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Veterinary Microbiology

Written by: Riley Holman • 2019 Scholar

The complex interplay between stress and bacterial infections in animals.

Stress -> glucocorticoids, catecholamines and neuroendocrine factors released into circulation Chronic stress -> shifts T helper 1- mediated cellular immunity to T helper 2 mediated humoral. This shift can increase susceptibility of host infection.


  • Stress = stimulus to brain that activates sympathetic nervous system
  • Chronic stress increases susceptibility to infection by suppressing the immune system What is released when stressed?
  • Catecholamines (norepinephrine and epinephrine) via SNS.
    • Most important and fast acting
  • Glucocorticoids (cortisol and corticosterone) secreted via adrenal gland Hypothalamic-pituitary-adrenal-axis. Slow acting
  • Microbial endocrinology = microbiology and neurophysiology intersect to become new research area
    • Stress-related hormones affect the pathogenic microorganism itself or the host-pathogen interaction directly GIT, Respiratory, or skin bacteria activate the neuroendocrine stress response
    • Stress factors: inadequate housing, overcrowding, heat, cold, poor nutrition, transportation
      • Increase pathogen carriage, disease susceptibility, carcass contamination and pathogen shedding

Stress and stress-related hormones:

  • Stressors can be different depending on the species or individual, however stress response is the same.
    • Activation of SNS and hypothalamic-pituitary-adrenal axis-> catecholamines-> glucocorticoids

Activation of the SNS: catacholamines

  • Stress-> SNS->acetylcholine from pre-gang sympathetic fibers->adrenal medulla->epinephrine->bloodstream->SNS nerve terminals-> lymphoid organs
  • Catecholamines (epi and NE) bind to adrenergic GPCRs: alpha 1 and 2, beta 1, 2, and 3 subtypes
    • All lymphoid cells express beta adrenergic (beta 2 is most important)
    • GTP guanosine triphosphate stimulates production of cAMP-> modulates cytokine expression

Activation of the hypothalamic-pituitary-adrenal axis: glucocorticoids

  • Stress->hypothalamus secretes corticotropin releasing factor that binds subtype 1 receptors located on anterior pituitary-> ant. pit then releases ACTH into systemic circulation-> triggers glucocorticoid (cortisol) secretion from adrenal glands ->unbound cortisol crosses cell membrane via passive diffusion
  • Glucocorticoids regulate wide range of functions: growth, metabolism, cardiovascular system, and immune modulation
  • Stress hormones can have a direct effect on all cells of the immune system because they all have receptors for cortisol

Effects of stress on the innate and acquired immune system

  • Chronic stress: stimulates humoral (antibody) immunity Inhibits cellular (T-cell) immunity
    • Inhibits cellular (T-cell) immunity by switching the cytokine majority from type-1 to type 2...increases risk of infection
  • Glucocorticoids suppress IL-12 production via APCs and down-regulate IL-12 receptor expression on NKs and T-cells
  • TH1 is down regulated d/t IFN-y secretion
  • IL-1, IL-2, IL-6, IL-8, IL-11, and macrophage colony-stimulating factor are suppressed, as well
  • Upregulate anti-inflammatory cytokines IL-4 and IL-10 production
    • Stress increases the IL-10 production by Th2 cells

Effects of stress on the intestinal barrier

  • Enteric nervous system controls GIT
    • Linked with CNS via sympathetic and parasympathetic
  • Intestinal barrier function: control nutrient uptake while protecting against noxious agents
    • Many cellular targets for glucocorticoids and catecholamines...stress mediators lead to bacterial invasion via altering commensal bacteria or altering mucosal integrity
  • Commensal bacteria-bacteriocin production (antimicrobial), alter pH
  • Mucous layer- physical barrier
  • Enterocytes- tight junctions for epithelial transport
  • Epithelium- antimicrobial peptides and barrier
  • Lamina propria- Enteric NS, endocrine system, immune system, intestinal motility
  • NE -> myenteric plexus (submucosa and mucosa) -> increases motility -> flushes out microbiota = pot. Pathogen exp

The effects of stress-related hormones on course of bacterial infections

  • Catecholamines stimulate bacterial growth and virulence (bacteria respond via quorum sensing)

Escherichia coli

  • Normal inhabitant of GIT in mammals, birds and reptiles
    • Includes commensal and virulent E. coli
  • Enterotoxogenic E. coli (ETEC)-> watery diarrhea from NE stimulating growth
  • Enterohemorrhagic E. coli (EHEC)-> hemorrhagic colitis and haemolytic uremic syndrome. Zoonotic Iron- bacteria need iron for growth and survival...host will dec. iron availability as defense
    • But catecholamines remove iron form host and make them available for bacteria and increase biofilms

Salmonella enterica

  • Salmonella Typhimurium most predominat serovar in pigs
  • Salmonella Enteritidis egg contaminator in birds
  • Systemic infections can cause encephalopathy in cattle
  • NE-> increases bacterial replication by increasing iron availability->increases risk of contaminating others

Campylobacter jejuni

  • Commensal colonies in intestines of chickens, turkeys, duck and pigs
  • Most common bacterial cause of food-borne disease (industrial countries)
  • Stress induced pathogenesis unknown
  • C. jejuni expresses CfrA ferric enterobactin receptor to eventually use as iron source Horizontal transmission


  • Macrophages are first line of defense
  • Adrenergic receptors influence whether macrophages are activated or suppressed by catecholamines
  • (stress hormones affect the outcome of mycobacterial infections by suppressing the macrophage-pathogen interaction) M. avium subsp. paratuberculosis-> dec. milk production in ruminants, weight loss, diarrhea without clinical signs during long incubation

Staphylococcus epidermis

NE stimulates biofilm proliferation
Stress response isn’t confined to just pathogens...affects commensal bacteria/microflora Coagulase-negative staphylococci protect against pathogens (S. aureus) and serves as a probiotic


  • Stress alters bacterial infections d/t host dependency and bacterium pathogenicity
  • In vitro studies prove catecholamines and glucocorticoids increase virulence and growth of many bacterial species


  • Duration of stress
  • Host’s immunity
  • Virulence of pathogen
  • Amount of pathogen exposure

Acute stress- enhanced host cell-mediated immunity (quick T-cell response)

Chronic stress- suppressed cell-mediated immunity...infection is dependent on chronic exposure to stress. Stress can increase biofilms and resistance of E. coli to antimicrobials. Animal welfare is crucial to minimizing stress.

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