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Contributors
May A. Beydoun Laboratory of Epidemiology and Population Sciences, National Institute on
Aging, NIA/ NIH/ IRP
Michael J. Boivin Global Neuropsychiatry Research Center, College of Osteopathic Medicine,
Michigan State University
Stuti Chakraborty Neural Plasticity and Neurorehabilitation Laboratory, Chan Division of
Occupational Science and Occupational erapy, University of Southern California
Arielle P. Davis Department of Neurology, Division of Infectious Diseases, University of
Washington
Soati Dian Department of Neurology & Research Centre for Care and Control of Infectious
Disease, Faculty of Medicine, Universitas Padjadjaran
Nicky Dunn Department of Clinical Neuroscience, Karolinska Institutet
Marisol Duran Department of Psychology, California State University
Ziad W. El- Hajj Department of Biology, McGill University
Lance D. Erickson Department of Sociology, Brigham Young University
Guy D. Eslick Managing Director, Clinical Links Using Evidence- Based Data (CLUED), PTY LTD
omas J. Farrer Idaho WWAMI Medical Education Program, University of Idaho
Patricia A. Fennell Albany Health Management Associates, Inc.
Jaroslav Flegr Laboratory of Evolutionary Biology, Department of Philosophy and History of
Science, Faculty of Science, Charles University
Anna Fogdell- Hahn Department of Clinical Neuroscience, Karolinska Institutet
Paul Bernard Foley Medical Journal of Australia
Kenneth J. Friedman Department of Medicine, School of Osteopathic Medicine, Rowan
University
Shawn D. Gale Department of Psychology and e Neuroscience Center, Brigham Young
University
Shane George Department of Psychology, e College of St. Rose
Dawson W. Hedges Department of Psychology and e Neuroscience Center, Brigham Young
University
Celia V. Holland Department of Zoology, Trinity College, Dublin
Mbusa J. Kombi Department of Neurology, University of Kinshasa, and Institut National de
Recherche Biomédicale
Rebecca A. Lundwall Department of Psychology and the Neuroscience Center, Brigham Young
University
xii Contributors
Chris H. Miller Department of Psychology, California State University
Leonard Ngarka Brain Research Africa Initiative (BRAIN); Neuroscience Lab, Faculty of
Medicine & Biomedical Sciences, e University of Yaoundé I; and Department of Neurology &
Clinical Neuroscience, Yaoundé Central Hospital
Alfred K. Njamnshi Brain Research Africa Initiative (BRAIN); Neuroscience Lab, Faculty of
Medicine & Biomedical Sciences, e University of Yaoundé I; and Department of Neurology &
Clinical Neuroscience, Yaoundé Central Hospital
Martins Nweke Department of Physiotherapy, Faculty of Health Science, University of Pretoria
Paulus Anam Ong Department of Neurology & Research Centre for Care and Control of
Infectious Disease, Faculty of Medicine, Universitas Padjadjaran
Peter K. Panegyres Neurodegenerative Disease Research Pty LTD, Western Australia School of
Medicine, e University of Western Australia
Liz Pritchard Department of Psychology, California State University
Ilene S. Ruhoy Cascadia Complex Health and Chiari/ EDS Center, Mount Sinai South Nassau
Matthew D. Sacchet Department of Psychiatry, Massachusetts General Hospital, Harvard
Medical School
Martin Shapiro Department of Psychology, California State University
Jonathan K. Stiles Department of Microbiology, Biochemistry and Immunology, Morehouse
School of Medicine
Rabporn Suntornlohanakul Division of Neurology, Department of Pediatrics, Hospital for Sick
Children, Toronto
Pegah Touradji Department of Physical Medicine and Rehabilitation, Johns Hopkins University
Desire D. Tshala- Katumbay Department of Neurology, University of Kinshasa, Institut National
de Recherche Biomédicale, and Oregon Health Sciences University
E l le n Wo o Department of Psychology, California State University and Department of Psychiatry,
University of California San Francisco
E. Ann Yeh Division of Neurology, Department of Pediatrics, Hospital for Sick Children, Toronto;
Division of Neurosciences and Mental Health, e Hospital for Sick Children Research Institute,
Toronto; and Faculty of Medicine, Department of Pediatrics, University of Toronto
Introduction to Infectious
Diseases in Neurocognitive and
Neuropsychiatric Medicine
Shawn D. Gale, Dawson W. Hedges, and Lance D. Erickson
In 1917, doctors rst in Europe and then throughout much of the world began
identifying an apparently new and mysterious disease. e epidemic of encephalitis lethargica, as the disease eventually became known, overlapped with the much
better- known inuenza epidemic of 1918 and 1919. While there was some confusion about whether encephalitis lethargica was actually distinct from inuenza, the
two diseases appeared to have dierent clinical features. Particularly striking about
encephalitis lethargica was its tendency to result in features of Parkinson’s disease
and a plethora of other neuropsychiatric and neurocognitive symptoms, including
psychosis, anxiety, and memory problems, some of which could be permanent
(Foley, 2018).
