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AS Biology > Chapter 10: Infectious Diseases > Flashcards

Chapter 10: Infectious Diseases Flashcards

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1
Q

What are antibiotics

A

Drugs that kill/stop growth of bacteria without harming cells of infected organism

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2
Q

From where are the 2 kinds of antibiotics derived

A

Natural: living things like plants, fungi, and sea creatures
Synthetic: industry. Change functional group in chemical structure to see how effective it is

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3
Q

2 types of antibiotics based on mechanism

A

Bactericidal - kill bacteria

Bacteriostatic - inhibit growth and hence reproduction

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4
Q

Types of antibiotics based on activity

A

Broad spectrum - active against wide range/no of bacteria

Narrow - active against one specific or few bacteria

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5
Q

Mechanism of action of antibiotics

A

They interfere with any aspect of growth or metabolism of the target bact

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6
Q

Sites (targets) of action of antibiotics

A

1) cell wall synthesis inhibition
2) transcription inhibition
3) protein synthesis inhibition
4) interfere with metabolic actions
5) interfere with DNA replication
6) membrane inhibitor

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7
Q

How does penicillin work

A

Bacteria need to grow by expanding but can’t due to cell wall. So they secrete Autolysine which makes holes in cell wall, so that bacteria can take in water by osmosis and stretch

Cell wall is made of cross links between peptidoglycan.
Now penicillin inhibits enzymes for cross link formations, while Autolysine continues making holes, so the cell expands but cell wall is not being and is weak made so bact bursts

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8
Q

How come penicillin only kills bact but doesn’t harm human cells or viruses

A

Human cells don’t have cell walls

Antibiotics are for prokaryotic protein only (viruses use host protein)

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9
Q

Why antibiotics are ineffective against virus

A

No cell itself

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10
Q

The antibiotics names which work on different sites of action of bacteria and state the mechanism

A

1) cell wall synthesis inhibition: penicillin, cephalosporin, vancomycin. All cidal
2) transcription inhibition: rifampicin. Cidal
3) protein synthesis inhibition: chloramphenicol, tetracycline. Static. Erythromycin, streptomycin. Cidal
4) interfere with metabolic actions: sulfa drugs. Static
5) interfere with DNA replication: quinolones. Cidal or static depending on conc.
6) membrane inhibitor: polymycin. Cidal

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11
Q

How does rifampicin kill bacteria by transcription inhibition

A

Dna not converted to Rna

So gene is not expressed so protein not formed

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12
Q

How does do antibiotics kill/halt growth bacteria by translation/protein inhibition

A

Rna is not converted to protein

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13
Q

How does quinolone kill/stop growth bacteria by interfering with DNA replication

A

Can be cidal or static

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14
Q

How does polymyxin kill bacteria by acting as membrane nhibitor

A

Inhibits specific protein in membrane which are used for cell signalling, facilitated diffusion, and channels for substance passage
So if these functions are prevented cell dies

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15
Q

How do sulfa drugs slow bacterial growth by interfering in metabolic reactions

A

Affect annabolic or catabolic reactions

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16
Q

Mechanism of antibiotic resistance

A

If bacteria is not sensitive or susceptible against antibiotic it is resistant and undergoes no action

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17
Q

4 mechanisms of antibiotic resistance

A

1) thick impermeable cell wall so antibio can’t pass into cell to work on sites
2) a gene acquired in bact that codes for enzyme β-lactamase/penicillinase which catalyses break down of penicillin

Bact gain gene coding for a protein protecting them from antibio:

3) develop mutation, spontaneous (change in nucleotide sequence). Altered protein, resulting from altered amino acid sequence/protein in membrane which is not affected by AB, or pumps antibio out of cell so it doesn’t affect sites, or inactivates it
4) vertical and horizontal transmission: repeated usage of antibio as small no of bact become resistant and survives due to mutation ie natural selection pressure and evolution

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18
Q

Why do bacteria become resistant so easily

A

Have only one set of chromosomes/1 circular dna
So any recessive change cannot be masked by another
And human misuse of AB exerts selection pressure on them

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19
Q

Soil is a harsh environment full of insecticides and fertiliser. It has _ bacteria

A 
Non pathogenic 
(don't cause diseases)
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20
Q

Vertical transmission:

A

Resistance is transmitted from one bacteria to another vertically along y axis
Bacteria divide by asexual binary fission, so bacterial chromosome/plasmid replicates and (function: resistance gene) divide into 2 into 2 daughter cells

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21
Q

Horizontal transmission:

A

(Mode/mechanism of sexual repro)
Bacteria come close
Conjugation tube formed
Pasmid are small loops of double stranded dna.
One strand (of either chromosome or plasmid) may be transferred from donor to recipient bacterium. So gene is transferred.
The donor will have 1 strand left, and will form another by complementary base pairing. Same happens with recipient with resistance gene

