Bacteria Flashcards
Opportunistic pathogen
Organisms that do not cause disease in a host that has a healthy immune system
True Pathogen
Equipped w/ virulence genes for adherence, invasion and evasion from the immune system and toxins
Nosocomial infection
Hospital acquired infections
ex. MRSA
Diarrhea
Staphylococcus
Gram Positive
-s. aureus
-Commensals on the skin and mucus membranes
-Pyogenic bacteria
-Abscesses, suppurative infections. post surgical
Virulence Factors
-Enterotoxins A-E (food poisoning)
-Exfoliation- Skin, scaled skin syndrome (infants)
-Porcine exudative epidermitis
-Eipidermolytic toxins-Skin
-Haemolysins
-Leukocidins
-Protein A-Present as surface component on most strains of virulent S. aureus (antiphagocytic and can bind to IgG)
Botryomycosis
Bacterial pseudomycosis Infrequent, chronic pyogramulmatus -Supportive wound infections and septicemia -Pyoderma -Pyemia -Lameness
Streptococcus
Gram Positive -Large group ( more than 68 species) -Occurs in nature and normal flora -Facultatively anaerobic S. pyogenes-Mostly human (scarlet fever) Mastitis, arthritis, meningitis S. equi equi- Stangles -Pyogenic -Hemolysis -Capsule interferes w/ phagocytosis S. pneumoniae-Pneumonia S. mutans
Bacillus
Gram Positive Rod -Bacillus anthacis- anthrax Virulence factors -Endospores -capsule -exotoxins- 3 heat libel protein components- work together as a complex Lethal factor-A part Edema Factor- A part Protective antigen- Binding part
Clostridium
Gram positive rod Histotoxic -Invasive clostridium C. chauvoel (black leg) C. perfringens (gas gangrene) Neurotoxic C. tetani C. botulinum
Clostridium tetani
Tetanus
Endotoxin (AB toxin)
-spastic paralysis
-trauma, surgical wounds, puncture, puncture wounds
Clostridium botulinum
BoNT- Flaccid paralysis
- *Intoxication not infection**
- Food borne
- Infant botulism
- Wound botulism
- Botox related
BoNT and TeNT
- Same mode of action
- Multiplies in dead carcuss and produce toxin
- Eating spoiled foods in which toxins have been produced under anaerobic conditions
- Different types of toxins depending on species
- Neurotoxin is heat labile
Facultative intracellular Bacteria
-Invades host cells when its advantageous
-Bacteria that can enter and survive in cells are shielded from humoral antibodies
-Can only be eliminated by a cellular immune response
-Must posses specialized mechanisms to protect them from the harsh environment of the lysosomal enzymes encountered within cells
Ex. Listeria monocytogenes
-Neisseria spp
-Brucells spp
Obligate intracellular Bacteria
-Cannot live outside the cell
-Need the host cell to supply then with ATP or other intermediates
Ex. Rikettsia spp
To cause disease a pathogen must…
- Gain access to the host
- Adhere to the host tissues
- Penetrate or evade host defenses
- Damage the host
- Directly
- Accumulation of microbial wastes
Preferred portals of entry
Mucus membranes
- Respiratory tract
- GI tract
- Urogenital tract
- Conjunctiva
Skin as a portal of entry
- Some pathogens infect follicles and sweat glands
- Unless broke, skin is usually an impermeable barrier to microbes
Parental Route
- Trauma
- Arthropods
- Injections
Numbers of invading microbes
- minimum infective dose
- likelihood of disease increases as the number of invading pathogens increases
- ID50= number of microbes required to produce infection in 50% of the population
- Different for each pathogen
- Different for different portals of entry
- LD50 (lethal dose)
Adhesions
Surface projections on pathogen, mostly made of glycoproteins or lipoproteins
-adhere to complementary receptors on the host cell
-can be part of the
-glycocalix
Ex. Streprococcus mutants
-Fimbrea- also pili and flagella
Ex. E.coli
Host cell receptors are most commonly sugars
Biofilms
Provide attatchment and resistance to antimicrobial agents
Capsules
overcoming host defenses
Inhibition or prevention of engulfment (by phagocytosis)
Cell wall components
overcoming host defenses
- Techoic acid
- Mycolic acid
- LPS
Antigenic Variation (overcoming host defenses)
-Avoidance of host immune response
Ex. Trypanosoma neisseria