A century later in 2019, a new viral disease began to make its way around the
world. Identied as being caused by a novel coronavirus, severe acute respiratory
syndrome coronavirus 2, coronavirus disease 2019 (Covid- 19) as it became known
oen presented with fever, a sore throat, and respiratory signs and symptoms, which
could culminate in pneumonia. In addition to the pulmonary features of Covid- 19,
people who survived the acute phase of the disease oen developed neuropsychiatric
and neurocognitive features such as fatigue, anxiety, depression, and problems with
memory, sometimes even aer what appeared to be only a mild acute illness. A study
of ten patients who had survived disorders of consciousness associated with Covid19 infection found decreased brain functional and anatomic connectivity compared
to healthy controls. Indeed, in this study, the degree of the decrease in structural
connectivity was like the decrease in structural connectivity found in patients who
have had severe traumatic brain injury (Fischer et al., 2022).
Although encephalitis lethargica and Covid- 19 are dramatic examples of how infectious diseases can cause a range of neuropsychiatric and neurocognitive problems,
many other infectious diseases appear to aect brain function resulting in impaired
behavioral and cognitive function. While some of these relationships are well
known, such as the association between neurosyphilis and psychosis and cognitive
Shawn D. Gale, Dawson W. Hedges, and Lance D. Erickson,
In: Infectious Diseases in Neurocognitive and Neuropsychiatric Medicine
Oxford University Press. © Oxford University Press 2024. DOI: 10.1093/ oso/
Infectious Disease and Neurocognition
impairment (see Chapter 8, this volume) and the tragic cognitive impairment that
can result from herpes encephalitis, the neuropsychiatric and neurocognitive effects of other infectious diseases can be more surprising and clinically relevant.
Accumulating ndings implicate multiple dierent viruses, bacteria, and parasites
in human cognitive and neuropsychiatric function.
Viruses are increasingly associated with cognitive decline, mild cognitive impairment, and dementia (Damiano et al., 2022), and adverse cognitive sequelae aer
acute infection have been associated with herpesviruses, including varicella zoster,
Japanese encephalitis, West Nile virus, and Covid- 19 (Damiano et al., 2022).
Further exemplifying how infectious diseases can aect neuropsychiatric outcomes, meningitis and measles along with febrile seizures are among the top six risk
factors for epilepsy in children in Nigeria (Watila et al., 2021), and neurocysticercosis,
caused by the pork tapeworm, Taenia solium, is a leading cause of epilepsy in regions
where Taenia solium is endemic (see Chapter 16, this volume).
Toxoplasma gondii is an intraneuronal protozoal parasite that in its latent
form infects approximately one- third of the world’s population. Unless there is
immunocompromise, the acute infection with T. gondii oen acutely results in
only a benign or even asymptomatic sickness, and its adverse eects on brain function were once considered limited to people with immunosuppression. Multiple
ndings, however, now show that latent infection in immunocompetent hosts
with T. gondii is a potential risk factor for a variety of adverse neuropsychiatric and
neurocognitive outcomes, including schizophrenia, obsessive– compulsive disorder, epilepsy, cognitive decits, and possibly dementia. Some evidence also indicates that T. gondii can aect brain volume (Erickson et al., 2021). Despite infecting
an estimated one- third of the world’s population, T. gondii has no known eective
treatment for its latent form, and eorts to develop a safe and eective vaccine for
T. gondii have so far been disappointing. Its widespread distribution and possible
associations with a range of neuropsychiatric and neurocognitive conditions make
T. gondii an important problem for public and personal health. Nonetheless, the
association between T. gondii and neuropsychiatric and neurocognitive outcomes
is complex. Even if T. gondii is a risk factor for schizophrenia, clearly with T. gondii
infecting one- third of the world’s population but only approximately 1 percent of
the world’s population having schizophrenia, not everyone who is infected with
T. gondii develops schizophrenia. Other factors must be involved, including host
genetic and immune factors, as well as other environmental and infection factors
and their interactions.
While T. gondii infection occurs in many regions throughout the world, other in-
fectious diseases that aect brain function are localized to particular regions. As an
example, the protozoans Trypanosoma brucei gambiense and Trypanosoma brucei
rhodesiense are the causative agents of human African trypanosomiasis or sleeping
sickness, a disease localized to central and east Africa, but which still aects thousands of people annually. Both organisms can enter the brain, where they can cause
sleeping sickness (Kennedy & Rodgers, 2019).
