infection control measure

1. EPIDEMIOLOGY IN HAIS
Dr. Anjalatchi Muthukumaran
Vice principal
Era college of nursing

2. 2
INTRODUCTION
The term epidemiology is derived from the Greek
word epidemic.
– Epi means-Among, upon,
– Demos means study population or people and
– Logos means scientific study.
So
– it is the scientific study of the disease pattern in
human population.
– In broad sense, it is the study of effects of multiple
factors on human health.
– It is multidisciplinary subject involving those of the
physician, Biologists, Public Health experts, Health
educators etc.

3. THE ULTIMATE AIMS OF EPIDEMIOLOGY CAN BE
CONCLUDED IN TO TWO FOLLOWINGS POINTS:-
• To eliminate or reduce the health
problem or its consequences
and
• To promote the health and
wellbeing of society as a whole.

4. EPIDEMIOLOGICAL FACTORS ON WHICH
HAI DEPENDS:-
There are 3 main factors related to development of
HAIs:-
 Agent factors
 Host factors
 Environmental factors

5. J

6. XAMPLE:-TYPHOID FEVER (DISEASE)
Salmonella
Typhi
Young age,
more in
males, Low
immunity,
Lack of
personal
hygiene
Polluted
water, Open
defecation

7. Mode of transmission
Portal of entry
Host
Infectious
agent
Reservoir
Portal of exit
CHAIN OF INFECTION -

10. CHAIN OF INFECTION:-
 In this chain of infection the agents of infection are
the microorganisms.
 A reservoir is defined as “any person, animal
arthropod, plant, soil or substance in which an
infectious agent lives and multiplies, on which it
depends primarily for survival.
 E.g in typhoid a case or carrier is reservoir of
infection, the reservoir of Clostridium botulinum is
soil.

11.  Human reservoir:- Reservoir of infection for human
is man itself ( a case or a carrier)
 A case is defined as “a person in a population
having a particular disease, health disorder or
condition under investigation”
 A carrier is defined as “an infected person or animal
that harbours a specific infectious agent in the
absence of discernible clinical disease and serves
as a potential source of infection for others”
 The “Typhoid Mary” is a classic example of a
carrier.

12.  Portal of exit is the path by which a pathogen leaves its
host.
 The portal of exit usually corresponds to the site where
the pathogen is localized.
 For example, influenza viruses and Mycobacterium
tuberculosis exit the respiratory tract,
 Schistosomes through urine,
 Cholera vibrios in feces,
 Sarcoptes scabiei in scabies skin lesions etc.

13. MODES OF TRANSMISSION OF HOSPITAL-ACQUIRED
PATHOGENS.
Route Description
Contact
transmission
Direct
contact
Skin to skin contact , MC
Indirect
contact
Contaminated inanimate objects such as-
 Dressings, or gloves, instruments (e.g.
stethoscope)
 Parenteral transmission through- NSI,
splashes, saline flush, syringes, vials etc

14. Route Description
Inhalational
mode
Droplet
transmissio
n
Droplets of >5 µm size can travel for shorter
distance (<3 feet).
 Generated while coughing, sneezing, and
talking
 Propelled for a short distance through the air
and deposited on the host's body.
 E.g -bacterial meningitis, diphtheria,
respiratory syncytial virus, etc.
Airborne
transmissio
n
Airborne droplet nuclei (≤ 5 µm size) or dust
particles
Remain suspended in the air for long time and
can travel longer distance.
 This is more efficient mode than droplet
transmission.
 E.g. Legionella, Mycobacterium tuberculosis,
measles and varicella viruses.

15. Route Description
Vector • Via vectors such as mosquitoes, flies, etc.
carrying the microorganisms
• Rare mode
Common
vehicle
such as food, water, medications, devices, and
equipment.

16.  The portal of entry refers to the manner in which a
pathogen enters a susceptible host. The portal of entry
must provide access to tissues in which the pathogen
can multiply or a toxin can act.
 For example, influenza virus exits the respiratory tract of
the source host and enters the respiratory tract of the
new host.
 Many pathogens that cause gastroenteritis follow a so-
called “fecal-oral” route because they exit the source host
in feces, are carried on inadequately washed hands to a
vehicle such as food, water, or utensil, and enter a new
host through the mouth.
 Other portals of entry include the skin (hookworm),
mucous membranes (syphilis), and blood (hepatitis B,
human immunodeficiency virus).

17.  The final link in the chain of infection is a susceptible
host.
 Susceptibility of a host depends on genetic or
constitutional factors, specific immunity, and nonspecific
factors that affect an individual’s ability to resist infection
or to limit pathogenicity.
 An individual’s genetic makeup may either increase or
decrease susceptibility.
 For example, persons with sickle cell trait seem to be at
least partially protected from a particular type of malaria.

