bacteriology wk 2

• necessary for colonization and to counteract washing action of fluids (innate response of host)
• adhesins interact with specific host receptors (host and cell-type specificity)
• pili (fimbral): bacteria only, pili interact with host glycoproteins/glycolipids
• afimbrial: bacteria and fungi. interact directly with host cell surface
• Use adherence to create biofilms

• product of adherence
• different cell types, non-specific adherence
• species act differently than free-living, more resistant.  Antibodies and antibiotics can't penetrate.  Stick to polysaccharids and extracellular matrix.  Protective.

• +: access to nutrients, no competing organisms, no clearance by immune system
• -: stuck, no new places

• love acid, somehow escape hydrolases or even raise pH
• escape from phagosome and live in cell
• pathway of phagosome to prevent full maturation (+/- acidification), live happily in specialized endosome

• prevent respiratory burst altogether
• detoxify toxic reactive oxygen intermediates
• superoxide dismutase converts O2- to H2O2 (which becomes OH- and HClO.  All aerobes produce this
• Catalase removes H2O2
• free radical scavengers

• inhibition of iNOS activity (deactivate induction enzyme or prevent induction or keep it from sticking to membrane so too far away)
• repair of RNI-induced damage
• detoxification of RNI

• downregulate gene expression
• make surface less negative so cations (defensins) won't bind
• pump antibiotics, toxins and antimicrobial proteins out of cell
• bind or cleave antimicrobials to prevent from attaching to membrane
• DO NOT REPAIR DAMAGE

• mask surface components with a capsule so mannose, etc can't recognize
• addition of sialic acid to LPS to inhibit complement fixation (degrades C3)
• long chain LPS - inhibits MAC access to surface (attack happens far from plasma membrane)
• C5a peptidase cleaves C5a chemotaxin
• prevent leukocyte extravasation (binds ICAM-1 to stop LFA-1 from binding)
• downregulate pro-inflammatory cytokines
• disable/kill phagocytic cells (toxin)

• bind IgG backwards/nonproductively (phagocytic cells not stimulated, antibody can grab another antibody, create huge clumps that also can't be phagocytized
• vary surface cell antigens regularly (vaccines impossible here) (biphasic illness--sick, better, sick)
• cleave IgA (just destroy antibody)
• inhibit T or B cell activation (prevent phosphorylation of receptor components or induce apoptosis)

• iron: siderophores, hemin binding proteins, transferrin binding proteins, iron reductases, metal transport proteins (bind transferrin or degrade so iron is released, take from host molecules.  Only borrelia doesn't need iron.
• some molecules like particular nutrients in particular sites, can help with ID

block dimorphism, block pathogenicity.  (some are polymorphic, depending on whether pseudohyphae count)

• product of microorganism that harms susceptible animals by altering cellular structure and/or function
• exotoxins are outside cells (protein)
• endotoxins are inside cell (lipopolysaccharide, only toxic under some circumstances, only released if cell is DEAD)

• low concentration: fever, vasodilation, increased antibody synthesis, inflammation (appropriate response)
• high concentration: endotoxic shock.  Hyperactivate TLR (produce IL-1, IL-6, IL-8, TNF-alpha, platelet activating factor, activates coag (DIC) and complement cascade, make prostaglandins and leukotrienes, endothelial damage), hyperinflammatory response, distributive shock, multiple system organ failure

lipotechoic acid, teichoic acid and peptidoglycan released by dying bacteria, sets off same series of reactions (Hyperactivate TLR (produce IL-1, IL-6, IL-8, TNF-alpha, platelet activating factor, activates coag (DIC) and complement cascade, make prostaglandins and leukotrienes, endothelial damage), hyperinflammatory response, distributive shock, multiple system organ failure)

• more potent than endotoxins and variable in response
• stimulate cytokine production
• damage membranes
• inhibit protein synthesis
• modify intracellular signaling pathways
• inhibit release of neurotransmitter
• spreading factors

• pyrogenic exotoxins = superantigens
• Hold together antigen presenting cell with T cell receptor so that even things that don't fit stimulate it.  But since they don't fit, they don't clear the infection.  Runaway inflammation

• phospholipases: destabilize phospholipid membrane, cause lysis.  
• pore-forming toxins: ion and water flux, lysis or even just phagocyte and inflammation activation

