Clinical Microbiology and Infection 24 (2018) 24e28

Contents lists available at ScienceDirect

Clinical Microbiology and Infection

journal homepage: www.clinicalmicrobiologyandinfection.com

Review

Body mass index and the risk of infection - from underweight

to obesity
J. Dobner 1, S. Kaser 1, 2, *
1)
Christian Doppler Laboratory for Metabolic Research, Medical University Innsbruck, Innsbruck, Austria
2)
Department of Internal Medicine 1, Medical University Innsbruck, Austria

a r t i c l e i n f o a b s t r a c t

Article history: Background: Nutritional status is a well-known risk factor for metabolic and endocrine disorders. Recent
Received 28 November 2016 studies suggest that dietary intake also affects immune function and as a consequence infection risk.
Received in revised form Aims: This reviews aims to give an overview on the effect of body weight on infection rate at different
11 February 2017
periods of life.
Accepted 12 February 2017
Available online 20 February 2017
Sources: Clinically relevant prospective, cross-sectional and caseecontrol community-based studies are
summarized.
Editor: L. Leibovici Content: In children and adolescents underweight is a significant risk factor for infection especially in
developing countries, probably reflecting malnutrition and poor hygienic standards. Data from indus-
Keywords: trialized countries suggest that infection rate is also increased in obese children and adolescents.
Anorexia nervosa Similarly, several studies suggest a U-shaped increased infection rate in both underweight and obese
Body mass index adults. In the latter, infections of the skin and respiratory tract as well as surgical-site infections have
Infection risk consistently been reported to be more common than in normal-weight participants. Paradoxically,
Obesity
mortality of critically ill patients was reduced in obesity in some studies.
Underweight
Implications: Several studies in children or adults suggest that both underweight and obesity are asso-
ciated with increased infection risk. However, confounding factors such as malnutrition, hygienic status
and underlying disease or co-morbidities might aggravate accurate assessment of the impact of body
weight on infection risk. J. Dobner, Clin Microbiol Infect 2018;24:24
© 2017 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All
rights reserved.

Introduction challenging due to several confounding factors such as malnutri-

Infectious and parasitic diseases are the second most common
cause of death worldwide and the most common cause of death in
low-income countries. Malnutrition and poor hygienic standards
might contribute to high infection rates in developing countries. On
the other hand, obesity has become a huge health burden in
western countries. Besides increased cardiovascular risk and higher
malignancy rates [1e3], obesity is also associated with impaired
immune responses, highlighting the close interaction between
metabolic control und immune tolerance [4]. Evaluation of the
clinical consequences of an altered immune response remains
* Corresponding author. S. Kaser, Christian Doppler Laboratory for Metabolic
Research, Department of Internal Medicine 1, Medical University Innsbruck,
Anichstrasse 35, 6020 Innsbruck, Austria.
E-mail address: susanne.kaser@i-med.ac.at (S. Kaser).
tion, underlying disease or co-morbidities.
Search criteria
We conducted a search for clinical studies or potentially relevant
meta-analyses or reviews by combining the following terms for
search in Medline: infection risk, obesity, body mass index, un-
derweight, overweight, anorexia, adiposity, immune function,
weight reduction, bariatric surgery and weight loss. Relevance of
studies was assessed by study size, study design and clinical char-
acterization of the study population including age and relevant co-
morbidities. Prospective, cross-sectional and caseecontrol
community-based studies were included. Unless otherwise indi-
cated, female and male participants were investigated in listed
studies. Literature research was focused on studies published be-
tween 2006 and 2016; however, some important studies published
before 2006 were considered due to missing recent data. Children

