characterized by seizures and fever was unrefined in the late 1800s [4, 9]. Diseases such as rabies, measles, varicella, mumps, and rubella that are complicated by encephalitis were, however, well recognized at that time and Keller's physician would very likely have easily diagnosed them clinically. Enteroviral encephalitis, which rarely results in severe sequelae, and insect-borne arboviral encephalitis both occur in the spring, summer, and fall whereas Keller's illness presented in February. Few studies document the outcome of herpes simplex virus encephalitis in the absence of antiviral treatment, although most patients died or had severe sequelae such as severe paralysis, aphasia, personality changes, or mental deterioration [10, 11].
Acute demyelinating encephalitis, an uncommon, immune-mediated inflammatory process, occurs most commonly in children and may be associated with visual impairment. Hearing loss, however, is rarely described and the disease is associated with few residua, other than occasional motor dysfunction [12].
In summary, although not clearly described in the medical literature, blindness and deafness could conceivably be sequelae of encephalitis, but would likely be accompanied by evidence of severe global cerebral damage, such as intellectual compromise or persistent seizures.
RUBELLA AS A POSSIBLE CAUSE OF HELEN KELLER'S DEAFBLINDNESS
Rubella (or German measles) is generally a mild infection. Although encephalitis occurs in about 1 per 5000 cases [13–15], it is nearly always associated with full recovery. Visual loss, secondary to cataracts or retinopathy, and deafness, however, are both well-known sequelae of the congenital rubella syndrome. Following the 1964 rubella epidemic in the United States, 3600 affected children were deaf and blind [14].
Thus, it is extremely unlikely Helen Keller suffered from rubella encephalitis and, because she was healthy before her febrile illness at 19 months of age, she definitely did not have congenital rubella.
SCARLET FEVER AS A POSSIBLE CAUSE OF HELEN KELLER'S DEAFBLINDNESS
The syndrome of scarlet fever has been recognized since ancient times and is characterized by its waxing and waning epidemiology. During the 18th century, this infection occurred in minor epidemics that were considered benign [16]. Then, in the mid-1820s–1830s, a pandemic of fatal scarlet fever appeared in Europe and in the United States, characterized by severe disease with case fatality rates ranging from 15% to 30%. For inexplicable reasons, the fatality rates from scarlet fever dropped precipitously by 1880 [16] in the United States, where it has remained, in general, a sporadic, relatively mild, and moderately uncommon infection.
Before the early 1900s, clinicians had difficulty distinguishing individual cases of scarlet fever from other febrile rash illnesses of childhood, so reports of cases were likely often misclassified. Epidemics, however, of infectious exanthema such as measles, varicella, and scarlet fever were well recognized and easily differentiated by clinicians during the late 19th century, the time of Keller's illness [17, 18].
Prior to the introduction of antibiotic treatment, the most frequent complications of scarlet fever were suppurative otitis media (14.1%) and mastoiditis (2.3%) [19] with occasional permanent deafness [20]. While both Corlett [20] and Koplik [21] cite the presence of eye complications with scarlet fever, neither mentions blindness among the extensive list of sequelae. Similarly, observations on the clinical courses of the large number of cases that occurred during the epidemic of the mid-1800s do not cite visual loss among the sequelae [17]. Furthermore, blindness with scarlet fever is not described in Osler's textbook of 1907 [22], in Holt's textbook of 1897 [4], nor in Fischer's textbook of 1907 [23]. In the largest report of sequelae of scarlet fever published, Louis Dublin, a biostatistician for the Metropolitan Life Insurance Company, described the outcomes of 1123 patients (82% of which were children 2–10 years of age) seen in 1911–1912 [24]. Among the 1063 survivors, 31 had nephritis, 31 otitis media, 22 adenitis, and 11 pneumonia, with no mention of hearing or vision loss.
Thus, while it may be tempting to assign scarlet fever as the cause of Helen Keller's deafblindness given the scarlet fever pandemic that was ending at the time of her illness, visual and/or hearing loss were extremely rare sequelae of this infection. Moreover, her physician very likely would have seen a large number of scarlet fever cases and would easily have made that diagnosis.
MENINGITIS AS A POSSIBLE CAUSE OF HELEN KELLER'S DEAFBLINDNESS
Based on their autopsy examinations, physicians in the mid-1700s recognized that the brains of deceased patients with symptoms similar to those Keller described, also called "brain fever," showed "dropsy," or congestion, of the ventricles [25], the result of impaired cerebrospinal fluid (CSF) flow from the fourth ventricle into the subarachnoid space and the spinal column. The word "meningitis" was first used in 1826 to describe inflammation of the arachnoid and/or pia mater [26].
In living patients, the etiology of bacterial meningitis could not be established until methods were developed to propagate bacteria on artificial media in the laboratory and until CSF could be analyzed. Quincke first described the technique for obtaining CSF by lumbar puncture in Germany in 1891 [27], only 5 months before Keller's illness. Thus, it would not have been used as a diagnostic aid by her physician in the Alabama countryside.