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22
Q

How can we prevent antibiotic resistance

A
  • only prescribe then when needed. Not for viral infection
  • reduce no of countries where AB sold without prescription
  • avoid using wide spectrum AB (less chance to becone resistant compared to narrow)
  • complete course of medication even if symptoms gone
  • avoid keeping unused medication for future
  • change type of AB prescribed for certain diseases so same one is not always prescribed -narrow AB
  • avoid using AB to prevent rather than cure infection ie famring. Unnecessarily exposing AB to any bacteria
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23
Q

what are infectious diseases

A

seases that are caused by organisms known as pathogens. communicable, passed from infected to uninfected

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24
Q

what are non infectious diseases

A

ot caused by pathogens. non communicable, not passed on as infection rather inherited

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25
Q

whats a disease

A

illness or disorderof body or mind that leads to poor health

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26
Q

who are carriers

A

people who have and spread the pathogen but do not show no symptoms

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27
Q

whats a transmission cycle

A

way in which a pathogen passes from one host to another. can be controlled by removing conditions that favor the pathogens spread

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28
Q

endemic:

A

Diseases that are always in populations

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29
Q

incidence:

A

no of people diagnosed with a disease over a certain period of time

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30
Q

prevalence:

A

no of people having the disease at one time

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31
Q

epidemic:

A

occuring in a region where theres a sudden increase of people having that disease

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32
Q

pandemic:

A

sudden increase of cases throughout the world

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33
Q

mortality:

A

death rate from different diseases

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34
Q

pathogen of cholera

A

vibrio cholerae (O1 classical strain)

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35
Q

method of transmission and site of action of cholera

A

contaminated food and water. bacteria transferred to uninfected people wtaer/food borne.

to reach small intestine (soa) have to go through stomach so if not enough acidic ie <4.5 bacteria will survive and pass. on reaching secrete toxin ie choleragen which disrupts function of epithelium lining wall and so that salts and water leave blood

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36
Q

clinical features and symptoms of cholera

A

severe diarrhoea, loss of salts and water, dehydration, weakness

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37
Q

method of diagnosis of cholera

A

microscopial analysis of faeces

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38
Q

treatment of cholera

A

intravenous salt and glucose solution
oral rehydration therapy
glucose is effective because it can be absorbed into blood along with ions

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39
Q

prevention of cholera

A

sewage treatment for clean drinking water
clean piped water for cleaning
avoid irrigation with water containing raw sewage
chlorination of water to kill water

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40
Q

pathogen of malaria

A

Plasmodium falciparum, .vivax, .orale, .malariae

41
Q

method of transmission of malaria

A

insect vector: female anopheles mosquito.
can also be during blood transfusion using unsterile needles
also mother to child via placenta

42
Q

global distribution of malaria

A

endemic in 106 countries such as the tropics

43
Q

site of action of plasmodium

A

liver
rbc
brain

44
Q

clinical features of malaria

A

fever, anaemia, shivering, sweating, headache, muscle pain, enlarged spleen, nausea

45
Q

method of diagnosis of malaria

A

microscopial examination of blood, or dip test for antigens in blood

46
Q

transmission cyle of malaria

A

1) infected mosquito takes blood meal to obtain protein needed to develop their eggs
2) if it has plasmodium the infective stages ie sporozoites pass onto human from salivary glands along with anticoagulent which is secreted to prevent blood clotting
3) sporozoite goes to liver quicly and multiplies asexually in next 7-10 days with no symptoms
4) merozoite- parasite- goes from liver to blood where plasmodium is asexually multiplied until rbc bursts and spread the parasite to invade more erythrocytes
5) some merozoites leave cycle of asexual multiplication and mature into sexual forms called gametocytes
6) mosquito bites infected human again and ingests gametocytes which develop into mature sex cells called gametes which fuse in its stomach which further divide into many malarial parasites

47
Q

how can malaria be treated

A

antimalarial drugs via iv drips such as artesunate (severe), quinine and chloroquine, which inhibit protein synthesis and prevents parasites spread in body

mefloquine used where there is drug resistance but can be expensive, and have bad side effects

prophylactic (preventative) drugs: taken before/during/after visit to endemic place. stop infection if bitten.
chloroquine, proguanil- fruther inhibits sexual reproduction inside mosquito, doxycycline

48
Q

prevention of malaria

A
  • reduce no of mosquitos: kill the vector by spreading oil over water where larvae are laid and hatchbut only breathe when in contact with air. marshes and vegetation drained. stock bodies of water with larvae eating fish. spray bacterium containing prep which kills larvae but not other life forms
  • avoid being bitten: sleep under mosquito nets, and soak them in insectiside every 6m, use repellents
  • use drugs to prevent infections
49
Q

worldwide control of malaria

A

worldwide eradication program
not successful cos plasmodium resistant to control drugs and mosquitos to insectisides
expensive
in areas of temporary eradication lost immunity and got infected when it returned
insectiside killed wasp that ate caterpillars and roofs came down