http://dx.doi.org/10.1016/j.cmi.2017.02.013
1198-743X/© 2017 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
 J. Dobner, S. Kaser / Clinical Microbiology and Infection 24 (2018) 24e28
or adolescents were defined as underweight or undernourished
when having a weight-to-height z-score < e2 standard deviations
(SD) or a body mass index (BMI) for age <2 SDs of WHO standards.
In adults, underweight was defined as a BMI <18.5 kg/m2, over-
weight as BMI between 25 and 30 kg/m2 and obese as BMI >30 kg/
m2 unless otherwise indicated.
Influence of BMI on infection risk in children and adolescents
Several studies in infants and young children suggest that un-
derweight rather than obesity is associated with raised infection
risk. In hospitalized sub-Saharan African children aged from 3
weeks to 2 years cytomegalovirus DNAemia was independently
associated with underweight defined as weight-for-height z-score
< e2 SD [5]. Other cross-sectional, community-based surveys also
revealed increased prevalence of helminth and parasitic
infections in children with low BMI aged between 6 months and
15 years in developing countries [6,7]. In another prospective
study performed in outpatient human immunodeficiency virus-
infected and -uninfected children aged 6 weeks to 1 year, stunt-
ing (which is defined as low height-for-age and indicative of
chronic malnutrition) but not underweight was associated with
increased incidence of malaria infection [8]. Not only risk of
infection but also infection-related morbidity was increased in In-
dian preschool children with low BMI for age when compared with
normal-weight children in a National Family Health Survey data-
base [9].
Underweight children are not only at higher infection risk in
developing countries but also in Western countries. In the USA,
observational chart review revealed that underweight children
were more frequently admitted to emergency units with respira-
tory infections than normal-weight, overweight or obese children
even when adjusted for age and sex [10]. Increased rates of surgical
site infections were also reported in underweight US children and
adolescents of both sexes aged between 2 and 19 years undergoing
clean orthopaedic procedures [11]. In these studies underweight
was defined as BMI <5th percentile for age and gender [10,11].
Risk of infection is less clear in overweight and obesity. In a
cross-sectional study performed in the Dutch PIAMA birth cohort,
obesity defined by a BMI >30 kg/m2 in 8-year-old children was
associated with more than fivefold increased bronchitis rates and
also raised use of antibiotics [12]. Similarly, in an inpatient US
database of participants aged 2e20 years risk of urinary tract in-
fections was significantly increased in obese females but not in
obese males. Obesity was defined by >95th percentile of weight in
this study [13]. In paediatric patients who had burns covering more
than 30%, sepsis incidence was similar in normal-weight (mean age
9 ± 4 years) and obese children (mean age 10 ± 5 years) despite
existing metabolic alterations in the obese group. Obesity was
defined as >85th percentile of BMI in this study [14].
Influence of BMI on infection risk in adults
In a prospective Danish cohort the association between BMI and
hospitalization or treatment for acute infections was investigated
in 75 001 middle-aged women over a median time period of 11.9
years. Risk of overall infection, infection of the respiratory tract and
the skin was U-shaped, suggesting that both underweight and
obesity predispose to community-acquired infections in women
[15]. An earlier meta-analysis of 25 studies investigating more than
2.5 million adults and children older than 12 years living in
industrialized countries revealed that only underweight but not
overweight or obesity was associated with an increased risk of
community-acquired pneumonia. However, a U-shaped relation-
ship between BMI and risk of Influenza-related pneumonia was
25
found in this analysis [16]. Remarkably, Braun et al. reported from a
US population-based, laboratory-based surveillance system that