18. IMMUNITY
 The term 'immunity' (Latin word ‘immunitas’,
means freedom from disease) is defined as the
resistance offered by the host against
microorganism(s) or any foreign substance(s).
 Immunity can be broadly classified into two
types-
o Innate immunity- present right from the birth
o Acquired / Adaptive- acquired during the
course of the life

19. DIFFERENCES BETWEEN INNATE AND ACQUIRED IMMUNITY
Innate immunity Acquired / Adaptive
immunity
Resistance to infection that an
individual possesses from birth
Resistance to infection
that an individual acquires
during his lifetime
Immune response occurs in
minutes
Immune response occurs
in days
Prior exposure to the antigen is
not required
Develops following the
antigenic exposure
Diversity is limited, acts through
a restricted set of reactions
More varied and
specialized responses

20. Innate immunity Acquired / Adaptive
immunity
Components of innate immunity
Anatomical barriers such as skin and mucosa
Physiological barriers (e.g. body temperature)
Phagocytes (neutrophils, macrophages &
monocytes)
Natural killer (NK) cells
Mast cells
Dendritic cells
Complement pathways- alternate & mannose
binding pathways
Fever and inflammatory responses
Normal resident flora
Cytokines- TNF-α, certain interleukin (IL-1, IL-6,
IL-8, IL-12, IL-16, IL-18), IFN-α, β and TGF- β
Acute phase reactant proteins (APRs)
Components of
acquired immunity
T cell
B cell
Classical complement
pathway
Antigen presenting
cells
Cytokines (IL-2, IL-4,
IL-5, IFN-γ)
Types of acquired
immunity-
It can be classified in
two ways:
 Active and passive
immunity
 Artificial and natural

21. INNATE IMMUNITY
 Innate immunity is the inborn resistance against infections
that an individual possesses right from the birth, due to his
genetic or constitutional makeup.

22. FEATURES OF INNATE IMMUNITY
 Acts in minutes
 Prior microbial exposure is not required
 Diversity is limited
 Non-specific
 No memory

23. INNATE IMMUNITY
Type of
innate
immunity
Explanation Examples
Species
immunity
Innate immunity towards
a microbe exhibited by all
members of a given
species
frogs are resistant to
Bacillus anthracis;
while toads are
susceptible.
Racial
immunity
innate immunity confined
to a particular race; may
be absent in other
communities
Negroes of America
are more susceptible to
tuberculosis than the
whites.
Individual
immunity
Antimicrobial defense
mechanisms that are
confined to a particular
individual; may not be
exhibited by others.
One exception is
identical twins who
exhibit similar degrees
of susceptibility to
infections

24. FACTORS INFLUENCING INNATE IMMUNITY
 Age
 Hormone
 Nutrition

25. COMPONENTS OF INNATE IMMUNITY
1. Anatomical and physiological barriers
2. Phagocytes
3. Natural killer (NK) cells and other classes of lymphocytes
4. Mast cells
5. Dendritic cells
6. Complement pathways
7. Inflammatory response
8. Normal resident flora
9. Cytokines
10. Acute phase reactant proteins (APRs)

26. ANATOMICAL AND PHYSIOLOGICAL BARRIERS
Anatomical
Barrier
Function
Skin Barrier
 Mechanically prevents entry of microbes
 Produces sebum containing antimicrobial peptides and fatty
acids
 Killing of microbes by intraepithelial lymphocytes
Mucosal Barrier
1. Mucous
membrane
Prevents entry of microbes mechanically and by producing
mucous which entraps microbes
2.Cilia Cilia present in the lower respiratory tract propel the microbes
outside
3.Normal
flora
Intestinal & respiratory mucosa are lined by normal flora.

27. Physiological
Barrier
Function
1.Temperature Normal body temperature inhibits the growth of some microbes
2.Low pH Gastric acidity inhibits most of the microbes
3.Secretory products of mucosa
Saliva Enzymes in saliva damage the cell wall and cell membrane of
bacteria
Tears Contains lysozyme, that destroys the peptidoglycan layer in
bacterial cell wall
Gastric juice HCl kills microbes by its low pH
Trypsin Hydrolyse bacterial protein
Bile salts Interfere with bacterial cell membrane
Fatty acids Denature the bacterial proteins
Spermine Present in semen, inhibits growth of Gram positive bacteria
Lactoferrin Binds to iron, thus interferes with acquisition of iron by bacteria

28. PROPERTIES OF ACQUIRED IMMUNITY
 Mediators- T cells & B cells are the chief mediators of
acquired immunity. Others include-
o Classical complement pathway
o Antigen presenting cells
o Cytokines (IL-2, IL-4, IL-5)
 Response occurs in days - It requires the activation of T and
B cells against the microbial antigens.
 Requires prior microbial exposure- Acquired immunity
develops only after the exposure to the microbes.

