4.1.1 Communicable Diseases, Disease Prevention and the Immune System Flashcards
four main types of pathogens that can cause disease in animals and plants
bacteria - prokaryotes
viruses - non-living parasites
protoctists - animal like or plant like; eukaryotes
fungi - eukaryotes
pathogen
an infectious micro-organism that causes disease
infectious
direct or indirect transmission caused by micro-organisms
communicable disease
diseases that can be transmitted from one organism to another
organism that causes tuberculosis
bacteria
organism that causes
bacterial meningitis
bacteria
organism that causes ring rot
bacteria
organism that causes HIV/AIDS
virus
organism that causes influenza
virus
organism that causes tobacco mosaic virus
virus
organism that causes black sigatoka
fungus
organism that causes blight
protoctist
organism that causes ringworm
fungus
organism that causes athlete’s foot
fungus
organism that causes malaria
protoctist
what is a protoctist
an animal like or plant like pathogen
how is tuberculosis transmitted
respiratory droplets
how is bacterial meningitis transmitted
respiratory droplets
how is ring rot transmitted
infected farming equipment
how is HIV/AIDS transmitted
needle sharing, unprotected sex, blood transfusion
how is influenza transmitted
respiratory droplets
how is tobacco mosaic virus transmitted
infected farming equipment
how is black sigatoka transmitted
spores
how is blight transmitted
aphids - VECTOR
how is ringworm transmitted
direct contact
spores
how is athlete’s foot transmitted
direct contact
fomite
what’s a fomite
an inanimate object that holds pathogens
how is malaria transmitted
anopheles
mosquito - VECTOR
antibiotic
a drug that slows bacterial growth or kills bacteria
bacteriostatic antibiotic
slows bacterial growth
bacteriacidal antibiotic
kills bacteria
reasons for the development of antibiotic resistance
over prescription of antibiotics
patients not finishing the course of antibiotics
routinely using antibiotics in farming
receptor mediated endocytosis
the toxin binds to a receptor site on the cell surface. the two are ‘swallowed’ into the inside of the cell
modes of transmission of communicable pathogens - animals
direct: contact, entry through skin, ingestion
indirect: fomites, inhalation, vectors
transmission of communicable pathogens in animals - direct: contact
contact with skin, bodily fluids, kissing
e.g STIs, diarrhoeal diseases
transmission of communicable pathogens in animals - direct: entry through the skin
wounds, animals bites, needles
e.g HIV, hepatitis, rabies
transmission of communicable pathogens in animals - direct: ingestion
contaminated food and drink
e.g diarrhoeal diseases
transmission of communicable pathogens in animals - indirect: fomites
bedding, socks, cosmetics
e.g athlete’s foot, cold sore viruses
transmission of communicable pathogens in animals - indirect: inhalation
breathing in respiratory droplets
e.g cold, flu, TB
transmission of communicable pathogens in animals - indirect: vectors
pathogens are carried from one host to another
modes of transmission of communicable pathogens - plants
direct: contact
indirect: soil contamination, vectors
transmission of communicable pathogens in plants - direct: contact
between healthy plants + diseased plants
infected farming equipment
e.g. tobacco mosaic virus
transmission of communicable pathogens in plants - indirect: soil contamination
reproductive spores are left in the soil
e.g. black sigatoka, ring rot
transmission of communicable pathogens in plants - indirect: vectors
wind, water, animals
e.g. blight
factors that affect the rate of transmission of communicable diseases (9)
how does penicillin work
inhibits cell wall synthesis
describe natural selection - bacteria resistance
•antibiotics are applied (selection pressure) - forcing bacteria to be selected
•susceptible bacteria killed, resistant bacteria survive, reproduce and pass on the resistance allele to offspring
•over repeated exposure to antibiotics, the resistant population grows + the allele frequency for resistance increases
where does the resistance allele come from
a mutation
how do viruses spread
virus binds to a receptor on plasma membrane of host cell, injects DNA into the nucleus of host cell.
host cell synthesises viral proteins that are assembled to form mature viruses.
viruses continue to be produced then burst out of host cell to infect others
how is HIV able to replicate
reverse transcriptase converts virus RNA into viral DNA
integrase inserts viral DNA into host cell DNA
active and passive defence in plants
passive - prevents entry of pathogens
active - induced when a pathogen is detected
two categories of passive defence mechanisms
physical, chemical
physical passive defence mechanisms in plants
- cellulose cell wall acts as a physical barrier
- lignin thickening of cell wall is indigestible + waterproof
*waxy cuticles prevent water from collecting on cell surface ( pathogens need water for survival) - callose prevents a pathogen spreading around the plant
- tyloses are balloon-like outgrowths of parenchyma cells to block xylem vessels
chemical passive defence mechanisms in plants
- usually produced when an infection is detected
- chemicals that have anti-pathogenic properties
*tylose contains a high concentration of chemicals
forms of active defence in plants
- production of chemicals
- additional cellulose
- deposition of callose
- oxidative bursts
- necrosis - cell suicide
- canker
active defence in plants: additional cellulose
cell walls become thicker and stronger = stronger barrier
active defence in plants: deposition of callose
deposition of callose between plant cell wall and cell membrane of invading pathogen - prevents cellular penetration at site of infection. strengthens cell wall, blocks plasmodesmata
active defence in plants: oxidative bursts
produce highly reactive oxygen molecules which are capable of damaging cells of invading organims
active defence in plants: necrosis
cells deliberately kill themselves to save the rest of the plant
killing cells that surround the infection can limit the pathogen’s access to water and nutrients = stopping further spreading.
