microbiology 2009

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Microbiology A branch of biology that studies organisms that can only be seen with a microscope

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Page 1: Microbiology 2009

Microbiology

A branch of biology that studies organisms that can only be seen with a microscope

Page 2: Microbiology 2009

Historical Overview

• Fossil evidence dating back 3.5 million years (Burton & Egelkirk 1999)

• Early civilizations isolated infected persons

• Soiled dressings were burned (Burton & Egelkirk

1999)

• Causes believed to be the action of gods• Early treatments – leeches, bleeding

Page 3: Microbiology 2009

Historical Overview (Cont’d)

• 1546 Girolamo Fracastorius – suggests disease is cause by living germs

• 1667 Antony van Leeuwenhoek – first light microscope – sees and describes microbes

• 1876 Robert Koch – develops culture plates• 1890’s Louis Pasteur – developed methods

of sterilization, pasteurisation.

Page 4: Microbiology 2009

Types of micro-organisms

Non-pathogen(ic) Pathogen(ic)

Non disease causingCommensal

Disease causing

Page 5: Microbiology 2009

Types of micro-organisms

bacteria

parasites

viruses

fungi

Page 6: Microbiology 2009

Bacteria

Single celled organisms Structure:

- rigid cell wall enclosing cytoplasm- nuclear body but no nuclear membrane- some develop a capsule for protection - some have flagellae for propulsion- some have fimbriae enabling attachment to

other cells

Page 7: Microbiology 2009

Requirements of bacteria

Oxygen: variable•aerobic

•anaerobic

pH:Most neutral/sl.alkaline

Some highly acidSome highly alkaline

Carbon:require a small

amount for cell structure

Temperature:Optimum – 37°CWide range from

5-60°C

Food and water:required by all

Page 8: Microbiology 2009

Properties of bacteria

Spore formation

Toxin production

Page 9: Microbiology 2009

Bacterial spores formation

Protective mechanism developed by some bacteria to survive in adverse conditions

Highly resistant to:- high temperatures- freezing- sunlight- disinfectants

Some spores (e.g. anthrax) have been found to be active after 100 years of being in inactive form

Page 10: Microbiology 2009

ANTHRAX

Page 11: Microbiology 2009

Production of toxins

2 types:

Exotoxins:Living bacteria

released into andcause damage to

surrounding tissues

Endotoxins:Remain in bacterial

wall

released on deathof bacterium

Page 12: Microbiology 2009

Classification of bacteria

1. Staining properties

Gram positivebacteria:

retainvioletcolour

Gram negativebacteria:

retain red

colour

Acid fast bacteria:stain unable to penetrate due to

waxy envelope

Reactions of bacteria to a staining technique

Page 13: Microbiology 2009

Classification by

shapeRound: cocci

diplococcistreptococci

staphylococci

Rod:bacilli

Spiral:spirillavibrioCorkscrew:

spirochaete

Page 14: Microbiology 2009

Cocci diseases (singular = coccus)

meningococci - meningococcal meningitis

(diplococci) streptococcus pyogenes - tonsillitis, pharyngitis, cellulitis

staphylococcus aureus - boils, carbuncles

pneumococci - pneumonia(diplococci)

Examples:

Page 15: Microbiology 2009

Bacilli diseases

Examples include:

Clostridium tetani - tetanus

Corynebacterium diphtheriae - diphtheria

Escherichia coli (E.Coli) – urinary tract infections

Pseudomonas aeruginosa - infected wounds

Page 16: Microbiology 2009

Bacterial disease examples: spiral shaped Spirilla:

Spirilla minus - rat bite fever

Vibrio: Vibrio cholerae - cholera

Spirochaete: Treponema pallidum - syphilis

Corkscrew shaped

Page 17: Microbiology 2009

CHOLERA

Page 18: Microbiology 2009

Specialised bacteria

Rickettsiae and chlamydiae o smaller than most bacteriao can only reproduce in living cells -

are therefore parasiteso rickettsiae often carried by fleas,

ticks, lice (vectors)Disease examples: Rickettsia australis - Queensland tick typhus Chlamydia trachomatis - trachoma, salpingitis

Page 19: Microbiology 2009

Specialised bacteria

Mycoplasma• ultramicroscopic bacteria• do not have a cell wall

Diseases caused:• certain respiratory and genital tract diseases

Page 20: Microbiology 2009

Viruses

• ultramicroscopic• no cell structure• no rigid cell wall• are intracellular parasites• can only reproduce within a host

cell• composed of either DNA or RNA but

not both• can lie dormant in cells with

activation occurring at a later time

Page 21: Microbiology 2009

VIRUS

Page 22: Microbiology 2009

Viruses

DNA viruses Herpes virus - herpes simplex, herpes zoster Adenovirus - conjunctivitis, URTI Poxvirus - variola (smallpox)RNA viruses Paramyxovirus - colds, measles, mumps, croup Piconavirus - infectious hepatitis A & B, polio.Retroviruses Human immunodeficiency virus (HIV) - AIDS Human T lymphotropic virus (HTLV) - lymphoma

