Vekselvirkning mellom menneske og bakterie: på slimhinner og hud Infeksjon: når bakterien gror i verten (trenger ikke merkes av verten) Sykdom: dersom bakterien forårsaker skade hos verten

Bacterial interactions with mucous membranes Figure: 21-01 Caption: Bacterial interactions with mucous membranes. (a) Loose association. (b) Adhesion. (c) Invasion into submucosal epithelial cells.

Normalflora på hud: Stort sett gram positive (som ikke krever så mye fuktighet): Corynebakterier (Propionebakterium acnes) Staphylococcus arter Acinetobacter (gram negativ) Figure: 21-02 Caption: The human skin. Microorganisms are associated primarily with the sweat ducts and the hair follicles.

Belegg på tannoverflaten: -mikrokolonier (noen typer Streptokokk) -glykoproteiner fra spytt Tykk biofilm: Mange typer bakterier, også anaerobe Karies: Streptococcus sobrinus Streptococcus mutants Figure: 21-05 Caption: Distribution of dental plaque, as revealed by use of a disclosing agent, on brushed (top) and unbrushed (bottom) teeth. The numbers give the total area of dental plaque. The red areas indicate plaque. Note that the plaque builds preferentially near the gum line, first occurring directly adjacent to the mucous membranes of the gingiva.

Figure: 21-08 Caption: The human gastrointestinal tract showing functions and the distribution of nonpathogenic microorganisms usually found in normal (healthy) individuals.

Staphylococcus aureus Streptococcus pneumoniae Nedre luftveier: Ingen Normalflora: Øvre luftveier: Staphylococcus aureus Streptococcus pneumoniae Nedre luftveier: Ingen Urinrør: Escherichia coli Proteus mirabilis (opportunistisk patogene) Skjede: Lactobacillus acidophilus (beskyttende) Figure: 21-10 Caption: The respiratory tract. The upper respiratory tract is populated with a large variety and number of microorganisms, but the lower respiratory tract has relatively few microbial inhabitants, unless there is an ongoing active infection (Figure 26.2).

Figure: 21-12 Caption: Microorganisms and pathogenesis. The presence and even growth of microorganisms on the host does not always lead to disease.

Spesifikke festemekanismer: -Glycocalyx/kapsel/slimlag -Adherens proteiner -Cellevegg komponenter -Fimbrier og pili Invasjon, kolonisering og vekst avhenger av: -evne til å omgå vertens forsvar -tilgang på næring, jern og sporstoffer

Virulens: Evne til å skape sykdom Avhenger av: -invasjonsevne (f.eks Streptococcus pneumoniae) -toksisitet (f.eks. Clostridium tetani) Figure: 21-15 Caption: Comparison of differences in microbial virulence based on the number of cells of Streptococcus pneumoniae or Salmonella typhimurium required to kill mice.

Proteiner (som oftest) som produseres av bakterien Virulensfaktorer: Proteiner (som oftest) som produseres av bakterien og eksporteres for å hjelpe kolonisering of vekst (eks. hyaluronidase som bryter ned et polysakkaridet mellom vertens celler) Exotoxiner (skilles ut av bakterien): -cytolytiske toksiner (forårsaker lysis av vertens celler) AB toksin (to komponenter, B binder til vertscelleoverflaten, A transporteres inn og virker som toksin) Superantigen (stimulerer immunresponsen og forårsaker forsterkede betennelsesreaksjoner) Endotoxin (er en del av bakterien): Forårsaker feber fordi endotoksin stimulerer vertens celler til å frigjøre faktorer som påvirker det temperaturkontrollerende senteret I hjernen. I tillegg: diaré og betennelsesreaksjoner. (eks. Lipopolysakkarid fra gram negative bakteriers yttermembran)

Eksempler på patogene bakterier som produserer AB exotoksiner: Organisme Sykdom Toksin Corynebacterium Difteri Difteritoksin (AB) diphteriae Vibrio cholerae Kolera Enterotoksin (AB) Clostridium botulinum Botulisme Nevrotoksin (AB) Clostridium tetani Stivkrampe Nevrotoksin (AB) Bacillus anthracis Miltbrann Letal faktor (LF), Ødem faktor (EF) og ”protective antigen” (AB)