chemicals in active response to an invading pathogen
terpenoids
phenols
alkaoloids
defensins
hydrolytic enzymes
non-specific response: expulsive reflexes
coughing + sneezing
expels pathogens that irritate lining of airways
non-specific defence: the skin
contains fibrous proteins: keratin, collagen - insoluble + impermeable
contains sebaceous glands: secrete antibacterial oils
non-specific response: inflammatory response
mast cells release histamines + cytokines
histamines increase permeability of capillaries = blood plasma to leak into tissues - pain, swelling
cytokines: increase diameter of arterioles, increases blood flow to wound + attracting phagocytes
non-specific response: wound repair
new skin cells formed: stem cells leave cell cycle, enter G0, become specialised + integrate themselves into existing tissues
scab formed while repairs are made
non-specific defence: mucous membrabes
airways and reproductive systems
goblet cells secrete mucus which traps pathogens
cilia wafts mucus along airway
non-specific response: blood clotting
enzyme catalysed cascade initiated by platelets at site of wound
process of blood clotting
tissue damages
platelets activated by tissue
platelets release thromboplastin
thromboplastin catalyses prothrombin into thrombin. calcium ions = cofactor
thrombin catalyses fibrinogen into fibers
fibers clot into thrombus
non-specific: other primary defences
eyes secrete tears - contain lysozyme
ear wax - physical barrier
phagocytosis
pathogen engulfed into phagocyte by phagocytosis into a phagosome
lysosomes fuse with phagosomes to form phagolysosomes - introduces hydrolytic enzymes e.g. lysozyme into phagosome + digestion occurs
useful digested products = reabsorbed
waste = excreted
where are t cells released from
thymus gland
where are b cells released from
bone marrow
t helper cells
clonally selected by an antigen-presenting cell
undergo clonal expansion
some form memory cells
others activate b cells
t killer cells
bind directly to infected cells
insert perforins into the plasma membrane
flood in hydrogen peroxide, nitric acid, hydrolytic enzymes
cause cell lysis
t regulatory cells
dampen down immune response
induce apoptosis of t helper, t killer and plasma cells - prevents autoimmunity
t memory cells
are clonally selected and expanded much quicker on 2nd infection by same pathogen
b lymphocytes
directly activated by antigen
clonally selected by t helper cell
clonally expanded by mitosis
some form memory cells
others differentiate to become plasma cells
what happens when an antigen is recognised
either:
macrophage engulfs + expresses antigen (APC)
antigen directly activates cell
antibody structure: variable region
specific shape to antigen
2 per antibody
antibody structure: hinge region
allows flexibility for antibody to bind to more than 1 antigen
antibody structure: constant region
non-specific binding site for neutrophils + macrophages
same in every antibody
opsonins
bind to antigen using its variable regions
marks out the antigen for destruction
neutrophil/macrophage binds to constant region + phagocytoses pathogen
bind to patogens, foreign cells
eases phagocytosis
agglutinins
each antibody has 2 variable regions
each variable region can attach to an antigen on a different pathogen - hinge provides flexibility = cross-links pathogens + clumps them together
eases phagocytosis for neutrophil
antitoxins
directly bind to toxin molecules secreted by pathogens
toxins neutralised which prevents damage to cells
primary immune response
first encounter with a particular pathogen
takes a few days to produce antibodies - clonal selection/expansion of t/b cells takes time
number of antibodies increase to low peak then drops rapidly
primary response has formed t/b memory cells - circulate in case of reinfection
secondary immune response
clonal selection + expansion must faster
number of antibodies increase at greater rate/ to a much higher conc.
levels of antibodies stay higher for longer
pathogens removed before symptoms are felt
natural active immunity
body’s own response to a new pathogen
memory cells produced
natural passive immunity
receipt of maternal antibodies through placenta or breast milk
no memory cells produced
artificial active immunity
injection of an antigen + immune response occurs
memory cells produced
artificial passive immunity
injection of antibodies made by another organism
no memory cells produced
type of immunity: vaccination
active: prompts immune response - results in memory cells
artificial: injected
principles of vaccinations
preventing severe illness which could result in death
promote herd immunity
promote ring immunity
herd immunity
vaccinating the majority of a population so that disease carriers are less likely to infect a vulnerable individual
ring immunity
vaccinating a smaller proportion than that required for herd immunity, but vaccinating those most likely to be affected
types of vaccine
weakened, live pathogen
dead, inactivated pathogen
toxoids
subunits
how does a weakened, live pathogen work?
modified pathogen that is active but not pathogenic
how does a dead, inactivated pathogen work?
pathogen killed but antigens are still present
how does a toxoid work?
modified toxins
how do subunits work?
isolated antigens
advantages of weakened, live pathogen vaccine
strongest response
long-lasting immunity
disadvantages of weakened, live pathogen vaccine
organism may revert + become pathogenic
advantages of dead, inactivated pathogen vaccine
stable
safer than live vaccines
disadvantages of dead, inactivated pathogen vaccine
response is weaker
boosters required
advantages of toxoids vaccine
safe
disadvantages of toxoids vaccine
may not give strong response
boosters required
advantages of subunits vaccine
vaccines for several strains can be produced
epidemic
disease spread across several countries in the same continent
pandemic
global spread of a disease across many continents
autoimmune disease
the immune system fails to recognise body cells as ‘self’
attacks itself and own cells, mistaking them for pathogens
destruction of self tissue
examples of autoimmune diseases
rheumatoid arthritis
lupus
type 1 diabetes
cytokines
attract phagocytes
