1.
Infectious Diseases
And Antibiotics

2.
Infectious Diseases
 Diseases caused by pathogens
 Some disease affect us for short periods of time –
common cold measles, influenza
 Others are more chronic – TB, AIDs
 Infectious diseases are not like COPD or coronary
heart diseases which are degenerative and are not
caused by pathogens

3.
Infectious Diseases
 Some diseases may even be transmitted without the
person contracting it – such person is called carrier
 Pathogens pass from one host to another in a
transmission cycle
 The 5 major diseases required in this syllabus include:
Cholera, Malaria, HIV-AIDs, Measles, TB

4.
More definitions
 Endemic: Describing a disease that is always present in
a population
 Incidence: The number of people diagnosed with a
disease over a period of time
 Prevalence: The number of people with the disease at
any one time
 Pandemic: An increase in number of cases throughout
a continent or across the world

5.
Cholera

6.
Cholera
 Caused by Vibrio cholerae
 Food-borne, Water-borne
 Distribution: Asia, Africa, Latin America
 Incubation period: 2 hours – 5 days
 Site of action: Small intestine
 Diagnosis: Microscopic examination of feces

7.
Cholera Causes
 Vibrio Cholerae inhibits the cell in the small intestine –
release choleragen
 Disrupting the osmotic balance, causing the cell to
release large quantity of water due to lost of salt
 Transmitted in water – uncontaminated food, feces, in
cooking utensils, vegetable irrigated with infected water
 Hence the disease is endemic in areas with poor
sanitation

8.
Cholera Symptoms
 Loss of fluid
 Loss of salt
 Dehydration
 Weakness
 Severe diarrhea (rice water)

9.
Treatment/ Prevention
 Rehydration – could be through Oral Rehydration Therapy
(ORT)
 Uses glucose is effective – it is taken right into the blood
 Prevention include development of sewage system
 Provision of clean water
 No inadequate cooking
 Always tracing cholera epidemic
 Vaccines are short term and not very effective

10.
Different Strains
 O1 – original strains
 EL TOR – transmitted by ship sewage and into sea
food
 1992: new strain O139 – replaces El Tor very quickly –
may be more virulent

11.
Malaria

12.
Malaria
 Caused by protoctist – Plasmodium
 Insect vector – female anopheles mosquitoes
 Distribution: The tropics
 Site of action: Liver, Red Blood Cells, Brain
 Incubation: A week to a year
 Diagnosis: Microscopial examination of blood. Dip stick
test

13.
Malaria transmissions
 Anopheles feeds on human blood that is infected
 Pathogen gametes taken up – fuses in the mosquito’s gut –
enters the salivary gland
 When it bites another person, it is released with the anticoagulant
the mosquito uses to prevent blood clot
 Malaria can be transmitted through placenta
 Also, by blood transfusion
 Plasmodium multiplies in both human and mosquito
 People can become immune from malaria – nut only as long as
they are constantly in contact with the disease

14.
Treatment
 Anti-malarial/ prophylactic (preventive) drug: Quinine, Mefloquine
 Chloroguine (inhibits protein synthesis)
 Proguanil (inhibits sexual reproduction)
 Strains of drug resistant plasmodium have developed (one
resisting mefloquine appear in Thailand-Laos border)
 Some doctors can misdiagnose initial malaria symptom as
influenza
 Some people do not realize they lose immunity when they re-
enter their home country after years of being away

15.
Prevention
 Reduce number of mosquitoes
- Destroy its habitat, release males with no gamete, use
of insecticides
 Avoid being bitten
- nets, insect repellants
 Drugs
- Chloroquine

16.
AIDs
Acquired Immuno Deficiency Virus

17.
AIDs
 A syndrome caused by a retrovirus
 Retrovirus: Those with RNA
 Human immunodeficiency virus

18.
HIV
 Infects and destroy T-helper cells of the immune
system
 Immune systems therefore do not respond effectively
 The body is made vulnerable to other diseases –
common cold and TB
 AIDs – is a conglomeration of opportunistic diseases