• inactivate ribosome
• ADP ribosylation

• cytotonic - elevate function of cell
• calmodulin-activated adenylate cyclase: not active with bacteria inside, only when TOXIN gets into cell, increases cAMP
• heat labile enterotoxic e coli: lock adenylyl cyclase in active form to increase cAMP in enterocytes, secrete ions into lumen, secretory diarrhea
• heat stable enterotoxic e coli: binds guanylate cyclase, changes conformation, increase in cAMP to increase secretion of ions, secretory diarrhea
• Disruption or activation of actin polymerization: directly breaks apart vs activates/inactivates via Rho family of small GTP binding proteins

• clostridium toxins
• endopeptidases: inactivate proteins required for neuroexocytosis
• tetanus toxin: inhibitory synapses in spinal cord (no more negative, so tetany/spastic paralysis
• botulinum toxin: peripheral nerve endings, blocks release of ACh at myoneronal junction, so flaccid paralysis (no +)
• same target, different neurons

• enhance dispersal of microorganisms in tissues
• breakdown ECM or debris in necrotic tissue

• two separate domains or subunits.  
• This gives them two ways into the cell (endocytosis, one portion escapes phagolysosome vs translocation, one sits on membrane while other gets into cytosol.  Both cause effect

protein injected only when there is contact between bacteria and host cell membrane.  can't make a vaccine because it is never free in the cytoplasm.

• gram -
• facultative anaerobe
• coccobacillus
• bipolar staining common
• Mannheimia hemolytica was previously believed to be a pasteurella

• gram negative, facultative anaerobe, coccobacillus, bipolar staining
• 12 capsular serotypes (A1, A2 or s.1, s.2), prevent phagocytosis
• previously thought to be pasteurella haemolytica
• Commensal of nasopharynx (esp ruminants) (OWN FLORA CAUSES DISEASE).  proteins weaken mucus and adhere, avoid mucociliary apparatus.  
• Leukotoxin produced kills alveolar macrophages, neutrophils, lymphocytes, platelets (via pore-forming at high concentration) and activates neutrophils at low concentration
• transmission by inhalation or direct contact
• A1 causes shipping fever in cattle
• A2 causes ovine pneumonic mannheimosis/enzootic pneumonia
• STRESS causes disease, causes INFLAMMATION WHICH CAUSES DAMAGE
• blood agar, beta-hemolysis (unlike pasteurella)
• lots of abx resistance, REDUCE STRESS.  Vax suck.

• mannheimia haemolytica A1 (cattle pneumonia)
• signs 1-2 weeks after STRESS
• fever, inappetance, listlessness
• respiratory signs seen later (cough, nasal d/c, crusty nose, ocular d/c, dyspnea, cranioventral pneumonia
• similar signs seen in secondary pneumonia (just systemic instead of localized)

• gram negative, facultative anaerobe, coccobacillus, bipolar staining
• five capsular serotypes
• commensal of UR, GI
• transmission by inhalation, adhere with pili
• secondary pneumonia in ruminants, swine (acute vs subacute) due to stress, LRT from inflamm response
• nonhemolytic on blood agar (not like mannheimia haemolytica)
• susceptible to abx
• progressive atrophic rhinitis in young pigs (infected at birth) (sneezing, epistaxis, tear duct obstruction, destruction of nasal turbinates and bones of snout, distorted face, zoonoses possible - vax for sow)
• snuffles in rabbits (mucopurulent rhinosinusitis, d/c, eye, URT, maybe LRT)
• fowl cholera, avian cholera (systemic.  Acute causes ADR, d/c.  Chronic is widespread - vax of bacterin or live attenuated)

• gram negative, coccobacillus, facultative anaerobe
• A. equuli: septicemia in newborn foals, pneumonia
• A. suis: respiratory disease in swine and horses
• A. pleuropneumoniae: swine pleuropneumonia

• swine pleuropneumonia
• transmission via inhaled, direct contact
• pore-forming toxins (ApxI, ApxII, ApxIII, ApxIV) like leukotoxin of M. haemolytica - activates neutrophils at low concentration, kill endothelial cells (hemorrhage), alveolar epithelial cells, neutorphils and macrophages at high concentration
• lung damage due to toxin and inflammation
• URT of sick or recovered, NOT COMMENSAL
• acute disease = severe fibrinous pleuropneumonia, ADR, acute respiratory distress (dyspnea, coughing, open-mouth breathing)
• chronic disease = intermittant cough, suboptimal weight gain, reduced appetite, intolerance to exercise
• death primarily in neonate piglets
• susceptible to abx
• bacterin and subunit vaccines
• HER ISOLATION BEST
• NEED NAD (grown on blood agar with it, beta hemolysis)