overweight and obesity (the latter defined as a BMI between
30
and <35 kg/m2) were associated with decreased pneumonia risk in
9048 young adults with laboratory-confirmed influenza even after
adjusting for clinical and demographic characteristics [17].
The effect of obesity on infection risk was especially stressed in a
registry-based analysis of 37 808 participants from the Danish
Blood Donor Study. Obesity was associated with a 50% increased
rate of hospital-based treated infections in healthy participants.
Abscesses occurred more commonly in obese participants of both
sexes, whereas infections of the skin and subcutaneous tissue were
found more frequently in males only. Rates of infection of the
respiratory tract and urinary tract (cystitis) were more common in
females [18]. Increased rates of bacterial or fungal skin infections in
obese participants were also found in other studies [19e21]. Data
are less clear for risk of urinary tract infections: although rates were
increased only in female but not in male, obese participants of the
Danish Blood Donor Study, a BMI
30 kg/m2 turned out to be a risk
factor for urinary tract infections and pyelonephritis in males and
females in a US insurance database analysis [22]. However, no in-
formation on co-morbidities was given in this report.
Obesity was also identified as an independent risk factor for
nosocomial infections such as pneumonia, Clostridium difficile co-
litis, bacteraemia and wound infections [23,24].
In a retrospective analysis of a US Quality Improvement Program
survey of 89 148 patients undergoing open abdominal procedures,
obesity and morbid obesity were identified as strong independent
risk factors of overall surgical site infection especially in clean or
clean-contaminated cases [25]. Similar results on increased surgical
site infection risk in obesity and morbid obesity were found in
several other studies [26e32].
Remarkably, Waisbren et al. [33] investigated the effect of body
fat content determined by body impedance analysis on surgical site
infection risk in patients undergoing elective surgery. Although
similar infection rates were observed in non-obese and obese
participants e as classified by BMI in this study e infection rates
were more than three times higher in obese patients defined by %
body fat than in non-obese participants. In this study, however,
diabetes rate was significantly higher in patients with post-
operative surgical site infection.
In a population-based longitudinal cohort study of 30 239 pa-
tients morbid obesity, but neither overweight nor obesity, was
associated with increased risk of sepsis even after adjusting for
sociodemographic factors, health behaviour, underlying disease,
statin use and high-sensitivity C-reactive protein [34]. In this study
waist circumference turned out to be a better predictor of sepsis
risk than BMI [34]. With respect to the clinical outcome the situa-
tion is partly different in obese intensive care patients: both short-
term and long-term mortality rates from surgical peritonitis were
found to be lowest in obese patients and highest in participants
with a BMI <21 kg/m2 despite a markedly increased length of stay
of obese patients at the intensive care unit and in hospital [35]. This
obesity paradox was also reported in patients with septic shock
[36]: in an international multicentre cohort study analysis of 8670
patients records showed significantly reduced mortality of obese
and morbidly obese participants. The authors suggested that dif-
ferences in sepsis interventions rather than different patient char-
acteristics might explain this finding. Other studies investigating
the association between obesity and sepsis mortality showed
mixed results with decreased, neutral or increased rates in obesity
as reviewed by Trivedi et al. recently [37].
Early studies suggest that patients with anorexia nervosa
represent an exception with regard to increased infection risk
found in underweight in general. Although some reports suggested
26 J. Dobner, S. Kaser / Clinical Microbiology and Infection 24 (2018) 24e28