Introduction 3
Increasingly, infectious diseases have been associated with neurodegenerative diseases such as Alzheimer’s disease. Better known for its associations with gastric ulcer
disease and gastric cancer, the globally distributed bacterium Helicobacter pylori is
associated with both worsened cognitive function (Erickson et al., 2023) and with
Alzheimer’s disease (Kountouras et al., 2006). Interactions between H. pylori and
some periodontal pathogens also have been associated with all- cause dementia
and with Alzheimer’s disease (Beydoun et al., 2021). Herpesviruses also appear associated with Alzheimer’s disease, with evidence suggesting that herpesviruses are
associated with the strongest known genetic risk factor for Alzheimer’s disease—
apolipoprotein E epsilon 4 allele— and with amyloid beta and tau protein deposition.
It may be that amyloid deposition is initially an adaptive response to herpesvirus
infection that later becomes maladaptive and leads to Alzheimer’s disease as amyloid deposition increases (Wainberg et al., 2021). Adding to the complexity of the
associations between infectious diseases and neurodegeneration is that not all types
of even herpesviruses have been associated with dementia. For example, in a large
study based on Danish health registries, herpes zoster was not associated with dementia (Johannesdottir Schmidt et al., 2022). Nonetheless, ndings suggest that
a variety of viruses, bacteria, and even some parasites might be associated with
Alzheimer’s disease (Piekut et al., 2022).
e gut microbiome is another potential source of bacteria and viruses that has
the potential to aect behavior and cognitive function (Davidson et al., 2018).
Housing approximately 100 times the number of genes in the human genome, the
gut microbiome is linked bidirectionally via the gut– brain axis to the brain and is
linked with the immune system and the hypothalamic– pituitary– adrenal axis. With
these extensive connections between the gut microbiome, the immune system, and
dierent brain regions, perturbations of the gut microbiome by diet, stress, and infectious diseases have the potential to account for at least some cognitive and behavioral dierences between individuals within the same species (Davidson et al., 2018).
e relationship between infectious diseases and neuropsychiatric and cognitive function is complex, with multiple factors potentially inuencing outcomes.
Genetic variants in the oligoadenylate synthetase 1 gene have been associated
with both Alzheimer’s diseases and with a severe outcome with Covid- 19 disease.
Oligoadenylate synthetase 1 is activated in microglial cells in the brain, and the association between allelic variants in this gene with both Alzheimer’s disease and
with Covid- 19 disease suggests that immunological function might be at play in
Alzheimer’s disease and in how brains respond to some infectious diseases (Magusali
et al., 2021). While this nding itself does not mean that having Covid- 19 is necessarily a risk factor for Alzheimer’s disease, it points to an underlying genetic vulnerability conferring risk for both Alzheimer’s disease and Covid- 19. Adding to the
complexity are ndings suggesting that the brain may have its own microbiome, variations of which could be associated with brain dysfunction (Zhan et al., 2016).
The accumulating evidence associating certain infectious diseases with several neuropsychiatric and cognitive outcomes has important clinical and public
Infectious Disease and Neurocognition
health implications. Recognition that some infectious diseases associated with
adverse neuropsychiatric and cognitive outcomes such as Covid- 19 have airborne patterns of transmission emphasizes the importance of addressing airborne routes of diseases transmission such as adequate indoor ventilation
(Jimenez et al., 2022).
Climate change can increase exposure to infectious diseases, including those that
are associated with neuropsychiatric and neurocognitive disease. Climate change
can alter the ranges of vectors, hosts, and reservoirs of infectious diseases (Louis
et al., 2023), resulting in increased exposure to some of the infectious diseases that
have been associated with worse neurocognitive and neuropsychiatric outcomes.
Mathematical modeling, for instance, suggests that unmitigated climate change has
the potential to increase the range of the Aedes aegypti mosquito, a vector for Zika
and dengue viruses, to include European cities by 2100, regions currently free of
this important vector (Liu- Helmersson et al., 2019). Further, interactions between
climate change and poverty have the potential to increase exposure to a variety of infectious pathogens, including the bacterium H. pylori, and are likely to increase with
climate change (Khalifa et al., 2010).
People living in low- income and middle- income regions may be especially vulnerable to some of the infections that have been associated with problems with
neurocognitive and neuropsychiatric function. e helminthic infection To xo c ar a ,
for example, is associated with regions that have a low human development index
(Rostami et al., 2019).
