MICROBIOLOGY OF PATHOGENIC FACTORS

Few are pathogenic

· Many benefit the host, or simply colonize the host without causing disease

Human body: 10 trillion cells + 100 trillion bacterial cells

· One organism benefits from the relationship

· Saprophytic mycobacteria of the ear and external genitals

· Escherichia Coli in the large intestine synthesize Vitamin K

o Vitamin K is absorbed into the blood stream and is used by the host

· large intestine of the host provides nutrients used by the bacteria, facilitating their survival

· One organism benefits from the relationship at the expense of the other

· Where harm is done

· Resident microbiota permanently colonize the host

· Transient microbiota temporarily colonize the host

· Secretory and excretory products of cells

· Bodily fluids

· Food in the gastrointestinal tract

· Temperature

· pH, O2, CO2, salt, sunlight

· Chewing

· Flow of saliva and peristalsis of gastrointestinal tract

· Mucous and ciliary action of respiratory system

· Age

· Nutritional Status

· Disability

· Stress

normal flora actually benefits the host by preventing growth of pathogenic microbes

§ Competes with the pathogen for nutrients

§ Produces substances harmful to the pathogen

Manipulates the host environment

o Age

o Antibiotic use – kill the normal flora and the pathogenic infecting us

o Changes in hygiene – changes quality of normal flora

Nutritional status

growth of C. diff in the large intestine

in the the GI normal flora creates an environment conducive to C. diff growth, resulting in disease

- microbes of normal flora move from a different environment than their habitat

- host's immune system is weekend/compromised

- changes in the composition of the host normal flora

Contact/Exposure

Adherence

Evasion of Host Defenses and Penetration

Damage of Host Cells

Transmission

Mucous membranes

skin

Direct deposition beneath mucous membranes or skin

portal of entry

§ Upper respiratory tract

§ Gastrointestinal tract

§ Genitourinary tract

§ Conjunctiva

portal of entry

§ unbroken or damaged, serves as an almost impenetrable barrier

some bacteria can gain access to the body via natural openings (ie: follicles, sweat gland ducts)

portal of entry

beneath mucous membranes or skin

§ Trauma (punctures, wounds, cuts), surgery, invasive procedures

o Ear

o Broken skin

o Insect bite

o Conjunctiva of Eye

o Nose

o Mouth

o Anus

o Placenta

o Vagina / Penis

Urethra

adherence is accomplished by cell surface molecules located on the pathogen

host and tissue specific

adhesin binding specifically to

located on the cells of host tissues

o produced by Streptococcus pyogenes (GAS) – appear as hair-like projections from the cell surface

o Mediates attachment of bacteria to epithelial cells of the host - many subtypes, some more strongly associated with specific diseases than others

Listerias – deli meat

surgical procedures

dental procedures

any some sort of replacement fro the body (i.e. hip replacement)

multiple bacterial species and consist of many layers

in many human bacterial infections (especially chronic infections)

Mechanisms of adhesion also contribute

- Capsule

- Cell wall

- Coagulase

- Kinase

Impairs phagocytosis, preventing phagocytic cell from adhering to the microbe, thereby increasing the virulence of the pathogen

With time, the host will produce antibodies against them

fibrinogen in the blood to form fibrin

Produced by some Staphylococci spp. – in circles, clusters, gram positive

a good place for bacteria to hide and thrive in

Degrades fibrin, and digest clots formed by the body to isolate the wound and clots created by the bacteria as protection from phagocytosis

facilitates a microbe’s entry into host tissues

produced by Streptococcus pyogenes and staphylokinase produced by Staphylococcus aureus

for survival in the immune ells

1. Escape phagosomes before fusing with host cell lysosomes

2. Prevent phagosome-lysosome fusion

3. Reducing effectiveness of toxic compounds within lysosome

4. Producing cell walls resistant to lysosomal proteases

o Invasive bacteria reach epithelial surface

o Bacteria produce hyaluronidase and collagenase

o Bacteria invade deeper tissues

NOT phagocytic

- produced by Salmonella spp. and E.coli spp

- rearrange actin filaments in epithelial cells of the intestinal lumen

NOT phagocytic

result of disruption in the cytoskeleton of the host cell

bacteria sinks into the ruffle and is engulfed by the host cell

induced when inside the host and the bacteria becomes enclosed in a vesicle

epithelial cells move into the blood stream, or enter phagocytes where they reproduce and grow

pathogen is successful in evading the host immune response, host cell damage and disease results

1. Appropriating host nutrients

2. Causing direct damage to tissues surrounding site of invasion

3. Producing toxins

4. Inducing hypersensitivity reactions (allergy)

o Iron is required for the growth of most pathogenic bacteria, determine strategies to obtain iron from host to reproduce

o In humans, iron is tightly bound to iron-transport proteins

o Low availability of iron produces a microbial iron deficiency

o Bind to iron more tightly than host iron-transport proteins

o Iron-siderophore complex taken up by receptors on bacteria

Direct binding to host iron-binding proteins

o intracellular bacteria and viruses metabolize and multiply in host cells, the host cell typically ruptures to facilitate their release, destroying the host cell

o Once released, pathogens spread to other tissues in great numbers

alter the normal metabolism of host cells

Inhibit protein synthesis, destroy blood cells and blood vessels, disrupt nervous system function

Enzymatic proteins produced inside some living pathogenic bacteria as a normal part of growth and metabolism

directly damages and destroys host cell

cytotoxin

by bacteria, gram + or gram –

into the surrounding environment, or during cell lysis

associated with the producing bacteria caused by the effect if the toxin host cells, not the pathogen

active enzymatic component

alters cell function by inhibiting protein synthesis

Binding component

binds to host cell receptor and exotoxin enters cell

Toxin increases cAMP in respiratory epithelial cells, causing increased mucous production and coughing

whooping cough

1. Bacterium produces and releases exotoxin

2. B (binding) component of exotoxin binds to host cell receptor and exotoxin enters cell

3. A (active) component of exotoxin alters cell function by inhibiting protein synthesis

Provoke an intense immune response – shock and disseminated intravascular coagulation

excessive IL-2, TNF, and TF production – cytokines

wants things fast - think about fast food

antigen wants to take time - fine dining

Lipid A

Released when Gram negative bacteria are killed (or multiply) - cell wall lyses, liberating them

Gram + not associated since they don’t have that outer membrane

macrophages to release high concentrations of IL–1

Chills, fever, weakness, generalized aches, shock ans death in severe cases

common mechanism of action, all produce the same signs and symptoms regardless of the pathogen

Increased tissue factor; activates extrinsic & intrinsic coagulation cascade

Disseminated intravascular coagulation (DIC); obstructive clots in capillaries, inducing tissue deat

superantigens

1. Macrophage ingest a Gram negative bacteria

2. Bacteria is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce IL -1

3. IL 1 is released by the macrophage into the bloodstream, travelling to the hypothalamus of the brain

4. IL-1 induces the hypothalamus to produce prostaglandins, resetting the bodies thermostat to a higher temperature producing fever

Exotoxins: No

- except superantigens

Endotoxins: Yes

Microorganisms leave the body via specific portals of exit in secretions, excretions, discharges or shed tissue

o Respiratory tract

o Gastrointestinal tract

o Genitourinary tract

o Skin, conjunctiva, blood, etc…