increased tuberculosis risk [38,39], others found no increased
infection risk in patients with anorexia nervosa [40,41]. Rates of
viral infections were reported to be even reduced in anorexia
nervosa [38,42]; however, this finding might be explained by
reduced fever response and symptoms in these patients [43].
Influence of BMI on infection risk in the elderly
Due to the aging of the immune system, elderly patients in
general are more susceptible to infections. When investigating
infection risk in inpatient geriatric patients aged
75 years both
underweight (BMI <20 kg/m2) and overweight (BMI >28 kg/m2)
patients were at increased risk for overall infection [44]. A meta-
analysis of 19 538 nursing home residents (median age 84.3
years) revealed higher infection-related mortality in underweight
patients whereas overweight and even obesity was associated with
lower infection-related mortality when compared with normal-
weight patients [45]. Retrospective analysis of 66 820 clients (age

65 years) of Elderly Health Centres in Hong Kong revealed a U-
shaped relationship between BMI and influenza-associated mor-
tality [46].
Effect of weight change on infection risk
The effect of weight change on community-acquired pneumonia
was investigated in participants of the Health Professionals Follow-
up Study and the Nurses' Health Study II. In males aged <60 years a
weight gain of >18 kg during a follow up of 6 years was associated
with a twofold increased risk of community-acquired pneumonia.
Similarly, weight gain was also positively associated with raised risk
of community-acquired pneumonia in adult women even after
adjusting for age, smoking status, physical activity, alcohol intake
and pre-study BMI [47]. Risk of community-acquired infection was
lowest in women with a BMI range from 21 to 22.9 kg/m2 and
highest in participants with BMIs of >30 kg/m2 (relative risk 2.22).
Regarding effects of weight loss on infection rate, postoperative risk
was analysed in 22 327 patients undergoing gastric bypass surgery.
Patients were introduced to weight-reducing regimens preopera-
tively, resulting in a median weight reduction of 4.8% before sur-
gical intervention. When participants with a preoperative mean
weight loss of 9.5% were compared with those whose weight
remained stable (þ0.5 kg), the risk of postoperative deep infection
or abscess was significantly reduced by 37% in weight-reduced
patients [48].
Confounding factors and mechanistic considerations
The causes of increased infection risk in obesity are various
and diverse. Despite increased susceptibility for co-morbidities
such as type 2 diabetes, obesity per se is associated with
altered cytokine synthesis, reduced antigen response and
diminished function of natural killer cells, dendritic cells and
macrophages. Disruption of lymphoid tissue integrity by fat
accumulation and altered secretion of adipocytokines such as
leptin or adiponectin have been suggested to explain immune
dysfunction in obese patients. Effects of obesity on immune
function and the metabolic control of immune response have
been described in detail elsewhere [4,49,50]. The controversial
results on the effects of obesity on infection risk might be partly
explained by categorization of obesitydalthough frequently
used, BMI does not necessarily reflect total body fat content. The
latter, however, might be a better and more reliable predictor of
infection risk at least from a pathophysiological point of view.
Additionally, the adipose tissue distribution might also influence
infection risk due to immunomodulatory effects of adipose tissue
depot-specific cytokine and adipocytokine secretion.
Interpretation of data from underweight patients seems even
more complex as underweight is a heterogeneous condition
found in otherwise healthy participants as well as in patients
with underlying chronic disease, malnutrition and also in pa-
tients with eating disorders. Anorexia nervosa was not found to
be associated with increased viral infection risk in some studies
as impaired immune function was suggested to be less frequent
and less severe in these patients [51]. Indeed, leucocyte,
lymphocyte and T-cell counts were found depleted, CD4/CD8
ratios increased and CD2/CD19 ratios decreased in early studies
of patients with anorexia nervosa or bulimia nervosa [52e54].
One explanation for differing infection risk in patients with
anorexia nervosa and malnourished starving participants is that
while carbohydrate and fat intake are critically limited, protein
deficiency is frequently found during starvation but not in pa-
tients with anorexia nervosa [55]. Besides the underlying causes
or co-morbidities discussed here, several other factors exert
immunomodulatory effects and so might contribute to infection
risk. These include physical activity [56], nutritional aspects (di-
etary composition or supplements) [57], smoking behaviour
[47,58] and well-being [59]. Potential confounding factors are
listed in Table 2.

Table 1
Summary of listed studies on the association between underweight (with exception of studies in patients with anorexia nervosa) or obesity and infection rates

Underweight Obesity

Children/adolescents Developing countries Viral, helminth, parasitic infection [ [5e7]

Industrialized countries
Adults Industrialized countries
Elderly Industrialized countries
Malaria infection 4 [8]
Respiratory tract infection [ [10]
Surgical site infection [ [11]
Community-acquired infections (f) [ [15]
Community-acquired pneumonia [ [16]
Influenza-associated pneumonia [ [16]
Overall infection [ [44]
Acute bronchitis [ [12]
Urinary tract infections (f)[ (m) 4 [13]
Sepsis 4 [14]
Community-acquired infections (f) [ [15]
Community-acquired pneumonia 4 [16]
Influenzaeassociated pneumonia [Y [16,17]
Hospital-based treated infections [ [18]
Skin infections [ [19e21]
Urinary tract infections (f)[ [18,22] (m) 4[ [18,22]
Nosocomial infections [ [23,24]
Surgical site infection [4 (BMI) [25e33]
Sepsis [ (morbid obesity) 4 (obesity) [34]
Overall infection [ [44]

Abbreviations: BMI, body mass index; (f), females; (m), males.