Infectious Diseases in Neurocognitive and Neuropsychiatric Medicine describes
how infectious diseases can adversely aect brain function to result in decreases
in neurocognitive function and in neuropsychiatric abnormalities. Infectious diseases that can aect brain function are widespread and can contribute to or result in substantial cognitive and neuropsychiatric morbidity. However, the extent
to which infectious diseases can aect cognition, behavior, and public health is
oen not fully appreciated. Rather than focusing on acute infections that aect the
brain such as meningitis and encephalitis, Infectious Diseases in Neurocognitive and
Neuropsychiatric Medicine explores the eects of chronic and latent infections on
brain function. Like many areas in medicine, the research ndings can sometimes
be unclear and even conicting. While the chapters in this book present ndings
suggesting associations between infectious disease and decits in neuropsychiatric
and cognitive function, they also describe gaps and inconsistencies in the research
ndings (see, e.g., Wang et al., 2022). Clearly, more research is needed, but Infectious
Diseases in Neurocognitive and Neuropsychiatric Medicine attempts to describe what
is known now and to outline future approaches to researching how infectious diseases can aect overall brain functioning.
Infectious Diseases in Neurocognitive and Neuropsychiatric Medicine starts with
a chapter that describes the neuropsychiatric sequelae of encephalitis lethargica.
While encephalitis lethargica is now rarely if ever encountered (Homan & Vilensky,
Introduction 5
2017), its eects on the brain in the early twentieth century were striking and provide
important examples of just how infectious disease can result in sometimes profound,
sometimes long- lasting, and sometimes delayed disturbances in neuropsychiatric
and cognitive function. Chapters then explore relationships between viral, bacterial, and parasitic infections on neurocognitive and neuropsychiatric function, and
later chapters describe the contributions of infectious diseases to dementia, multiple
sclerosis, depression, obsessive– compulsive disorder, schizophrenia, chronic fatigue
syndrome, and brain development. Additional chapters discuss acute necrotizing
encephalopathy and associations between the microbiome and neurocognitive and
neuropsychiatric function.
References
BEYDOUN, M. A., BEYDOUN, H. A., WEISS, J., HOSSAIN, S., EL- HAJJ, Z. W. & ZONDERMAN, A.
B. 2021. Helicobacter pylori, periodontal pathogens, and their interactive association with incident
all- cause and Alzheimer’s disease dementia in a large national survey. Mol Ps ych iatry, 26, 6038– 6053.
DAMIANO, R. F., GUEDES, B. F., DE ROCCA, C. C., DE PADUA SERAFIM, A., CASTRO, L. H. M.,
MUNHOZ, C. D., NITRINI, R., FILHO, G. B., MIGUEL, E. C., LUCCHETTI, G. & FORLENZA, O.
2022. Cognitive decline following acute viral infections: Literature review and projections for postCOVID- 19. Eur Arch Psychiatry Clin Neurosci, 272, 139– 154.
DAVIDSON, G. L., COOKE, A. C., JOHNSON, C. N. & QUINN, J. L. 2018. e gut microbiome as a
driver of individual variation in cognition and functional behaviour. Philos Trans R Soc Lond B Biol
Sci, 373, 20170286.
ERICKSON, L. D., BROWN, B. L., GALE, S. D. & HEDGES, D. W. 2021. Association between
Toxoplasma gondii and seropositivity and serointensity and brain volume in adults: A crosssectional study. PLoS One, 16, e0245994.
ERICKSON, L. D., WHITE, D. S., BASSETT, P., GALE, S. D., BROWN, B. L. & HEDGES, D. 2023.
Cognitive function in UK adults seropositive for Helicobacter pylori. PLoS One, 18, e0286731.
FISCHER, D., SNIDER, S. B., BARRA, M. E., SANDERS, W. R., RAPALINO, O., SCHAEFER, P.,
FOULKES, A. S., BODIEN, Y. G. & EDLOW, B. L. 2022. Disorders of consciousness associated with
COVID- 19: A prospective multimodal study of recovery and brain connectivity. Neurology, 98,
e315– e325.
FOLEY, P. B. 2018. Encephalitis Lethargica: e Mind and Brain Virus. New York: Springer.
HOFFMAN, L. A. & VILENSKY, J. A. 2017. Encephalitis lethargica: 100 years aer the epidemic. Brain,
140, 2246– 2251.
JIMENEZ, J. L., MARR, L. C., RANDALL, K., EWING, E. T., TUFEKCI, Z., GREENHALGH, T.,
TELLIER, R., TANG, J. W., LI, Y. & MORAWSKA, L. 2022. What were the historical reasons for the
resistance to recognizing airborne transmission during the COVID‐19 pandemic? Indoor Air, 32,
e13070.