29. PROPERTIES OF ACQUIRED IMMUNITY
 Specific-Acquired immunity is highly specific; directed
against specific antigens that are unique to the microbes.
 Memory present- A proportion of T and B cells become
memory cells following primary contact of the microbe,
which play an important role when the microbe is
encountered subsequently.
 Diversity is wide- Acquired immunity though takes time to
develop is active against a wide range of repertoire of
antigens.

30. TYPES OF ACQUIRED IMMUNITY
 Active and passive immunity
 Artificial and natural immunity

31. ACTIVE IMMUNITY
 Active immunity is the resistance developed by an individual
towards an antigenic stimulus.
 Active immunity may be induced naturally or artificially:
o Natural active immunity occurs following an exposure to a microbial
infection (e.g. measles virus infection)
o Artificial active immunity develops following an exposure to an
immunogen by vaccination (e.g. measles vaccine).

32. ACTIVE IMMUNITY
 Long-lasting- Active immunity usually lasts for longer
periods but the duration varies depending on the type
of pathogen.
o Last life long- e.g. following certain viral infections
such as chicken pox, measles, small pox, mumps
and rubella.
o Last short- e.g. following influenza infection.
o Premunition or concomitant immunity – Immunity
may last as long as the microbe is present. Once the
disease is cured, the patient becomes susceptible to
the microbe again (Spirochaetes and Plasmodium).

33. ACTIVE IMMUNITY
o Premunition or concomitant immunity – Immunity may
last as long as the microbe is present. Once the disease
is cured, the patient becomes susceptible to the microbe
again (Spirochaetes and Plasmodium).
o Active immunity may not be protective at all- e.g. for
Haemophilus ducreyi, the patient may develop genital
lesions following reinfection even while the original
infection is active.

34. PASSIVE IMMUNITY
 Passive immunity is defined as the resistance that is
transferred passively to a host in a 'readymade' form
without active participation of the host’s immune
system.
 Passive immunity can also be induced naturally or
artificially.
o Natural passive immunity involves the IgG antibody
transfer from mother to fetus across the placenta.
o Artificial passive immunity develops following
readymade transfer of commercially prepared
immunoglobulin (e.g. Rabies immunoglobulin)

35. ROLE OF PASSIVE IMMUNITY
 Immunodeficient individuals (as host’s immune apparatus is
not effective)
 Post exposure prophylaxis; when an immediate effect is
warranted.
 Passive immunity develops faster; there is no lag phase or
negative phase.
 There is no immunological memory as the memory cells are
not involved.
 Booster doses are not effective

36. DIFFERENCES BETWEEN ACTIVE AND PASSIVE IMMUNITY
Active immunity Passive immunity
Produced actively by host
immune system
Immunoglobulins received passively
Induced by
 Infection (natural)
 Vaccination (artificial)
Acquired by-
 Mother to fetus IgG transfer
(natural)
 Readymade antibody transfer
(artificial)
Long lasting Lasts for short time
Lag period present No Lag period
Memory present No Memory
Booster doses-useful Subsequent doses-Less effective
Negative phase may occur No Negative phase
In immunodeficiency individuals
not useful
Useful in immunodeficient individuals

37. Primary immune response Secondary immune response
Immune response against primary
antigenic challenge
Immune response against
subsequent antigenic challenge
Slow, sluggish (appear late) and
short lived
Prompt, powerful & prolonged (long
lasting)
Lag period is longer (4-7 days) Lag period is absent or short (1-3
days)
No negative phase Negative phase may occur
Antibody produced in low titer & is
of IgM type.
Antibodies are more specific but
less avid
Antibody produced in high titer & is
of IgG type
Antibodies are less specific but more
avid
Antibody producing cells- Naive B
cells
Antibody producing cells- Memory B
cells
Both T dependent and T
independent antigens are
processed.
Only T dependent antigens are
processed.

38. LOCAL (OR MUCOSAL) IMMUNITY
 Immune response that is active at the mucosal surfaces such as
intestinal or respiratory or genitourinary mucosa.
 Mediated by a type of IgA antibody called secretory IgA.
 Local immunity can only be induced by natural infection or by live
vaccination (but not by killed vaccines).

39. HERD IMMUNITY
 Herd immunity is defined as the overall immunity of a
community (or herd) towards a pathogen.
 Elements that contribute to create a strong herd immunity are-
o Occurrence of clinical and subclinical cases in the herd
o On-going immunization programme
o Herd structure i.e. type of population involved
o Type of pathogen-Herd immunity may not be strong in a community
against all the pathogens.

40. HERD IMMUNITY
 Herd immunity develops following effective vaccination
against some diseases like:
o Diphtheria and Pertussis vaccine
o Measles, Mumps and Rubella (MMR) vaccine
o Polio (Oral polio vaccine)
o Smallpox vaccine

41. THANK YOU