 J. Dobner, S. Kaser / Clinical Microbiology and Infection 24 (2018) 24e28
Table 2
Potential confounders of reported associations between underweight or obesity and
infection risk independent of age, sex and hygienic standard
 Underlying disease (e.g. unintentional weight loss in chronic illness)
 Co-morbidities (e.g. type 2 diabetes) [60]
 Nutrition (e.g. specific diets, dietary supplements) [57]
 Physical activity [56]
 Smoking behaviour [47,58]
 Well-being [59]
Conclusions
Several epidemiological data suggest that body weight is asso-
ciated with rate of infection risk and also outcome of disease(see
Table 1). Whereas in children and adolescents underweight en-
hances the risk of several infections especially in developing
countries, enhances the risk of several infections, both obesity and
underweight have been found to increase infection risk in adults in
a U-shaped manner in several studies indicating that normal
weight is associated with the lowest infection risk in most subjects.
Mixed results of studies might be explained by heterogeneity of
study populations and environmental factors including diet and
lifestyle factors [61].
From the listed studies two major striking findings warrant
further investigation. First, despite alterations in immune function
anorexia nervosa was not associated with increased viral infection
risk in most studies. Second, obesity turned out to be protective
with respect to mortality in critically ill patients. Better patho-
physiological understanding of the responsible mechanisms in both
settings will help to better identify patients at risk.
Acknowledgement
Financial support from the Austrian Federal Ministry of Science,
Research and Economy and the National Foundation for Research,
Technology and Development is gratefully acknowledged.
Transparency Declaration
The authors declare no conflict of interest.
References
[1] Gluvic Z, Zaric B, Resanovic I, Obradovic M, Mitrovic A, Radak D, et al. Link
between Metabolic Syndrome and Insulin Resistance [Internet]. Current
Vascular Pharmacology 2017:30e9. Available from: http://www.eurekaselect.
com/node/146175/article.
[2] Tune JD, Goodwill AG, Sassoon DJ, Mather KJ. Cardiovascular consequences of
metabolic syndrome. Transl Res 2017; Jan 9 (epub ahead of print).
[3] Vucenik I, Stains JP. Obesity and cancer risk: evidence, mechanisms, and
recommendations. Ann N Y Acad Sci 2012;1271:37e43.
[4] Carbone F, La Rocca C, De Candia P, Procaccini C, Colamatteo A, Micillo T, et al.
Metabolic control of immune tolerance in health and autoimmunity. Semin
Immunol 2016;28:491e504.
[5] Tembo J, Kabwe M, Chilukutu L, Chilufya M, Mwaanza N, Chabala C, et al.
Prevalence and risk factors for betaherpesvirus DNAemia in children >3
weeks and <2 years of age admitted to a large referral hospital in sub-Saharan
Africa. Clin Infect Dis 2015;60:423e31.
[6] Sayasone S, Akkhavong K, Odermatt P. Multiparasitism and intensity of hel-
minth infections in relation to symptoms and nutritional status among chil-
dren: s cross-sectional study in southern Lao People's Democratic Republic.
Acta Trop 2015;141:322e31.
[7] Mahmud MA, Spigt M, Mulugeta Bezabih A, Lo
pez Pavon I, Dinant G-J, Blanco
Velasco R. Risk factors for intestinal parasitosis, anaemia, and malnutrition