Within a span of 6 years, beginning 10 years after Keller's illness, the major bacterial causes of meningitis were identified. Haemophilus influenzae meningitis (then called influenzal meningitis under the mistaken belief that it was associated with influenza) was first described in September 1892 [28]. Neisseria meningitidis meningitis was first recognized during epidemics of meningococcal infection in 1894 [29] and Streptococcus pneumoniae meningitis was first described in 1898 [30]. What we now call group B streptococci, a notable cause of neonatal meningitis, and group A Streptococcus were referred together as "hemolytic streptococci" [31]. In the early 20th century, the relative incidences of the bacterial causes of meningitis varied from study to study. A 1911 review of 199 children in New York with culture-proven bacterial meningitis found Mycobacterium tuberculosis in 70%, meningococci in 12%, pneumococci in 11%, staphylococci or streptococci in 5%, Bacillus influenzae (H. influenzae) in 2%, and the "colon bacillus" (Escherichia coli) in 0.5% [32].
Clinically, bacterial meningitis in children is characterized by its abrupt onset, with intense headache, vomiting, convulsions, chills, and high fever. Following the appearance of posterior neck pain, opisthotonos occurred, often along with general muscle rigidity. Rash was occasionally present, as well as conjunctivitis, retinitis, and optic neuritis [32]. Furthermore, the children were very irritable and intolerant of light and sound, and their skin was hypersensitive to touch. If the anterior fontanelle had not closed, it was seen to be bulging [21]; at age 19 months, Helen's anterior fontanelle was no longer open. Meningitis caused by H. influenzae, the meningococcus, or the pneumococcus could not be distinguished from each other by clinical symptoms alone.
Prior to the introduction of antibiotic therapy, the outcomes of children with meningitis were usually disastrous. Tuberculous and "hemolytic streptococcal" meningitis were uniformly fatal [23, 33], as was pneumococcal meningitis, with the single exception of one patient in Holt's series who, upon recovery, remained partially paralyzed and "mentally defective" [32]. Thus, because of their extremely high fatality rates, neither tuberculous, pneumococcal, nor group B streptococcal meningitis likely explain the illness that caused Keller's deafblindness.
During the fatal scarlet fever pandemic of the 1800s, streptococcal meningitis was a rare complication among hospitalized children, occurring in 19 of 17311 scarlet fever patients [34]. Only 2 of the 19 meningitis patients (10%), compared to 44% of all scarlet fever cases [24], were children <5 years of age. Only 1 of the 19 survived, and that patient, a 5-year-old, had no apparent sequelae. Furthermore, the appearance of meningitis, which was often associated with suppurative otitis media (75%) or sinusitis (20%), was delayed during the course of scarlet fever and presented from 4 to 117 days following its onset, with more than half appearing after >21 days. Of note, in the absence of antibiotics, the scarlet fever rash lasted 3–4 days and desquamation occurred 4–15 days after onset of the illness [22]. Helen Keller's physician very likely would have recognized scarlet fever if it preceded meningitis that left her deaf and blind.
In 1922, Dr Thomas Rivers reported a mortality rate of 97% among children with H. influenzae meningitis <2 years of age and 71% among those >2 years of age. Of the 17 survivors, 4 had neurologic sequelae including partial blindness (n = 2), nerve deafness (n = 1), and partial hemiplegia (n = 1) [35].
After 1937, anti-influenzal serum was routinely used in patients with H. influenzae meningitis at major medical centers with marginal benefit, and within a short time, treatment with sulfonamides was introduced. Of 110 H. influenzae meningitis patients treated with various combinations of serum, sulfonamide drugs, streptomycin, and penicillin, the mortality rate was 21%. In follow-up of the surviving patients, 52 had no neurologic sequelae whereas 12 had significant neurologic sequelae, including one child who was deaf, blind, and "talks little" [36]. Although the survival rate of untreated cases was very low, H. influenzae meningitis could have caused Keller's deafblindness, based on the reported sequelae of deafness or blindness among untreated patients and a deafblind child among treated patients.
Studies of "epidemic meningitis," caused by N. meningitidis, in the early 1900s cited a wide range of mortality rates ranging from 60% to >80%, with the highest in young children [23]. Among survivors, deafness occurred in 12% and blindness in 10%, but intellectual deficits were rare (1%–3%) [37]. Surviving patients recovered either by "lysis," with gradual improvement of symptoms, or by "crisis" marked by sudden improvement [37]. Among 1300 patients treated with antimeningococcus serum, the mortality rate was 31% and among the survivors, 45 were permanently deaf, 3 were blind, 3 were mentally impaired, and 2 were deafblind [37]. Thus, the meningococcus, likely a sporadic case rather than related to a local epidemic, is a credible cause of the illness that left Keller deaf and blind, based on its higher survival rate among untreated (albeit adult) patients, the apparent sudden resolution of her disease by crisis, and the description of 2 deafblind children among survivors treated with serum therapy.
PATHOPHYSIOLOGY OF DEAFNESS WITH MENINGITIS
Hearing loss is a common complication of bacterial meningitis; in a large study of children treated with antibiotics, 14% had transient conductive hearing loss (accompanied by otitis media in 60%) [38]. Furthermore, despite the availability of excellent antibiotic therapy, 10% had permanent sensorineural hearing loss (half was bilateral). The rate of permanent deafness varied by the causative pathogen: 31% of those with pneumococcus, 6% with H. influenzae, and 10% with meningococcus. Hearing loss correlated with low CSF glucose on admission [38] and, in a rabbit model, occurred with the onset of inflammation in the CSF [39].
