第6章 细菌的感染与免疫

							Chapter 11

        bacterial
infection and immunity
Pathogen: A microorganism capable of
 causing disease.

Nonpathogen: A microorganism that
 does not cause disease.
Opportunistic pathogen: some non-
 pathogens may cause diseases under
 some special conditions.
                   infection
 Theprocess of interplay between M. and
 host.

 M.                      Host defenses

 Different   results after infection
Section 1

    normal microbial
flora and opportunistic B.
  1.Normal flora

 The  various B. and F. that are permanent
  residents of certain body sites
 vary in number and kind from one site to
  another
 the locations are usually skin, oropharynx,
  colon, and vagina (mucous membranes)
Role of normal flora

 keep   health

 Cause   disease
2. beneficial effects of the normal
                flora

   Priming of immune system
     play an important role in the
      development of immunologic
      competence
     Induce cross-reaction with
      pathogenic organisms
   exclusionary effect --- colonization
    resistance

   Production of essential nutrients ---
    - produce several B vitamins and
    vitamin K
3. opportunistic B.

 Many  species among the normal
 flora are opportunists.

 Member  of the normal flora may
 themselves produce disease under
 certain circumstances.
  three conditions correlated with
       opportunistic infection

 Change   of inhabiting places

 Immune   system compromise

 dysbacteriosis
dysbacteriosis

 When the resident flora is disturbed,
 some little significant M. may
 colonize, proliferate and produce
 diseases.

 Mainlyresult from long term and
 large doses antibiotics taken
Section 2

    bacterial
  pathogenesis
Pathogenicity: the capacity of B. to initiate
 diseases


virulence :A quantitative measure of
  pathogenicity
  LD50: the number needed to kill half the
hosts
  ID50: the number needed to cause infection
In half the hosts
    Bacterial virulence factors

 Adherence   factors
 Invasion of host cells and tissues
 Toxins
 Enzymes
 Antiphagocytic factors
 Bacterial biofilms
A. Adherence factors

 Surface hydrophobicity and net
  surface charge
 Surface molecules of B.
   pili
   lipoteichoic acid, protein F, M protein
 B. Invasion of host cells and tissues

 Invasion: the entry of B. into host cell

 The bacteria produce virulence factors that
 influence the host cells, causing them to
 engulf (ingest) the bacteria

 enzymes
Antiphagocytic factors

   Capsule: prevent the phagocyte from
    adhering to the B.

 The   cell wall proteins of the G+ cocci
     M protein: antiphagocytic
     protein A: binds to IgG
                prevent the activation of C
C. toxins
Two groups
   exotoxin
   endotoxin


  P85 table 11-2
1. exotoxin

 Excreted  by living cell
 produced by G+ and G- B.
 Polypeptides
 Relatively unstable ( heating )
 Highly antigenic:
  antitoxins---- prevention
  toxoids----used in protective vaccines
    exotoxin
 toxicity is high
 Usually bind to specific receptors on cell
 polypeptides, encoded by plasmid or
  bacteriophage DNA
 have an A-B subunit structure
  A: toxic activity
  B: bind the exotoxin to
     specific receptors
 2. endotoxin

 component   of the cell wall
 present only in G- B.
 LPS, encoded by genes on the bacterial
  chromosome
 Relatively stable
 2. endotoxin

 weakly  antigenic
 toxicity is low
 No specific receptors found on cells
 all produce the same generalized effects
The activities of LPS

 Fever
 Leukopenia and hypoglycemia
 Hypotension and shock
 Complement cascade
 Disseminated intravascular coagulation
The biologic effects of endotoxin

1.   Fever: the release by macrophages of
     endogenous pyrogen
2.   Hypotension, shock, impaired perfusion
     of essential organs: vasodilation,
     increase vascular permeability, decrease
     peripheral resistance
3. DIC: activation of the coagulation
    system
4. Inflammation and tissue damage:
    activate the C. cascade
5. Activation of macrophages and B
    lymphocytes
D. enzymes

 tissue-degrading   enzymes

 IgA1   proteases
 E. Antiphagocytic factors
Antiphagocytic surface structures
 Capsule
 Impede phagocytosis
 Protein A
 M protein
F. Bacterial biofilms
 An aggregate of interactive B. attached
 to a solid surface or to each other and
 encased in an exopolysaccharide matrix

         from planktonic or free-living
 Distinct
 bacterial growth
Asingle species of B. may be involved, or
 more than one species may coaggregate

 Genes may be activated that influence
 metabolic pathways and the production of
 virulence factors

   deep within the matrix tend to have
 B.
 decreased metabolism
 Someof the B. within the biofilm show
 marked resistance to antimicrobials

            of M. occur within the biofilm
 Interactions
 (community)

 Drug-resistance   can spread fast

 Areimportant in human infections that are
 persistent and difficult to treat
Section 3

 host defence against
bacterial infection
Section 4

  the initiation and
course of infection
 Sources of infection

   exogenous infection

 Endogenous      infection
    ( opportunistic pathogen infection)
A. Exogenous infection

 Patients


 Carriers


 animals
patients

 May transmit the pathogens from
 the incubation period to recovery
 stage of the disease
   carriers
 Healthy carries: harbor the pathogens
  but are not ill
 Incubatory carriers: incubating the
  pathogens in large numbers but are not
  yet ill
 Convalescent carriers: have recovered
  from the infectious disease but continue
  to harbor large numbers of the
  pathogens
 carries

 May harbor the pathogens for only a brief
 period or for long periods

 May be the important sources of
 infection
 animals
 Existprimarily in animals and
 incidentally infect humans

 Produce  infection of humans that is
 inadvertent, a mistake in the normal life
 cycle of the organism
 B. Endogenous infection
   causing diseases come from host
 B.
 where they reside

     of endogenous infections are
 Most
 opportunistic pathogen infections
Pathway of bacterial entrance
  Contact
  Inhalation
  Ingestion
  Inoculation
  Animal   vectors
Types of bacterial infection

 Inapparent infection
 Apparent infection
 carrier

   M.                  Host defenses
     induce various types
A. Inapparent infection
 Subclinical
 Theindividual is sometimes referred to
 as a carrier
          overpower
 M.                  Host defenses
B. Apparent infection
 The   hosts have evident clinic symptoms

         overpower
 M.                   Host defenses
If B. spread to whole body
 Bacteriemia:   B. circulate but not multiply
 in the blood

 Septicemia: B. circulate and multiply in
 the blood, produce toxic products and
 cause high swinging type of fever and
 other toxic symptoms
 Pyemia:pyogenic B. produce septicemia
 with multiple abscesses in internal
 organs

 Toxemia:B. multiply at invading location
 and do not enter blood stream, but the
 exotoxins enter blood and cause
 corresponding toxic symptoms

 Endotoxemia:   G- B. release a lot of
 amount endotoxin released from
 bacterial cell rupture
C. carrier
 Afterinapparent or apparent infection
 the pathogens are not eliminated in time,
  the B. still survive and multiply in host at
  low speed
 B. spread into the environment
 Important sources of infection