among school children in Ethiopia. Pathog Glob Health 2013;107:58e65.
[8] Arinaitwe E, Gasasira A, Verret W, Homsy J, Wanzira H, Kakuru A, et al. The
association between malnutrition and the incidence of malaria among young
HIV-infected and -uninfected Ugandan children: a prospective study. Malar J
2012;11:90.
[9] Ramachandran P, Gopalan H. Undernutrition & risk of infections in preschool
children. Indian J Med Res 2009;130:579e83.
27
[10] Wyrick S, Hester C, Sparkman A, O'Neill KM, Dupuis G, Anderson M, et al.
What role does body mass index play in hospital admission rates from the
pediatric emergency department? Pediatr Emerg Care 2013;29(9).
[11] Cies JJ, Chan S, Hossain J, Brenn BR, Di Pentima MC. Influence of body mass
index and antibiotic dose on the risk of surgical site infections in pediatric
clean orthopedic surgery. Surg Infect (Larchmt) 2012;13:371e6.
[12] Wijga AH, Scholtens S, Bemelmans WJE, de Jongste JC, Kerkhof M, Schipper M,
et al. Comorbidities of obesity in school children: a cross-sectional study in
the PIAMA birth cohort. BMC Public Health [Internet] 2010;10:184. http://
dx.doi.org/10.1186/1471-2458-10-184. Available from.
[13] Grier WR, Kratimenos P, Singh S, Guaghan JP, Koutroulis I. Obesity as a risk
factor for urinary tract infection in children. Clin Pediatr (Phila) [Internet].
SAGE Publications 2016 Jan 24;55:952e6. Available from: http://journals.
sagepub.com/doi/abs/10.1177/0009922815617974.
[14] Kraft R, Herndon DN, Williams FN, Al-Mousawi AM, Finnerty CC, Jeschke MG.
The effect of obesity on adverse outcomes and metabolism in pediatric burn
patients. Int J Obes 2012;6:485e90. http://dx.doi.org/10.1038/ijo.2011.224.
Available from.
[15] Harpsøe MC, Nielsen NM, Friis-Møller N, Andersson M, Wohlfahrt J,
Linneberg A, et al. Body mass index and risk of infections among women in
the Danish national birth cohort. Am J Epidemiol 2016;183:1008e17. Avail-
able from: http://aje.oxfordjournals.org/content/183/11/1008.abstract.
[16] Phung DT, Wang Z, Rutherford S, Huang C, Chu C. Body mass index and risk of
pneumonia: a systematic review and meta-analysis. Obes Rev 2013;14:
839e57.
[17] Braun ES, Crawford FW, Desai MM, Meek J, Kirley PD, Miller L, et al. Obesity
not associated with severity among hospitalized adults with seasonal influ-
enza virus infection. Infection 2015;43:569e75.
[18] Kaspersen KA, Pedersen OB, Petersen MS, Hjalgrim H, Rostgaard K, Møller BK,
et al. Obesity and risk of infection: results from the Danish Blood Donor Study.
Epidemiology 2015;26:580e9.
[19] Thorsteinsdottir B, Tleyjeh IM, Baddour LM. Abdominal wall cellulitis in the
morbidly obese. Scand J Infect Dis 2005;37:605e8.
[20] Roujeau J-C, Sigurgeirsson B, Korting H-C, Kerl H, Paul C. Chronic dermato-
mycoses of the foot as risk factors for acute bacterial cellulitis of the leg: a
caseecontrol study. Dermatology 2004;209:301e7.
[21] García Hidalgo L. Dermatological complications of obesity. Am J Clin Dermatol
2002;3:497e506.
[22] Semins MJ, Shore AD, Makary MA, Weiner J, Matlaga BR. The impact of obesity
on urinary tract infection risk. Urology 2012;79:266e9.
[23] Huttunen R, Karppelin M, Syrj€ anen J. Obesity and nosocomial infections.
J Hosp Infect 2013;85:8e16.
[24] Falagas ME, Kompoti M. Obesity and infection. Lancet Infect Dis 2006;6:
438e46.