Penetration in the host cell cytoskeleton
overcoming host defenses
Ex. salmonella
E.coli
-Produce invasins
Invasins
Protein that cause the actin of the host cells cytoskeleton to form a base that carries the bacteria into the cell
Production of enzymes
overcoming host defenses
Digest tissues
Intracellular Bacteria survival following phagocytosis
overcoming host defenses
- escape from phagocytic vacuoles into cytosol
- prevention of lysosomal fusion to phagosomes
- resistance to hydrolytic enzymes
Cogulase
promotes blood clotting
fibrinogent-fibrin
walls of bacteria from phagocytosis
Kinase
Breaks down fibrin
blood clot dissolve
hyaluronidase
spreading factor
digestion of intracellular cement
tissue penetration
Collagensase
Collagen hydrolysis
IgA protease
IgA destruction
Hemolysins
Lyse blood cells
Leukocidins
Lyse neutrophils and macrophages
Direct host cell damage
- Growth and replication in host cells results in host cell lysis
- penetration through host cells causes damage
- lysis of host cells to obtain nutrients
Using the hosts nutrients to damage the host
Iron
-required from all cells
-host cell usually does not have free iron
Pathogens can produce siderophores
-compounds secreted by bacteria capable of binding iron from host proteins
Ex. enterobactin (gram - bacteria such as E.coli and salmonella)
Siderophores
iron chelators
-iron complex is absorbed by bacteria
Bacteria factors that disturb host functions
-Protein exotoxins with specific target receptors
Ex. Gram - and Gram +
-Hydrolytic Enzymes
-Broad substrate specificities
Ex. nucleases, proteases, lipases
Products that evoke aberrent host response
-Cross creative antigens (autoimmunity)
-superantigens
Endotoxins
-gram - only LPS, Lipid A part, release upon cell death due to vigorous inflammation
-massive release (endotoxic shock)
Exotoxins
-proteins produced inside pathogenic bacteria
-most commonly gram + as part of their grown and metabolism
Exotoxins are then excreted into surround medium following lysis
Endotoxins
- Lipid portions of LPS that are part of the outermsmbrane of the cell wall of gram negative bacteria
- Lipid A
- Endotoxins are liberated when the bacteria die and cell wall breaks apart.
Toxemia
Presence of toxins in the blood
Toxigenicity
ability to produce toxins
Antitoxins
antibodies produced against exotoxins
Type l exotoxin
Superantigens -bacterial proteins that non specifically stimulate t-cells -Cause intense immune response due to cytokines from host cell -excessive cytokines can cause -fever -nausea -vomiting -diarrhea -shock -death (septic shock) Ex. Toxic shock syndrome (staphylococcus) staphylococcal food poisoning
Type ll exotoxin
Membrane disrupting toxins
-disrupt host cell plasma membranes
-leads to ion imbalance and uncontrolled entry of water from surrounding tissues into the cells- cell swells and bursts
Ex. Leukocidins- kills WBCs
-Hemolysins- Kills erythrocytes
Streptolysins- Hemolysins produced by streptococci
Type lll exotoxins
A-B toxins
-MOST EXOTOXINS
-consists of two polypeptides
A part-enzyme
B part- Binding component
-Bacterium produces and releases exotoxin
-B component attaches to host cell receptor
-A-B exotoxin enters host cell by endocytosis
-A-B exotoxin enclosed in pinched off portion of plasma membrane during pinocytosis
-A-B components separate
-A part alters cell function by inhibiting protein synthesis
-B part is released from host cell
Ex. Botulinum and tetanus toxins
Neurotoxins
Interfere with neurological signal transmission
Leukotoxins
Destroy leukocytes
Enterotoxins
Effect the intestinal tract
Cytotoxins
Kills host cells
Endotoxins
-Release of endotoxins by
-Cell death
-antibiotics
-Antibodies
Cause
-fever
-shock
-Tumor necrosis factor allows bacteria to cross the blood brain barrier
-LAL assay detects endoroxins
Quorum sensing
- Bacteria appear relativity innocuous as they quietly grow in numbers
- When population reaches a certain level, behavior, appearance, metabolism are altered
- these changes cumulate in an infection that can ambush and overwhelm immune system
How can bacteria acquire virulence factors?