19.
HIV Transmission
 HIV is transmitted by sexual intercourses – bodily fluid
exchange
 Transmitted in blood transfusion
 Across placenta from mother to child
 Needle sharing
 If someone is discovered to have HIV – they are asked
to contact sexual partner immediately

20.
HIV Transmission
 Pregnant woman are advised not to breastfeed their
children
 Viral particles can be found in breast milk
 HIV positive woman use antiretroviral drug before
delivery

21.
Treatment
 Cannot be cured
 Spreads of AIDs can be slowed down
 Using variety of drugs – problems here are side effects
and cost
 Zidovudine – binds to/ block action of reverse
transcriptase – stopping replication
 Increasing life expectancy

22.
Prevention
 Controls of HIV include contact tracing
 Programs to exchange used needles for better ones
 More care/ control into working on blood transfusion
 Ante-natal care

23.
TB
Tuberculosis

24.
Tuberculosis
 Pathogens: Mycobacterium Tuberculosis, Mycobacterium
Bovis
 Transmissions: Airborne droplets, undercooked meat,
unpasteurized milk
 Distribution: Worldwide
 Incubation: Weeks – years
 Site of action: primary infection in lungs, secondary in lymph
nodes, bones, guts
 Diagnosis: microscopic examination of sputum, chest X-ray

25.
Tuberculosis Symptoms
 Coughing blood
 Coughs
 Chest pain
 Shortness
of breath
 Fever
 Sweating
 Weight Loss

26.
Transmission
 Airborne disease – in aerosol droplets
 Infect the malnutritioned
 Those living in overcrowded conditions – at risk
 Opportunistic infection of AIDs
 TB transmission can come from cattle milk/ meat
 1940s: introduction of Streptomycin
 1950s: Introduction of Vaccines
 The disease was thought to have been eradicated, now it’s on
the rise

27.
Treatment Tuberculosis
 When diagnosed – the patient should be isolated
 Treatment: Uses several drugs to ensure death to the
bacteria
 6 – 9 months long
 The bacteria – slow growing and not sensitive to drugs
 The patient MUST complete the whole course of drug
or risk the bacteria becoming resistant

28.
Drug Resistance
 Some bacteria survive the treatment, mutate and
become drug resistance
 DOTS (Direct Observational Treatment Program) used
to ensure complete process in the course of treatment
 Isoniazid/ Rifampicin used

29.
Drug Resistance
 MDR-TB (Multiple-Drug-Resistant) are on the rise
 They are now resistant to Isoniazid and Rifampicin

30.
Tuberculosis prevention
 BCG Vaccine
 Protects 70-80% of people receiving it
 Effectiveness of vaccine reduces with age unless
exposed to TB
 TB can still be transmitted between cattle and human
– cattle are tested on routines, milk is always
pasteurized
 Contact tracing is very important

31.
Measles

32.
Measles Cause
 Virus enters the body and infects respiratory tract
 Rash appears, runny nose, cough, watery eyes, white
spots inside the cheek
 Pneumonia
 Sinus infection
 Brain damage
 Are all symptoms

33.
Measles transmission
 One of the most contagious disease
 Sneezing/ Coughin can release droplets with millions of
viruses
 Initial immunity provided for infant from antibodies
 May infect those deficient of vitamin A

34.
Antibiotics

35.
Antibiotic
 Selective toxins
 Kill or disable pathogen without harming the host
 Only work on bacteria and some on virus
 They are derived from living organisms
 Bacteriostatic: Stop/ prevent bacterial growth
 Bactericidal: Kills Bacteria

36.
Penicillin
 When bacteria grow – they punch holes into their walls
with enzyme autolysin – then they use peptidoglycan
to form crosslinks within those holes to strengthen the
cell wall
 Penicillin prevents Peptidoglycan from forming – hence
the cell wall of the bacteria continues to find new holes
until they take up too much water and burst