50
Q

reasons for worldwide concern over malaria

A
  • increase in drug resistant forms of plasmodium
  • increase in proportion of cases caused by P/ falciparum which is fatal
  • difficulties in developing vaccines
  • increase in epidemics due to environmental changes that favour mosquito spread
  • migration of people from endemics who can spread it
51
Q

what had kinda helped the malaria eradication program

A
  • diagnosis easy without labs using dip stick tests
  • whole plasmodium genome has been sequenced, help us in making effective vaccines
  • using drugs in combination to reduce resistance
52
Q

improvement which will help with malaria prevention

A
  • modern techniques of genome sequencing and drug design
  • develop vaccines agaisnt diffrent stages of parasites lifecycle
  • international will to remove disease from poor countries via generous donations from organisations
53
Q

pathogen causing AIDS

A

HIV

54
Q

method of transmission of hiv

A

semen and vaginal fluids during intercourse
infected blood
mother to baby via placenta or milk
contaminated syringes

55
Q

global aids distribution

A

sub saharan africa and south east asia

56
Q

incubation period of HIV

A

initial infection symptoms in first few days but years before aids symptoms

57
Q

site of action of hiv

A

T helper lymphocytes,macrophages, brain cells

58
Q

symptoms of hiv and aids

A

infection- flu like
aids has opportunistic infections eg pneumonia, TB, cancer (less effective in finding and destroying tumours),fungi ; weight loss,dementia, sweating and fever, diarrhoea

59
Q

method of hiv diagnosis

A

test blood urine or saliva for antibody presense againt hiv

60
Q

structure of hiv

A

outer envelope of lipid membrane has gp120 and g041 proteins
has capsid
inside protein core is RNA, and protease and and reverse transcriptase enzymes

61
Q

hiv life cycle:

A
  • is a retrovirus ie rna not dna
  • binds to a receptor and empties contents into cell
  • reverse transcriptase makes comlementary mirror image of rna as a double stranded dna whihc is integrated into human chromosomes
  • when dna is transcipted and translation sets of viral protein chains assemble
  • immature virus buds out of cell and protease hydrolyses the protein chains into individual proteins which combine to form viral core, new virus

-destroys helper t cells and macrophages which control immune response to infection so if their nos decrease so does defense ability so pathogens impose opportunistic infections

62
Q

if hiv is the infective agents aids is an

A

aquired immunodeficiency with is a set of opportunistic diseases

63
Q

transmission of hiv

A
  • intercourse and exchange of body fluids
  • blood donation
  • needle sharing in drug takers
  • mother to child in placenta
64
Q

hiv treatment

A

dna nucleotides such as zidovunine similar to thymine binds to viral reverse transcriptase enzyme and blocks its action which stops replication of rna and body lymphocyte count goes up

65
Q

why is hiv spread difficult to reduce

A

it has a long latent stage so it can be transmitted by HIV positive people who dont know theyre infected

it keeps changing its surface proteins, making it hard for the body to identify

66
Q

hiv prevention

A
  • contraceptive methods which reduce risk of infection by being barriers between fluids and thus reduce transmission
  • contact tracing. hiv+ person identifies people they may have transmitted it to and theyre offered tests
  • stop doing needle sharing drugs or atleast use sterile ones, or take it in another form
  • donated blood is screened for hiv and heat treated to kill it
  • in developed countries high risk groups offered testing
  • women and babies are given drugs to safely let the child recieve milk
67
Q

pathogens of tb

A

mcyobacterium tuberculosis and m. bovis

68
Q

method of tb transmission

A

mt- airborne droplets

mb- uncooked meat and unpasteurised milk

69
Q

global distribution and incubation period of TB

A

worldwide

few weeks upto many years

70
Q

site of action of tb

A

primary-lungs

secondary-bones,gut,lymph nodes

71
Q

clinical features of tb

A
  • raking cough
  • coughing blood
  • chest pain
  • shortness of breath
  • fever+sweating
  • weight loss
72
Q

methods of tb diagnosis

A
  • microscopial examination of sputum
  • chest xray
  • tuberculin test
73
Q

tb life cycle

A

bacteria are mainly captured by the alveolar macrophages, but can invade immune systme and remain dormant and only reactivate when immune system is under compromised conditions

74
Q

2 types of tb

A

latent tb- dormant and not contagious but treatment needed bcos can become active
active tb- makes you sick and contagious

75
Q

treatment of tb

A

DOTS-direct observation therapy short course, 6-8 months patient made sure to be taking their meds

76
Q

antitb drugs in treatment

A

first line but they often fail
One reason being multidrug resistant bacteria so need…
second lines

77
Q

difference between MDR-TB and XDR-TB

A

M is resistant to at least one of first line

X is to one first and at least one second line

78
Q

why does tb become resistant

A

Drug resistance occurs as a result of mutation in the bacterial DNA.