Page 23: Microbiology 2009

“BIRD FLU” VIRUS

Page 24: Microbiology 2009

SMALLPOX VIRUS

Page 25: Microbiology 2009

VIRUS

Page 26: Microbiology 2009

Fungi

• Plant organisms: mainly moulds and yeasts

• Do not contain chlorophyll• Present in soil, air, water• Multiply by producing spores• Most non-pathogenic• A few are pathogenic

Page 27: Microbiology 2009

Pathogenic fungi (mycoses)

Superficial:

skin, mucous membranes,

hair,nails

Intermediate:

subcutaneoustissue

Systemic:

deep tissues organs

3 types of mycotic infections

Page 28: Microbiology 2009

Fungi

Diseases causedDermatophytes:o Tinea pedis - athlete’s footo Tinea unguium – toenail

infectionsCandidiases (moniliasis):o Candida species - oral thrush,

skin infectionso Aspergillus - aspergillosis

(respiratory disease)

Page 29: Microbiology 2009

TINEA PEDIS

Page 30: Microbiology 2009

Parasites

• Survival requirements depend on a living organism – the host

• Parasite-host effects variable: from little damage to death

• Classification includes:helminths – multicellular animals (worms) e.g. flatworms (platyhelminths) : roundworms (nematodes) : flukes (trematodes)protozoa - single celled animal organisms transmitted to humans by insects

Page 31: Microbiology 2009

Pathogenic parasites

o Trematodes (flukes) : liver, lungs or intestinal infestation

o Nematodes – round worm infestation

o Echinococcus granulosis (dog tapeworm) – hydatid cysts

o Protozoa – malaria, toxoplasmosis

Page 32: Microbiology 2009

PEDICULI CAPITUS

Page 33: Microbiology 2009

PEDICULI

Page 34: Microbiology 2009

Prevention

• Immunisation• Cleaning processes:

environment & equipment• Health status of staff, visitors

etc• Provision of clean water, food &

sanitation

Page 35: Microbiology 2009

Prevention

• PPE• Management of waste and

body fluids• Handwashing

Page 36: Microbiology 2009

Transmission modes the mode of movement of pathogen from exit point to

new host

Airborne:droplets

dust particles

Contact:direct

indirect

Ingestion:infected food/water/utensils/

objectshands

Vectors:Flies, rats, mosquitos

Page 37: Microbiology 2009

ENTRY POINT

ways in which pathogen enters the body

ingestion

inhalationbroken skin/

mucousmembranes

trans-placental

Page 38: Microbiology 2009

EXIT POINT

the point from which pathogens emerge to enable entry to a new site of residence

human exit points include:- breaks in skin and mucous membranes : discharging wounds- gastro-intestinal tract : faeces, vomitus, bile, drainage tube- respiratory tract : sneezing, coughing, expectorating sputum- urinary tract : infected urine- blood : bleeding wounds- reproductive tract : semen, vaginal discharge

Page 39: Microbiology 2009

Prevention

• Handwashing• Isolation• Cleaning systems:

environment and equipment• Use of appropriate PPE

Page 40: Microbiology 2009

SUSCEPTIBLE HOST

o Degree of resistance an individual has to a pathogen

o Resistance to disease influenced by such factors as:- healthy nutrition- adequate rest and sleep- effective management of stress- effective hygiene practices- adequate exercise

Page 41: Microbiology 2009

Prevention• Procedures to manage

indwelling lines: catheters, IV• Aseptic techniques for wound

care• Handwashing• Immunisation• Treat disease processes • Encourage mobility, self care

Page 42: Microbiology 2009

Lunch

• Please return in 45 min

Page 43: Microbiology 2009

BODY DEFENCES AGAINST INFECTION

External mechanical and chemical barriersFirst line of defence

Inflammatory responseSecond line of defence

Immune responseThird line of defence

Non-specific defences

Specific defences

Page 44: Microbiology 2009

External mechanical and chemical barriers

intact skin and mucous membranes: acid mantle, sweat, sebum, normal flora

gastro-intestinal tract: mucous membranes, normal bowel flora, saliva, stomach acidity, bile alkalinity

respiratory tract: mucous membranes, cilia, nasal secretions

eyes: tears urinary tract: acidity of urine

Page 45: Microbiology 2009

Inflammation

second line of body defence is non-specific: occurs whenever body

tissues are injured classic clinical manifestations:

- redness- heat- swelling- pain/tenderness

- restricted movement pus formation occurs when injured area

becomes infected

Page 46: Microbiology 2009

Inflammatory response

Tissue injured

Release of chemicals (e.g. histamine, kinins)

Blood vessels to dilateCapillaries to leakActivation of pain receptors

cause

Page 47: Microbiology 2009

Inflammation

Heat and rednessdue to vasodilation

resulting in increasedblood supply to injured

area

Tenderness/Paincaused by pressure on underlying sensory

nerve receptors from swelling.Send impulses to spinal cord to brain

Swelling (oedema)results from

capillary leakage intosurrounding

tissues

Page 48: Microbiology 2009

Pus

Mixture of: -dead or dying neutrophils-broken down tissue cells-dying and living pathogens

If area not completely cleared of infection, remnants become walled off to form an abscess

Surgical drainage may be necessary before healing occurs

Page 49: Microbiology 2009

Other non-specific defences

• Complement fixation- 22 plasma proteins

- attach to foreign cells • Interferons

- proteins secreted by virus infected cells

• Natural Killer Cells– Lymphocytes that destroy infectious microbes

plus certain spontaneously arising tumour cells

• Fever- temperature rise may kill certain pathogens

Page 50: Microbiology 2009

Phagocytosis

• Ingestion of microbes or any foreign particulate matter by cells called phagocytes

• Two major types of phagocyte:– Neutrophils (white blood cells)– Macrophages (scavenger cells derived

from monocytes)

Page 51: Microbiology 2009

Mechanism of Phagocytosis

• Three phases:– Chemotaxis – activated complement proteins

cause chemical attraction of phagocytes to a particular location

– Adherence – attachment of the plasma membrane of the phagocyte to the surface of the foreign material.

– Ingestion – the cell membrane of the phagocyte extends projections that engulf the micro-organism

Page 52: Microbiology 2009

Immune Response

o Third line of body defenceo Response is specific,

systematic and has a memoryo Cells of the immune system

are:- B lymphocytes- T lymphocytes- Macrophages

Page 53: Microbiology 2009

Immune response

o Two kinds – closely allied o Both triggered by antigens

o Cell-mediated (cellular) immune responses (CMI)

o T cells proliferate into “killer” cells and directly attack the invading antigen

o Antibody-mediated (humoral) immune responses (AMI)

o B cells transform into plasma cells which synthesize and secrete specific proteins called antibodies or immunoglobulin's

Page 54: Microbiology 2009

Formation of T Cells and B Cells

• Both develop from haemopoietic stem cells in red bone marrow

• B cells complete maturity in bone marrow

• T cells leave as pre-T cells and migrate to the thymus gland to mature

Page 55: Microbiology 2009

Immune system cells

B lymphocytes:-produce antibodies(immunoglobulins)

T lymphocytes:-non-antibody

producing

Macrophages:-engulf foreign

particles

Humoral (antibodymediated) immunity

Cell mediated andhumoral immunity

Cell-mediated (cellular)immunity

Page 56: Microbiology 2009

Immunity

Any substance capable of

stimulating the immune system and

causing animmune response

Are immunoglobulins (Igs)

produced in the bodyin response to

Antigens

Five classes:-IgM, IgA, IgD,

-IgG, IgE

Antigens: (Ags) Antibodies: (Ab)

Page 57: Microbiology 2009

Functions of Antibodies

• Neutralizing antigen• Immobilization of bacteria• Agglutination and precipitation of

antigen• Activation of complement• Enhancing phagocytosis• Providing foetal and newborn

immunity

Page 58: Microbiology 2009

Immunity

Innate(genetic, inborn)

Acquired

Naturally acquiredArtificially acquired

ActiveProtection acquired by

getting the disease

PassiveAntibodies passively cross

from mother to babyvia placenta or breast milk

ActiveProtection acquired by

immunisation with vaccinethat stimulates body toactively produce own

antibodiesPassive

Protection acquired by direct injection

of antibodies(immunoglobulins)Ref: Tabbner, 2005, p.331 (Adapted from Herlihy and Maebius: 2000,

p.354)

Page 59: Microbiology 2009

Immunological Memory

• Memory for certain antigens triggers immune responses

• Immune responses are much quicker and more intense after a second exposure to an antigen

• Basis for immunization

Page 60: Microbiology 2009

References• Burton, G., and Engelkirk, P., (1999).

Microbiology for the Health Sciences, Lippincott Williams & Wilkins, Philadelphia

• TAFE Frontiers, (2003). Learners Resource: Microbiology and Wound Management, Dept. of Education, Employment and Training. Victoria

• Marieb, E., (2006). Essentials of Human Anatomy & Physiology (8E). Pearson. San Francisco

• Tortora, G. J., & Grabowski, S., (1996). Principles of Anatomy and Physiology (8 E). Harper Collins. New York