[25] Winfield RD, Reese S, Bochicchio K, Mazuski JE, Bochicchio GV. Obesity and
the risk for surgical site infection in abdominal surgery. Am Surg 2016;82:
331e6.
[26] Zahr F, Genovese E, Mathier M, Shullo M, Lockard K, Zomak R, et al. Obese
patients and mechanical circulatory support: weight loss, adverse events, and
outcomes. Ann Thorac Surg 2011;92:1420e6.
[27] Lilienfeld DE, Vlahov D, Tenney JH, McLaughlin JS. Obesity and diabetes as risk
factors for postoperative wound infections after cardiac surgery. Am J Infect
Control 1988;16:3e6.
[28] Crabtree TD, Codd JE, Fraser VJ, Bailey MS, Olsen MA, Damiano RJ. Multivariate
analysis of risk factors for deep and superficial sternal infection after coronary
artery bypass grafting at a tertiary care medical center. Semin Thorac Car-
diovasc Surg 2004;16:53e61.
[29] Tjeertes EKM, Tjeertes EEKM, Hoeks SE, Hoeks SSE, Beks SBJ, Beks SSBJC, et al.
Obesityda risk factor for postoperative complications in general surgery?
BMC Anesthesiol 2015;15:112.
[30] Vilar-Compte D, Mohar A, Sandoval S, de la Rosa M, Gordillo P, Volkow P.
Surgical site infections at the National Cancer Institute in Mexico: a case-
control study. Am J Infect Control 2000;28:14e20.
[31] Thelwall S, Harrington P, Sheridan E, Lamagni T. Impact of obesity on the risk
of wound infection following surgery: results from a nationwide prospective
multicentre cohort study in England. Clin Microbiol Infect 2015;21:
1008.e1e8.
[32] Olsen MA, Mayfield J, Lauryssen C, Polish LB, Jones M, Vest J, et al. Risk factors
for surgical site infection in spinal surgery. J Neurosurg 2003;98(2 Suppl):
149e55.
[33] Waisbren E, Rosen H, Bader AM, Lipsitz SR, Rogers SO, Eriksson E. Percent
body fat and prediction of surgical site infection. J Am Coll Surg 2010;210:
381e9.
[34] Wang HE, Griffin R, Judd S, Shapiro NI, Safford MM. Obesity and risk of sepsis:
a population-based cohort study. Obesity (Silver Spring) 2013;21:E762e9.
[35] Utzolino S, Ditzel CM, Baier PK, Hopt UT, Kaffarnik MF. The obesity paradox in
surgical intensive care patients with peritonitis. J Crit Care 2014;29:887.e1e5.
[36] Arabi YM, Dara SI, Tamim HM, Rishu AH, Bouchama A, Khedr MK, et al. Clinical
characteristics, sepsis interventions and outcomes in the obese patients with
septic shock: an international multicenter cohort study. Crit Care 2013;17:R72.
[37] Trivedi V, Bavishi C, Jean R. Impact of obesity on sepsis mortality: a systematic
review. J Crit Care 2015;30:518e24.
[38] Dally PJ, Sargant W. Anorexia nervosa. Br Med J 1969;1(5643):529e30.
[39] Crisp AH, Palmer RL, Kalucy RS. How common is anorexia nervosa? A prev-
alence study. Br J Psychiatry 1976 Jun 1;128:549e54 [cited 2016 Nov 28].
28 J. Dobner, S. Kaser / Clinical Microbiology and Infection 24 (2018) 24e28
[40] Bowers TK, Eckert E. Leukopenia in anorexia nervosa: lack of increased risk of
infection. Arch Intern Med 1978;138:1520e3.
[41] Palla B, Litt IF. Medical complications of eating disorders in adolescents. Pe-
diatrics 1988;81. 613 LP-623.
[42] Armstrong-Esther CA, Lacey JH, Crisp AH, Bryant TN. An investigation of the
immune response of patients suffering from anorexia nervosa. Postgrad Med J
1978;54(632):395e9.
[43] Brown RF, Bartrop R, Beumont P, Birmingham CL. Bacterial infections in
anorexia nervosa: delayed recognition increases complications. Int J Eat Dis-