- Encoded in DNA
- Encoded on- bacteriophage DNA
- Plasmid DNA
- Transposons - lysogenic conversion
- transduction
- conjugation
- transformation
Bacteriophages
Virus particles which attack bacteria
-phage can be transmitted to non-pathogenic strains making them virulent
Lysogenic conversion with bacteriophages
-Can result in bacteria with virulence factors such as toxins, fimbriae or capsules
Transduction
-The process by which DNA is transferred from 1 bacterium to another by phage
-Mediated conjugation
-transfer of genetic material from a donor cell to a recipient cell by cell to cell contact
–Plasmids may carry genes for antibiotic resistance and or virulence factors between bacteria, allowing new bacteria to become pathogenic
Ex. tetanus neruotoxin
staphylococcus enterotoxins (superantigen)
Hemorrhagic E. coli (fimbriae and shiga toxin)
Plasmids
Circular DNA present in bacteria
Conjugation
-The process by which on bacterium (w. fertility factor) transfers genetic material to another through direct contact
Transformation
-The genetic alteration of a cell, resulting from the direct uptake and incorporation of exogenous genetic material from its surroundings and taken up though the cell membrane
Listeria monocytogenes
Gram positive rod
non sporulating
-Septicemia, abortion, meimgeoenephalitis
-Food bourne->pathogen
-(milk, cheese, ready to eat meals)
-Neural form- circling disease
-gets into eyes and mm while eating
-effects neural system
-milk producing animals
-cillage eating animals
-Visceral form
-ingestion
Virulence factors
-invasinsMycobacterium
- Acid fast positive
- Intracellularl (facultatively obligate)??
- M. tuberculosis- humans
- M. bovine- induces granulomas
- M. avium- avian
- M. avium sbsp. paraturburculosis- Johne’s disease
- chronic granulomatus enteritis**
enterobacteriaceae
Gram negative rods Facultative anearobe -Escherichia -Salmonella -Yersinia
Gram (-) oxidase negative rods
- Ferment glucose
- Motile
- many non pathogenic species*
- present in water, soil environment and the GI tract of humans and animals
- Coliform bacteria
Coliform bacteria
- E.coli
- Klebsiella
- Enterobactor
- Faecal streptococcus and Enterococcus (human)
- *Indicators**
E. coli
gram (-) bacteria
Enterotosigenic E. coli
Diarrhea neonatal colisepticemia in cows and pigs First 6 weeks of life in piglets (lose receptors as they age) K88 (F4)- Pigs K99 (F5)- Calves **adhesions** Exotoxins
Enterohemorrhagic E. coli
Shiga toxin producing (verotoxins)
Causes edema disease in piglets
0157H7 in humans
-Hemmorrhagic enteritis
- Hemolytic uremic syndrome and irreversible kidney failureSalmonella
gram negative Salmonella enterica animals- septicemia, acute, subacute and chronic enteritis **some are host specific** S. dublin- cattle S. typhi- humans S. enteritidis- chickens and humans
Typhoid
only cause systemic disease in humans resulting from material invasion of the blood stream
Yersinia
gram (-) bacteria
Yersinia enterocolitica
pathogen of humans and animals
-causes gastroenteritis and other infections
Yersinia pseudotuberculosis
Mainly animals
acute enteric disease
gastrointestinal tract of domestic and wild animals and birds
transmission by ingestion of contaminated food and water
Yersinia pestis
causes plague in humans, rodents and cats
Gram negative rods and cocci
Non-fermenting, aerobic/microaerophilic
psuedomonas
P. aeruginosa (environmental microorganism)
-opportunistic
-high antimicrobial resistance (can form biofilms)
-all animals
-wound infections, absesses diarrhea, ear and urogenital infections. nosocomial infections
-Dogs-> ear and urinary tract infections
Spiral shaped
Campylobacter -pathogenic (animals and humans) C. jejuni- GI diseases in goats, dogs, cats, sheep, calves Leptospira spirochete->endoflagella gram (-) L. interrogans- leptospirosis -spread in urine -natural hosts- swine, rodents, dogs -can live in water for days -direct or indirect infection
Class molicutes
-no cell wall
-no peptidoglycan
Mycoplasmas
M. pneumonia- walking pneumonia
M. bovis-pneumonia and arthritis in cattle
fried egg colonies
Obligate intracellular pathogens
Chlamydia
-gram (-) pleomorhpic
-do not generate ATP needs hosts ATP
-C. psittaci- psittacosis in humans and avians
chlamydosis in avians and bovine abortion
-zoonotic
-infect mucus membranes of respiratory and GI tracts of normal animals
Rikettsia
Gram (-) cocobacilli -obligate intracellular R. rikettsia -rocky mountain spotted fever -humans and dogs -ticks as vectors
Enterotoxigenic Clostridium
C. preferingens (enterotoxemia)
C. deficile (pseudomembenous colitis in humans and enterocolitis in lab animals)
Atypical Clostridium
C. piliforme-obligate intracellular pathogen
- ONLY GRAM NEGATIVE CLOSTRIDIUM
- Tyzzers disease, necrotising hepatitis, ileitis, typhlitis and colitis
- laboratory rodents, rabbits and horses
