Department of Molecular Virology and Microbiology Swine ‘09 The 2009 H1N1 Influenza Pandemic.
Microbiology 2009
Transcript of Microbiology 2009
Microbiology
A branch of biology that studies organisms that can only be seen with a microscope
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
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.
Types of micro-organisms
Non-pathogen(ic) Pathogen(ic)
Non disease causingCommensal
Disease causing
Types of micro-organisms
bacteria
parasites
viruses
fungi
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
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
Properties of bacteria
Spore formation
Toxin production
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
ANTHRAX
Production of toxins
2 types:
Exotoxins:Living bacteria
released into andcause damage to
surrounding tissues
Endotoxins:Remain in bacterial
wall
released on deathof bacterium
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
Classification by
shapeRound: cocci
diplococcistreptococci
staphylococci
Rod:bacilli
Spiral:spirillavibrioCorkscrew:
spirochaete
Cocci diseases (singular = coccus)
meningococci - meningococcal meningitis
(diplococci) streptococcus pyogenes - tonsillitis, pharyngitis, cellulitis
staphylococcus aureus - boils, carbuncles
pneumococci - pneumonia(diplococci)
Examples:
Bacilli diseases
Examples include:
Clostridium tetani - tetanus
Corynebacterium diphtheriae - diphtheria
Escherichia coli (E.Coli) – urinary tract infections
Pseudomonas aeruginosa - infected wounds
Bacterial disease examples: spiral shaped Spirilla:
Spirilla minus - rat bite fever
Vibrio: Vibrio cholerae - cholera
Spirochaete: Treponema pallidum - syphilis
Corkscrew shaped
CHOLERA
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
Specialised bacteria
Mycoplasma• ultramicroscopic bacteria• do not have a cell wall
Diseases caused:• certain respiratory and genital tract diseases
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
VIRUS
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
“BIRD FLU” VIRUS
SMALLPOX VIRUS
VIRUS
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
Pathogenic fungi (mycoses)
Superficial:
skin, mucous membranes,
hair,nails
Intermediate:
subcutaneoustissue
Systemic:
deep tissues organs
3 types of mycotic infections
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)
TINEA PEDIS
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
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
PEDICULI CAPITUS
PEDICULI
Prevention
• Immunisation• Cleaning processes:
environment & equipment• Health status of staff, visitors
etc• Provision of clean water, food &
sanitation
Prevention
• PPE• Management of waste and
body fluids• Handwashing
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
ENTRY POINT
ways in which pathogen enters the body
ingestion
inhalationbroken skin/
mucousmembranes
trans-placental
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
Prevention
• Handwashing• Isolation• Cleaning systems:
environment and equipment• Use of appropriate PPE
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
Prevention• Procedures to manage
indwelling lines: catheters, IV• Aseptic techniques for wound
care• Handwashing• Immunisation• Treat disease processes • Encourage mobility, self care
Lunch
• Please return in 45 min
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
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
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
Inflammatory response
Tissue injured
Release of chemicals (e.g. histamine, kinins)
Blood vessels to dilateCapillaries to leakActivation of pain receptors
cause
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
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
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
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)
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
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
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
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
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
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)
Functions of Antibodies
• Neutralizing antigen• Immobilization of bacteria• Agglutination and precipitation of
antigen• Activation of complement• Enhancing phagocytosis• Providing foetal and newborn
immunity
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)
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
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