• gram negative bacillus, facultative anaerobe, require NAD and/or heme
• blood agar with staph species to provide NAD or on "chocolate" agar (nutrient agar with heated blood) w/CO2
• susceptible to abx
• vaccine for infectious coryza -- bacterin does not prevent infection but does prevent serious disease

• gram negative, bacillus, facultative anaerobe, require NAD and/or heme
• commensal
• bronchopneumonia
• disease occurs secondary to viral infection

• gram negative, bacillus, facultative anaerobe, require NAD and/or heme
• "infectious coryza"
• Not commensal
• transmission by inhalation, direct contact
• acute respiratory disease of chickens d/c, facial swelling, diarrhea, ADR, decreased weight gain and egg production

• gram negative facultative anaerobe bacillus
• normal inhabitant of respiratory tract (commensal)
• bronchopneumonia, disease induced by stress
• usually associated with M. haemolytica infections

• gram negative, obligate aerobic coccobacillus
• B. parapertussis (rarely pneumonia in sheep) 
• B. bronchiseptica (non-progressive atrophic rhinitis in pigs, kennel cough in dogs)
• B. avium (turky coryza)

• gram negative obligate aerobic coccobacillus
• commensal in URT
• transmission by inhalation
• non-progressive atrophic rhinitis (less severe than pasteurella multocida).  damage, sneezing, snuffling, mucopurulent nasal discharge.
• Kennel cough - usually with adenovirus and parainfluenza, spasmodic coughing with hacking, retching
• mild or inapparent resp disease in a variety of hosts.
• grow on blood or macConkey agar.  Sometimes hemolytic.  Susceptible to abx but response can be poor (takes time for respiratory to repair and mucociliary damaged)
• live attenuated vaccines for kennel cough
• bacterins or bacterin-toxoids for atrophic rhinitis.  
• Turkey coryza vaccines are live attenuated or bacterins, don't work.

• gram negative obligate anaerobic coccobacillus
• turkey coryza - young turkey poults, spread by close contact.  Brownish exudate at first, then sneezing, exudate, conjunctivitis, rales, dyspnea, altered vocalization, decreased activity and feeding

• gram negative facultative anaerobe bacillus
• commensal in intestines (opportunistic), great in environment
• secondary in mycoplasma birds
• causes air sacculitis, colibacillosis, colispeticemia
• acquired by inhalation (fecal-oral)
• resp distress, decreased feeding
• bacteria causes inflammation, fibrin on organs
• blood/MacConkey agar. Large lactose-fermenting colonies
• commonly resistant to antimicrobials (avian).  ENVIRONMENT.  
• killed or attenuated vaccines, effective against homologous.

• small round gram negative bacterium, too small to be coccus.  
• obligate intercellular.  
• Complex life cycle (elementary body is infectious, reticulate body is metabolically active).  Inhale elementary, live in vacuole, don't fuse with lysosome,become reticulate, change back to elementary for cell lysis (occasional exocytosis).  
• Bird commensal
• psittacosis, ornithosis, avian chlamydiosis.  
• REPORTABLE, zoonotic
• stress reactivates
• inappetance, weight loss, reduction in eggs in birds.  eye/nose d/c, lethargy, anorexia, dyspnea, fever, exudative bronchopneumonia in mammals
• Inclusion bodies, growth in tissue culture.  
• Tetracycline, regs on exotics.

• gram positive, facultative anaerobic coccus
• commensals of URT, digestive, lower genital
• pyogenic causes resp dz with thick yellow pus
• not good in environment
• Lancefield groupings based on polysaccharides in cell wall.  Lots of types.
• blood agar with CO2.  Equi, canis, porcinus beta-hemolytic; suis, pneumoniae alpha-hemolytic.  
• not abx resistant usu (penicillin) 
• vax: suis has bacterin, equi-equi has bacterin and attenuated.

• gram positive facultative anaerobic coccus
• strangles
• NOT commensal
• URT, lymph node abscesses
• hard to swallow
• anorexia, depression, (biphasic) fever, serous nasal d/c
• bastard strangles spreads to other lymph nodes.
• Strep canis and strep porcinus similar in cats/pigs

• gram positive facultative anaerobic coccus
• inhalation or injection of resp secretions or pus
• NOT commensal, avoids clearance (adherance, kill phagocytes (pore) or avoid uptake via capsule, kill NETs), kill/avoid antibodies
• SUPERANTIGENS (overactivate T cells)
• carry in gutteral pouch