Microbiology is the study of microorganisms that can only be seen with a microscope. Historical evidence shows early civilizations isolated infected individuals and burned soiled dressings. Girolamo Fracastorius first suggested disease was caused by living germs in 1546. Robert Koch developed culture plates in 1876 and Louis Pasteur developed sterilization methods. Microorganisms include bacteria, viruses, fungi, parasites and can be pathogenic or non-pathogenic. The human body defends against infection through mechanical barriers, inflammation, phagocytosis, and specific and non-specific immune responses using B cells, T cells and antibodies.

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

2. 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

3. 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.

4. Types of micro-organisms
Non-pathogen(ic)
Pathogen(ic)
Non disease
causing
Commensal
Disease causing

5. Types of micro-organisms
bacteria
parasites
viruses
fungi

6. 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

7. Requirements of bacteria
Oxygen:
variable
•aerobic
•anaerobic
pH:
Most neutral/sl.alkaline
Some highly acid
Some highly alkaline
Carbon:
require a small
amount for
cell structure
Temperature:
Optimum – 37 C
Wide range from
5-60 C
Food and water:
required by all

8. Properties of bacteria
Spore formation
Toxin production

9. 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

10. ANTHRAX

11. Production of toxins
2 types:
Exotoxins:
Living bacteria
released into and
cause damage to
surrounding
tissues
Endotoxins:
Remain in bacterial
wall
released on death
of bacterium

12. Classification of bacteria
1. Staining properties
Gram positive
bacteria:
retain
violet
colour
Gram negative
bacteria:
retain
red
colour
Acid fast bacteria:
stain unable to penetrate due to
waxy envelope
Reactions of
bacteria to a
staining
technique

13. Classification by shape
Round: cocci
diplococci
streptococci
staphylococci
Rod:
bacilli
Spiral:
spirilla
vibrio
Corkscrew:
spirochaete

14. Cocci diseases (singular =
coccus)
 meningococci - meningococcal
meningitis
(diplococci)
 streptococcus pyogenes - tonsillitis,
pharyngitis, cellulitis
 staphylococcus aureus - boils,
carbuncles
 pneumococci - pneumonia
(diplococci)
Examples:

15. Bacilli diseases
Examples include:
 Clostridium tetani - tetanus
 Corynebacterium diphtheriae -
diphtheria
 Escherichia coli (E.Coli) – urinary
tract infections
 Pseudomonas aeruginosa -
infected wounds

16. Bacterial disease examples:
spiral shaped
Spirilla:
Spirilla minus - rat bite fever
Vibrio:
Vibrio cholerae - cholera
Spirochaete:
Treponema pallidum - syphilis
Corkscrew shaped

17. CHOLERA

18. Specialised bacteria
Rickettsiae and chlamydiae
o smaller than most bacteria
o can only reproduce in living cells - are
therefore parasites
o rickettsiae often carried by fleas, ticks,
lice (vectors)
Disease examples:
 Rickettsia australis - Queensland tick
typhus
 Chlamydia trachomatis - trachoma,
salpingitis

19. Specialised bacteria
Mycoplasma
• ultramicroscopic bacteria
• do not have a cell wall
Diseases caused:
• certain respiratory and genital tract
diseases

20. 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

21. VIRUS

22. 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

23. “BIRD FLU” VIRUS

24. SMALLPOX VIRUS

25. VIRUS

26. 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

27. Pathogenic fungi (mycoses)
Superficial:
skin, mucous
membranes,
hair,
nails
Intermediate:
subcutaneous
tissue
Systemic:
deep tissues
organs
3 types
of
mycotic
infections

28. Fungi
Diseases caused
Dermatophytes:
o Tinea pedis - athlete’s foot
o Tinea unguium – toenail infections
Candidiases (moniliasis):
o Candida species - oral thrush, skin
infections
o Aspergillus - aspergillosis
(respiratory disease)

29. TINEA PEDIS

30. 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

31. 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

32. PEDICULI CAPITUS

33. PEDICULI

34. Prevention
• Immunisation
• Cleaning processes: environment &
equipment
• Health status of staff, visitors etc
• Provision of clean water, food &
sanitation

35. Prevention
• PPE
• Management of waste and body
fluids
• Handwashing

36. 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/
objects
hands
Vectors:
Flies, rats, mosquitos

37. ENTRY POINT
 ways in which pathogen
enters the body
ingestion
inhalation
broken skin/
mucous
membranes
trans-
placental

38. 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

39. Prevention
• Handwashing
• Isolation
• Cleaning systems: environment
and equipment
• Use of appropriate PPE

40. 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

41. Prevention
• Procedures to manage indwelling
lines: catheters, IV
• Aseptic techniques for wound
care
• Handwashing
• Immunisation
• Treat disease processes
• Encourage mobility, self care

42. Lunch
• Please return in 45 min

43. BODY DEFENCES AGAINST INFECTION
External mechanical and chemical barriers
First line of defence
Inflammatory response
Second line of defence
Immune response
Third line of defence
Non-specific defences
Specific defences

44. 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

45. 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

46. Inflammatory response
Tissue injured
Release of chemicals
(e.g. histamine, kinins)
Blood vessels to dilate
Capillaries to leak
Activation of pain receptors
cause

47. Inflammation
Heat and redness
due to vasodilation
resulting in increased
blood supply to injured
area
Tenderness/Pain
caused by pressure on underlying sensory
nerve receptors from swelling.
Send impulses to spinal cord to brain
Swelling (oedema)
results from
capillary leakage into
surrounding
tissues

48. 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

49. 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

50. 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)

51. 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

52. Immune Response
o Third line of body defence
o Response is specific, systematic
and has a memory
o Cells of the immune system are:
- B lymphocytes
- T lymphocytes
- Macrophages

53. 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

54. 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

55. Immune system cells
B lymphocytes:
-produce antibodies
(immunoglobulins)
T lymphocytes:
-non-antibody
producing
Macrophages:
-engulf foreign
particles
Humoral (antibody
mediated) immunity
Cell mediated and
humoral immunity
Cell-mediated (cellular)
immunity

56. Immunity
Any substance capable
of
stimulating the
immune system and
causing an
immune response
Are immunoglobulins
(Igs)
produced in the body
in response to
Antigens
Five classes:
-IgM, IgA, IgD,
-IgG, IgE
Antigens:
(Ags) Antibodies: (Ab)

57. Functions of Antibodies
• Neutralizing antigen
• Immobilization of bacteria
• Agglutination and precipitation of
antigen
• Activation of complement
• Enhancing phagocytosis
• Providing foetal and newborn
immunity

58. Immunity
Innate
(genetic, inborn)
Acquired
Naturally acquired Artificially acquired
Active
Protection acquired by
getting the disease
Passive
Antibodies passively cross
from mother to baby
via placenta or breast milk
Active
Protection acquired by
immunisation with vaccine
that stimulates body to
actively produce own
antibodies
Passive
Protection acquired
by direct injection
of antibodies
(immunoglobulins)Ref: Tabbner, 2005, p.331 (Adapted from Herlihy and Maebius: 2000, p.354)

59. 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

60. 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