The mechanism of sensorineural hearing loss in meningitis is inflammation of the cochlea and/or labyrinth, as demonstrated during ear dissection at autopsy [40], in animal models of bacterial meningitis [39], and by neurovestibular testing [41]. Animal studies show that sustained bacteremia leads to increased permeability of the blood–cochlear barrier, thus promoting access of the bacteria to the cochlea/inner ear [42].
PATHOPHYSIOLOGY OF VISION LOSS WITH MENINGITIS
Loss of vision secondary to bacterial meningitis was occasionally seen prior to 1940, usually as the result of metastatic endophthalmitis following the entry of organisms into the retinal or uveal circulation by bacterial penetration of the blood–ocular barrier [43]. This pathophysiologic process is identical in meningococcal, pneumococcal, or H. influenzae meningitis [44–46].
In a series of 350 cases of meningococcal meningitis prior to the availability of antibiotic therapy, 19 patients (5.7%) developed endophthalmitis and 4 were bilateral [47]. No relation was seen between its occurrence and severity of the meningitis. Most patients did not complain of pain (but many were likely obtunded), although 3 of the 19 complained of severe eye discomfort. Photophobia was rare. All affected eyes became totally blind. None of the affected eyes demonstrated phthisis bulbi (atrophic globe) and many showed no shrinkage of the globe at all. Six of the eyes were enucleated and all showed inflammation of the iris, ciliary body, and choroid, as well as inflammatory infiltrates of the retina, usually with detachment. Abscesses occurred in the vitreous with organization and formation of a cyclitic membrane.
Another potential mechanism of vision loss with bacterial meningitis is orbital cellulitis/orbital abscess with central retinal artery necrosis, as was seen in 2 of 350 cases of meningococcal meningitis [47]. An additional cause is septic thrombi to the retinal artery with dissemination of bacteria through the retinal vessels and rapid destruction of the retina [43]. A very rare cause is immune panophthalmitis as described in meningococcal meningitis [48].
In her autobiography, Helen Keller wrote:
"I fancy I still have confused recollections of that illness. I especially remember the tenderness with which my mother tried to soothe me in my waking hours of fret and pain, and the agony and bewilderment with which I awoke after a tossing half sleep, and turned my eyes, so dry and hot, to the wall, away from the once-loved light, which came to me dim and yet more dim each day. But, except for these fleeting memories, if, indeed, they be memories, it all seems very unreal, like a nightmare."[1]
These symptoms suggest ocular inflammation, but Helen was only 19 months old and unlikely to have retained actual memories of that time.
Upon recovery from her illness, Helen's left eye was proptotic with a cloudy cornea (Figure 1), so most photos of her were taken from her right side. In approximately 1911, at the age of about 30 years, both her eyes were removed and replaced with glass prostheses [8]. The reason for her unilateral proptosis is unknown, but she may have had an orbital abscess in the left eye.
Figure 1.
Helen Keller studying geometry at Radcliffe College, 1900. Photographer Studio F. W. Burchall, Boston. Photo courtesy of the American Foundation for the Blind, Helen Keller Archive.
Figure 1.
Helen Keller studying geometry at Radcliffe College, 1900. Photographer Studio F. W. Burchall, Boston. Photo courtesy of the American Foundation for the Blind, Helen Keller Archive.
CONCLUSIONS
In summary, the historical record does not elucidate, with certainty, the cause of Helen Keller's deafblindness. In her autobiography, she said she was unconscious, her physician expected her to die, and her family was told her illness was "congestion of the stomach and brain." The meaning of this diagnosis is obscure. In 1881, "congestion of the stomach" was considered a meaningless term and "congestion of the brain" referred to altered cerebral blood flow [18]. If she had meningitis, she very likely would have experienced vomiting from increased intracranial pressure, which may have been interpreted as "congestion of the stomach." Furthermore, at that time physicians knew that patients who died of "brain fever" had congestion of the cerebral vessels upon autopsy and her doctor may have used the term "congestion of the brain" to reflect the process that he suspected was occurring in her head.
Prior to the use of antibiotics, bacterial meningitis was usually a fatal disease, although 20%–40% survived N. meningitidis meningitis and <5% survived H. influenzae meningitis. The sequelae included a variety of neurologic deficits, including deafness and blindness, which, similar to a fatal outcome, were more common among young children compared with older children. Amazingly, like Keller, some children survived with intact intelligence. Of the bacteria that cause meningitis, the most likely to explain her illness are N. meningitidis or, possibly, H. influenzae. Fortunately, because of the widespread use of vaccines against H. influenzae and S. pneumoniae, along with the use of meningococcal vaccines in at-risk individuals, bacterial meningitis among children in the United States today is rare.
Note
Potential conflicts of interest. The author: No reported conflicts of interest. The author has submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
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What Made Helen Keller Blind and Deaf
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