JOHANNESDOTTIR SCHMIDT, S. A., VERES, K., SORENSEN, H. T., OBEL, N. & HENDERSON,
V. W. 2022. Incident herpes zoster and risk of dementia: A population- based Danish cohort study.
Neurology, 99, e660– e668.
KENNEDY, P. G. E. & RODGERS, J. 2019. Clinical and neuropathogenetic aspects of human African
trypanosomiasis. Front Immunol, 10, 39.
KHALIFA, M. M., SHARAF, R. R. & AZIZ, R. K. 2010. Helicobacter pylori: A poor man’s gut pathogen?
Gut Pathog, 2, 2.
KOUNTOURAS, J., TSOLAKI, M., GAVALAS, E., BOZIKI, M., ZAVOS, C., KARATZOGLOU, P.,
CHATZOPOULOS, D. & VENIZELOS, I. 2006. Relationship between Helicobacter pylori infection
and Alzheimer disease. Neurology, 66, 938– 940.
Infectious Disease and Neurocognition
LIU- HELMERSSON, J., ROCKLOV, J., SEWE, M. & BRANNSTROM, A. 2019. Climate change may
enable Aedes aegypti infestation in major European cities by 2100. Environ Res, 172, 693– 699.
LOUIS, S., CARLSON, A. K., SURESH, A., RIM, J., MAYS, M., ONTANEDA, D. & DHAWAN, A. 2023.
Impacts of climate change and air pollution on neurologic health, disease, and practice: A scoping
review. Neurology, 100, 474– 483.
MAGUSALI, N., GRAHAM, A. C., PIERS, T. M., PANICHNANTAKUL, P., YAMAN, U., SHOAI,
M., REYNOLDS, R. H., BOTIA, J. A., BROOKES, K. J., GUETTA- BARANES, T., BELLOU, E.,
BAYRAM, S., SOKOLOVA, D., RYTEN, M., FRIGERIO, C. S., ESCOTT- PRICE, V., MORGAN, K.,
POCOCK, J. M., HARDY, J. & SALIH, D. A. 2021. A genetic link between risk for Alzheimer’s disease and severe COVID- 19 outcomes via the OAS1 gene. Brain, 144, 3727– 3741.
PIEKUT, T., HURLA, M., BANASZEK, N., SZEJN, P., DORSZEWSKA, J., KOZUBSKI, W. &
PRENDECKI, M. 2022. Infectious agents and Alzheimer’s disease. J Integr Neurosci, 21, 73.
ROSTAMI, A., RIAHI, S. M., HOLLAND, C. V., TAGHIPOUR, A., KHALILI- FOMESHI, M., FAKHRI,
Y., OMRANI, V. F., HOTEZ, P. J. & GASSER, R. B. 2019. Seroprevalence estimates for toxocariasis in
people worldwide: A systematic review and meta- analysis. PLoS Negl Trop Dis, 13, e0007809.
WAINBERG, M., LUQUEZ, T., KOELLE, D. M., READHEAD, B., JOHNSTON, C., DARVAS, M. &
FUNK, C. C. 2021. e viral hypothesis: How herpesviruses may contribute to Alzheimer’s disease.
Mol Psychiatry, 26, 5476– 5480.
WANG, X., JIANG, D. M., LI, T. X., ZHANG, X., WANG, R., GAO, S., YANG, F. Y., WANG, Y., TIAN,
Q., XIE, C. R. & LIANG, J. H. 2022. Association between microbiological risk factors and neurodegenerative disorders: An umbrella review of systematic reviews and meta- analyses. Front Psychiatry,
13, 991085.
WATILA, M. M., BALARABE, S. A., KOMOLAFE, M. A., IGWE, S. C., FAWALE, M. B., OTTE, W. M.,
VAN DIESSEN, E., OKUNOYE, O., MSHELIA, A. A., ABDULLAHI, I., MUSA, J., HEDIMA, E. W.,
NYANDAITI, Y. W., SINGH, G., WINKLER, A. S. & SANDER, J. W. 2021. Epidemiology of epilepsy
in Nigeria: A community- based study from 3 sites. Neurology, 97, E728– E738.
ZHAN, X. H., STAMOVA, B., JIN, L. W., DECARLI, C., PHINNEY, B. & SHARP, F. R. 2016. Gram-
negative bacterial molecules associate with Alzheimer disease pathology. Neurology, 87, 2324– 2332.
PART I
VIRAL DISEASES IN NEUROCOGNITIVE
AND NEUROPSYCHIATRIC MEDICINE