37.
Antibiotic Resistance
 Tuberculosis has impermeable wall and has an enzyme
that can break down penicillin
 Bacterial membranes can sometimes pump out
antibiotics
 Eg. Enzyme beta-lactamase can be found in soil
bacteria which grow in unfavorable condition – this
enzyme can break down penicillin – it is transmitted via
horizontal and vertical transmission to other bacteria

38.
Antibiotic Resistance
 Pathogens can develop resistance to antibiotics
 Developing enzymes for destroying penicillin
 Can develop if people misuse antibiotic
 There are two ways by which resistance can be
transmitted – vertical and horizontal

39.
Effectively Using
Antibiotic
 Widespread use of antibiotic can lead to bacteria
developing multiple resistance (one plasmid carrying
resistance for many antibiotics)
 Should be used sparingly
 Only use against bacteria and not virus

40.
Immunity
And Vaccines/ Monoclonal Antibodies

41.
External Defences
 Defenses that act as the first line of defense for our
body
 The external defenses of our body include:
 Our skin
 Our respiratory tract’s goblet cells and nasal hair
 Our stomach acid

42.
Internal Defences

43.
Phagocytes

44.
Phagocytes
 White blood cells produced in bone marrows
 When pathogens attack a cell – the cell releases
histamine
 In the process of chemotaxis – the cell uses histamine,
in combination with bacterial chemical to call for
phagocytes
 The phagocytes connect with the antigen – engulfing
them in phagocytosis and destroying them

45.
Neutrophils
 Produced in the bone
marrow
 Travel throughout the
body
 Usually conduct
phagocytosis on
antigens
 Short lived cells
 Patrol tissues

46.
Macrophages
 Larger
 More like bodyguard – found in specific parts of the
body – spleen, kidney etc.
 Travels in blood as monocyte until reaching the place
of guardian
 They cut up pathogens to be displayed to T-Cells

47.
Lymphocytes

48.
Lymphocytes
 Smaller than phagocytes
 Have large nucleus that fill most of the cell
 B-Lymphocytes
 T-Lymphocytes
 Only mature lymphocytes can carry out immune
responses
 Each lymphocyte specialized to respond to specific
antigens

49.
T-Cells
 Have specific receptors – specific to one antigen
 Activated when antigen is in contact with cells or
presented to them by macrophages
 Release cytokines – stimulate B-cells to divide –
stimulates Cytotoxic T-cells to differentiate

50.
B-Cells
 B-cells produce antibodies
 They can only produce for one type of pathogen
 When received messages from T-cells the B-cells
begin the process of clonal selection

51.
Clonal Selection
 B-cells specific to the antigen begins to divide
 Some differentiate into memory cells
 Others into plasma cells

52.
Clonal Expansion
 Plasma cells divide and release antibodies
 Memory cells divide and remain in the body
 If the pathogen returns, they respond pretty much
immediately

53.
Primary Responses
 Macrophage will attack
 B-cells will go through clonal selection and expansion
 It will take more time for antibodies to be produced and
invaders to be suppresses

54.
Secondary Responses
 The memory cells recognize the pathogens
 Immediate attacking
 The invaders are immediately suppresses
 Memories are over a lifetime
 Except for common cold and influenza that mutate all
the time

55.
Antibodies
 Globular glycoproteins
 Used to identify and neutralize foreign objects
 They can protect the cells by neutralizing toxins, kill
the bacteria by causing bursting, top the pathogen by
sticking to it, attaching to its flagella

56.
Antibodies

57.
Immunity
Active, passive, Artificial, Natural

58.
Active Immunity
 Immunity that are derived from real infections
 Can be artificial: In the form of vaccination
 Can be natural: in the form of actual infection

59.
Passive Immunity
 Immunity that is given and is usually temporary
 Artificial: Usually by injections of anti toxins
 Natural: Antibodies passed on the children in breast
milk (in colostrum – has IgA)