Mutation is a random event and occurs with a frequency of about one in every thousand bacteria

79
Q

first line drugs are

A

FLD, INH, PZA, EMB, SM

80
Q

second line drugs are

A

fluoroquinolones- OFX, LEV, MOX, CIP
injectable antitb drugs- CAP, KAN, AMK
any others are less effective

81
Q

why is tb incidence so high in some areas

A
  • some strains are resistant to drugs
  • poor housing
  • partial treatment via programs increases resistance
82
Q

sputum test:

A

mucus and pus from lungs analysed via microscopy for the bacterium

83
Q

tuberculin test:

A

A small amount of a substance called PPD tuberculin is injected just below the skin of your forearm. Within 48 to 72 hours, a health care professional will check your arm for swelling at the injection site. A hard, raised red bump means you’re likely to have TB infection. The size of the bump determines whether the test results are significant.

84
Q

tb prevention

A
  • contact tracing and subsequent testing of those people
  • BCG vaccine protects upto 70-80% of people who get it
  • cattle regularly tested for tb and killed. milk pasteruised
85
Q

causative agent of measles

A

morbillivirus

86
Q

measles mechanism

A

virus enters the body and multiplies inside cells in the upper respiratory tract (nasal cavity and trachea).

87
Q

measles symptoms

A

no symptoms for 8–14 days after the initial infection and then a rash appears and a fever develops

Other symptoms are a runny nose, a cough, red and watery eyes (conjunctivitis) andsmall white spots that may develop inside the cheeks

88
Q

treating measles:

A

bed rest+medicines to lower the fever; no specific medicines. After about ten days the disease clears up and there are rarely any complications
if any it gets serious: pneumonia, ear and sinus infections,brain damage and convulsions may follow and even childhood blindness

89
Q

measles transmission

A

very contagious, when people sneeze or cough droplets carry it

90
Q

why does measles hardly affect infants

measles affects malnourished children with _ deficiency

A

passive immunity ie antibodies from mother

vitamin A

91
Q

where is measles major

A

places of overcrowded, insanitary conditions and where there is a high birth rate
virus is transmitted easily in these conditions

92
Q

measles prevention and why it may be difficult to eradicate

A
  • could be eradicated with surveillance and vaccination
  • but a programme of one-dose vaccination has not eliminated the disease in any country, despite high coverage of the population. This is explained by the poor responseto the vaccine shown by some children who need several boosters to develop full immunity
  • migrants cause epidemics by forming infection reservoirs
  • immunity of 93–95% is required to prevent transmission
93
Q

causative agent of smallpox

A

variola virus

94
Q

transmission method and symptoms of smallpox

A

direct contact

Red spots containing a transparent fluid would appear all over the body. These then filled with thick pus. Eyelids became swollen and could become ‘glued’ together. Sufferers often had to be prevented from tearing at their flesh. Many people who recovered were permanently blind and disfigured by scabs left when the pustules dried out.

95
Q

why was the worldwide small pox eradication program successful

A
  • ring vaccination: upon a reported case everyone in the area at risk due to contact was vaccinated
  • virus was stable; it did not mutate and change its surface antigens. so same vaccine used everywhere hence cheap
  • vaccine was made from a harmless strain of a similar virus (vaccinia) and was thus effective
  • vaccine was freeze-dried and could be kept at high temperatures for as long as 6 months so used in tropics
  • the infected were easy to identify
  • vaccine easy to adminster effectively due to stainless steel reusuable needle
  • virus did not linger in the body afterwards to become active later and form a reservoir of infection
  • animals werent infected so easy to break cycle
  • youngsters volunteered to vaccinate and spread info
96
Q

susceptible and resistant bacteria

A

ones which are sensitive are susceptible

if they gain gene coding that protects them from AB are resistant

97
Q

rise of multiple resistant bacteria such as MRSA

A

resistance may first appear in a non-pathogenic bacterium, but then be passed to a pathogenic species. Bacteria living where there is widespread use of antibiotics may have plasmids carrying resistance
genes for several different antibiotics, giving multiple resistance.

98
Q

How to choose effective antibios

A

Testing antibiotics against the strain of the bacterium isolated from people ensures that the most effective antibiotic can be used in treatment.

99
Q

why is it a race against time developing new antibiotics

A

bacteria become resistant as fast as ABs are developed

so we need to find ones which work in a completely different way from our current ones

AS Biology (11 decks)

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