ord 2005;37:261e5.
[44] Dorner TE, Schwarz F, Kranz A, Freidl W, Rieder A, Gisinger C. Body mass index
and the risk of infections in institutionalised geriatric patients. Br J Nutr
2010;103:1830e5.
[45] Veronese N, Cereda E, Solmi M, Fowler SA, Manzato E, Maggi S, et al. Inverse
relationship between body mass index and mortality in older nursing home
residents: a meta-analysis of 19,538 elderly subjects. Obes Rev 2015;16:
1001e15.
[46] Yang L, Chan KP, Lee RS, Chan WM, Lai HK, Thach TQ, et al. Obesity and
influenza associated mortality: evidence from an elderly cohort in Hong Kong.
Prev Med (Baltim) 2013;56:118e23.
[47] Baik I, Curhan GC, Rimm EB, Bendich A, Willett WC, Fawzi WW. A prospective
study of age and lifestyle factors in relation to community-acquired pneu-
monia in us men and women. Arch Intern Med 2000;160:3082e8.
[48] Anderin C, Gustafsson UO, Heijbel N, Thorell A. Weight loss before bariatric
surgery and postoperative complications. Ann Surg 2015;261:909e13.
[49] Andersen CJ, Murphy KE, Fernandez ML. Impact of obesity and metabolic
syndrome on immunity. Adv Nutr 2016;7:66e75.
[50] Naylor C, Petri WA. Leptin regulation of immune responses. Trends Mol Med
2016;22:88e98.
[51] Mustafa A, Ward A, Treasure J, Peakman MT. Lymphocyte subpopulations in
anorexia nervosa and refeeding. Clin Immunol Immunopathol 1997;82:
282e9.
[52] Marcos A, Varela P, Toro O, Lo
pez-Vidriero I, Nova E, Madruga D, et al. In-
teractions between nutrition and immunity in anorexia nervosa: a 1-y follow-
up study. Am J Clin Nutr 1997;66:485Se90S.
[53] Marcos A, Varela P, Toro O, Nova E, Lo
pez-Vidriero I, Morande
G. Evaluation of
nutritional status by immunologic assessment in bulimia nervosa: influence
of body mass index and vomiting episodes. Am J Clin Nutr 1997;66:491Se7S.
[54] Marcos A, Varela P, Santacruz I, Mun ~ oz-Ve
lez A, Morande
G. Nutritional status
and immunocompetence in eating disorders. A comparative study. Eur J Clin
Nutr 1993;47:787e93.
[55] Nova E, Varela P, Lo
pez-Vidriero I, Toro O, Cen ~ al MJ, Casas J, et al. A one-year
follow-up study in anorexia nervosa. Dietary pattern and anthropometrical
evolution. Eur J Clin Nutr 2001;55:547e54.
[56] Krüger K, Mooren FC, Pilat C. The immunomodulatory effects of physical ac-
tivity. Curr Pharmaceut Design 2016;22:3730e48.
[57] Urwin HJ, Miles EA, Noakes PS, Kremmyda L-S, Vlachava M, Diaper ND, et al.
Effect of salmon consumption during pregnancy on maternal and infant faecal
microbiota, secretory IgA and calprotectin. Br J Nutr 2014;111:773e84.
[58] Nuorti JP, Butler JC, Farley MM, Harrison LH, McGeer A, Kolczak MS, et al.
Cigarette smoking and invasive pneumococcal disease. N Engl J Med
2000;342:681e9.
[59] Lasselin J, Alvarez-Salas E, Grigoleit J-S. Well-being and immune response: a
multi-system perspective. Curr Opin Pharmacol 2016;29:34e41.
[60] Pearson-Stuttard J, Blundell S, Harris T, Cook DG, Critchley J. Diabetes and
infection: assessing the association with glycaemic control in population-
based studies. Lancet Diabetes Endocrinol 2016;4:148e58.
[61] Veonese N, Li Y, Manson JE, Willett WC, Fontana L, Hu FB. Combined as-
sociations of body weight and lifestyle factors with all cause and cause
specific mortality in men and women: prospective cohort study. BMJ
2016;355:i5855.