60.
Vaccines

61.
Vaccines as an Artificial
immunity
 A prepared antigen used to stimulate an immune
response artificially
 May use dead pathogens
 Or those that attenuated

62.
Problem: Poor Responses
 Sometimes there is poor response
 The person may have a lack lusting immune system
 May be malnutritioned – cannot produce antibodies
 May require buffer

63.
Problem: Live Virus/ Herd
immunity
 Sometimes virus can continue to infect other people
 Herd immunity is required to protect the entire
community
 This means the entire or most of the population are
vaccinated sot he virus cannot survive

64.
Problem: Antigenic
Variation
 Virus may mutate into many forms
and strains
 For example, Cholera has mutated
several times over the past
decades
 Tuberculosis mutated to resist drug
treatments in the forms of MDR-TB
(Multiple-Drug Resistant
Tuberculosis)

65.
Problem: Antigenic
Concealment
 Virus may hide itself
 For example, Cholera can conceal itself in the small
intestine

66.
Autoimmune Disease

67.
Autoimmune Disease
 Usually when T-cells are produced that are somehow
meant to attack self-antigen they are destroyed in
early stages
 But in rare circumstances, they escaped detection
 These T-cells proceed to order the attack of the
human it was create to protect

68.
Myasthenia Gravis
 This is caused by a complex
process where certain inhibition by
antibodies caused by the deformed
T-Cells stop transmission of
electrical impulse between nerve
cells and muscle cells
 This causes muscle weakness

69.
Multiple Sclerosis
 Destruction of the myelin sheath on the nerve cells
 Nerve impulses not transmittedLost of work in the
CNS (Central Nervous System)
 MRI scan can detect the plaque/ degenerative area
 Symptoms: Muscle weakness, loss of sensory input,
poor vision, mental problems

70.
Rheumatoid Arthritis
 Attack the joints and spread to the rest of the body
 Start in fingers, hands then spread to the rest of the
body
 Tendons inflames, muscle spasm and pain

71.
Type 1 Diabetes
 Inhibition of the islets of Langerhans
 Stop the production of insulin
 Hence leads to high blood sugar content

72.
Monoclonal Antibodies

73.
Monoclonal Antibodies
 Antibodies that are produced by human over and over
again for uses that we want
 Important because it can be use for diagnosis and
treatment
 Normal antibodies are hard to replicate because B-
cells that divide do not produce antibodies and plasma
cells that produce antibodies, do not divide.

74.
Making such Antibodies
 Inject an animal with an antigen that would induce an
immune response that would produce the kind of
plasma cell we want
 Extract the plasma cell from the spleen of the animal
 Fuses the plasma cell with cancer cell
 The cell will begin to divide

75.
Diagnosis with Mabs
 Mabs are marked by radioactive markers
 They are sent into the blood (sometimes to detect
blood clot)
 When they reach the ‘destination’ – the doctors can
detect the clot

76.
Treatment with Mabs
 Can pose problems because they have to be
administered more than once
 Because the Mabs are from animals – they are still
non-self, so our immune response will soon detect that
too
 We can still modify the sugar chains of the antibodies
to make them look like ours
 Or change the gene that code for those chains… same
result

77.
Trastuzumab
 Treat breast cancer
 Binds to cells that multiply in abnormal quantity
 Marks for destruction for immune response

78.
Ipilumab
 Treat for Melanoma – a skin cancer
 Blocks the actions of the proteins that stop the
production of T-cells
 Hence sustain the immune response

79.
Infliximab
 Treat Rheumatoid Arthritis
 Binds to the proteins secreted by T-cells that
damage the joints
 Usually takes up to 2 months to treat
 Important that these antibodies are humanized

80.
Rituximab
 Binds to the surface membrane of B-cells
 Cause the death of the cell eventually
 Used to treat diseases where there are over
production of B-cells – leukemia (cancer of the bone
marrow – causing deformed cells to be created)
 May be used against Rheumatoid arthritis, Multiple
Sclerosis and Myasthenia Gravis