Vertscellens proteinsyntese avhenger av at elongeringsfaktor 2 henter en t-RNA med aminosyre til ribosomet Figure: 21-18a Caption: The action of diphtheria toxin from Corynebacterium diphtheriae. (a) Elongation factor 2 (EF-2) normally binds to the ribosome and brings an amino acid-charged t-RNA to the ribosome, causing protein elongation.

vertscellens proteinsyntese ved å inaktivere elongeringsfaktor 2 Difteritoksin hemmer vertscellens proteinsyntese ved å inaktivere elongeringsfaktor 2 Kun Corynebacterium diphteriae lysogen med -fag (som bærer tox genet) er patogen Figure: 21-18b Caption: The action of diphtheria toxin from Corynebacterium diphtheriae. (b) Diphtheria toxin binds to the cell membrane, where it is cleaved and the A peptide is internalized. The A peptide catalyzes the ADP-ribosylation of elongation factor 2 . The modified elongation factor no longer aids transfer of amino acids to the growing polypeptide chain, resulting in shutdown of protein synthesis and death of the cell.

Sammentrekning av muskelcelle avhenger av at acetylcholin frigjøres fra nervecelle enden Figure: 21-19a Caption: The action of botulinum toxin from Clostridium botulinum. (a) Upon central nervous stimulation, acetylcholine (A) is normally released from vesicles at the neural side of the motor end plate. Acetylcholine then binds to specific receptors on the muscle, inducing contraction.

Botulinumtoksin hindrer frigjøring av acetylcholin, som resulterer i mangel på sammentrekning i muskelceller Figure: 21-19b Caption: The action of botulinum toxin from Clostridium botulinum. (b) Botulinum toxin acts at the motor end plate to prevent release of acetylcholine (A) from vesicles, resulting in a lack of stimulus to the muscle fibers, irreversible relaxation of the muscles, and flaccid paralysis. (Section 29.5).

Figure: 21-20a Caption: The action of tetanus toxin from Clostridium tetani. (a) Muscle relaxation is normally induced by glycine (G) release from inhibitory interneurons. Glycine acts on the motor neurons to block excitation and release of acetylcholine (A) at the motor end plate.

Figure: 21-20b Caption: The action of tetanus toxin from Clostridium tetani. (b) Tetanus toxin binds to the interneuron to prevent release of glycine from vesicles, resulting in a lack of inhibitory signals to the motor neurons, constant release of acetylcholine to the muscle fibers, irreversible contraction of the muscles, and spastic paralysis. (Section 27.8 and Figure 27.19).

Enterotoxiner: Exotoxiner som virker i tynntarmen. Forårsaker massiv utskillelse av væske. Lages av både patogene i tarmen (eks. Escherichia coli, AB toksin, Vibrio cholerae, AB toksin) og bakterier som forurenser mat (eks. Bacillus cereus , Clostridium perfringens (cytolytisk toksin), Staphylococcus aureus, superantigen).

Figure: 21-21a Caption: Action of cholera enterotoxin. (1) The normal process of ion movement in the intestine and colonization of the epithelium by Vibrio cholerae followed by binding of the enterotoxin by specific interaction with the GM1 ganglioside on host cells. (2) The A-B toxin acts by internalizing the toxic A component and activating adenyl cyclase.

Figure: 21-21b Caption: Action of cholera enterotoxin. (3) leading to disruption of normal sodium influx, (4) loss of into the lumen, and diarrhea. Treatment for cholera is by ion replacement and rehydration therapy. Antibiotic treatment may shorten the course of the disease by limiting V. cholerae growth, but has no effect on toxin that has already been produced.

Vertens forsvarssystemer: Spesifikke (immunrespons) Uspesifikke: inflammasjon og feber Fysiske og kjemiske barrierer Konkurrerende normalflora Figure: 21-23 Caption: Physical, chemical, and anatomical barriers to infection.