OVERVIEW of

INFECTIOUS DISEASES

WINARTO
Dept of Clinical Microbiology and
Ophthalmology
Fac of Medicine, Diponegoro University
2016
The top seven killers (1997)
 emerging infectious diseases
• Legionellosis
• Toxic shock syndrome
• Lyme disease: Borrelia
• Cat scratch disease:
Bartonella
• Gastric ulcers : Helicobacter
• Wipple’s disease:
Tropheryma
• Ehrlichiosis
• Chlamydial pneumonia
• Invasive streptococcal
infections
• Tuberculosis
• Cholera
• Diphtheria
• MRSA & community-MRSA
• Multiple antibiotic resistance
• Human immunodeficiency virus
• West Nile virus
• Hepatitis virusses
• African hemorrhagic fever
• Hantavirus infections
• Human herpes virusses 6,7,8
• Herpes B virus
• Parvovirus B19
• Rotavirus
• Norwalk virus & other SRV’s
• Rabies
• Human T-cell lymphotropic virus
• Human metapneumo virus
• SARS Corona virus
• Resistance to antiviral agents
 emerging infectious
diseases
• Malaria • Invasive candidiasis
• Cryptosporidiosis
• Invasive aspergillosis
• Microsporidiosis
• Scabies • Invasive
mucormycosis
• Pneumocystis carinii
• Kawasaki syndrome
• Prion disease
 Infection ?

Inflammation ?
HOST AGENT RELATIONSHIP
HOST AGENT RELATIONSHIP
Temperature
Dust and humidity
ENVIRONMENT The use of AB
Pesticides

AGENT HOST

Pathogenicity Innate immunity

Virulence Adaptive immunity
Infective dose Normal microflora
Infectiousness Nutritional factors
AB resistance Socio-economic factors
Behavioral factors
HOST AGENT RELATIONSHIP

ENVIRONMENT

AGENT HOST

HEALTHY or DISEASE
 INFECTION
Microbe entry
Innate immunity
Invasion

Colonization

Evasion toxin

Adaptive immunity
Tissue injury inflammation

Functional impairment
 Adhesion

Colonization

Invasion –
Multiplication

Infection
11
INFECTION CURVE
INFECTIOUS AGENT
1. BACTERIA
2. VIRUS
3. FUNGUS
4. PRION
5. PARASITES
 Size of
Eukaryotes, Prokaryotes, and Virus

PROKARYOTE
EUKARYOTE

More than 500 virus could

enters within bacterial cell VIRUSES
 Prokaryote Eukaryote
Nucleoid contain DNA Nucleus contain DNA &
& RNA RNA

Cytoplasmic structures Cytoplasmic structures

- plasmid - mitochondria

Cell membrane Surface layers

Cell envelope Motility Organelles

- bacteria, viruses. - human, parasite, fungi,

animal.
BACTERIA
GROWTH, SURVIVAL &
DEATH of
Microorganisms
The population of microorganisms in the
biosphere is roughly balanced

Growth is counter balanced by death

 MICROBIAL GROWTH
Microbial growth requires:

Polymerization of proteins,
biochemical building nucleic acids,
blocks polysaccharides
and lipids

Needs Energy
building blocks:
. Synthesized by cell  require co-enzyme
. Provided in the growth medium
Microbial metabolism ca be divided:

1. Pathways for the interconversion of

focal metabolites.
2. Assimilatory pathways for the
formation of focal metabolites.
3. Biosynthetic sequences for the
conversion of focal metabolites to end
products.
4. Pathways that yield metabolic energy
for growth and maintenance.
When provided:
building blocks and Cell synthesize
source of metabolic macromolecules
energy

The sequence of building blocks determined by

1. Nucleic acid and protein: template
directed
- DNA  DNA & RNA
- RNA  messenger RNA  protein
2. Carbohydrate and lipids: enzymes
specificities
Once macromolecules have been synthesized

Self assemble of supramolecular

structures of the cell:
- ribosomes
- membrane
- cell wall
- flagella
- pilli
Medium
Building blocks
synthesized

Carbohydrate
Macromolecules protein
lipid

Cell wall
Supramolecular Membrane
structure Flagella, etc

Regulated by control mechanism

Growth is the orderly increase in the sum of
all components of organism.
Increase in size due takes up water or lipid
or polysaccharides is not true growth.
Cell multiplication is consequence of
growth  microbial concentration
increased.

1  2  4  16  etc nt
Binary fission
Measurement of microbial concentration:
1. Cell concentration:
the number of viable cells per unit
volume of culture
2. Biomass concentration:
dry weight of cells per unit volume
of culture
GROWTH CURVE
The Lag phase:
Period during cell depleted metabolic
activities as results of unfavorable
conditions and adapt to new environment.

The Exponential phase:

New cell material is being synthesized at
constant rate and the mass increase in an
exponential manner.
This continues up to nutrient become
exhausted or toxic metabolites accumulate
& inhibit the growth.
The Maximum Stationary phase:
Nutrients exhausted and toxic metabolites
accumulate  growth cease completely.
Cell death and new cell is just balanced.

The Phase of Decline: The Death phase:

The death rate reached a steady level.
After the majority of the cell have died, the
death rate decrease drastically, so a small
number of survivors persist for months or
even years.
 CULTIVATION of Microrganisms

Cultivation is the propagating organisms

by providing the proper environmental
conditions.
Factors must be controlled:
1. Nutrients
2. pH
3. Temperature
4. Aeration
5. Salt concentration
6. Ionic strength.
Oxygen (-) Oxygen (+)

anaerob Facultative anaerob aerob

CO2

microaeriophilic
 CLASSIFICATION of Microrganisms

1. Morphology:
a. Rods: spore / no spore
b. Cocci
c. Spiral
2. Gram Staining:
a. Positive gram
b. Negative gram
3. The presence of Oxygen:
a. Aerob
b. Anaerob
Classification of bacteria
 EXAMPLES
1. Staphylococcus aureus Cocci, gram positive,

Streptococcus pyogenes aerobic

1. Escherichia coli

2. Clostridia tetani

3. Clostridia botulinum

4. Neisseria gonorrhea
 EXAMPLES
1. Staphylococcus aureus
Rod, gram negative,
2. Escherichia coli
facultative
3. Clostridia tetani
anaerobic
4. Clostridia botulinum

5. Neisseria gonorhoea
 EXAMPLES
1. Staphylococcus aureus

2. Escherichia coli
Rod, gram positive,
3. Clostridia tetani
anaerobic, spore
Clostridia botulinum
forming
4. Neisseria gonorrhea
 EXAMPLES
1. Staphylococcus aureus

2. Escherichia coli

3. Clostridia tetani

4. Clostridia botulinum
Cocci, in pairs, gram
5. Neisseria gonorhoea
negative, aerobic
FUNGUS
 Mycology: study of fungi
Mycoses: fungal infection
80,000 species have been described
< 400 species medically important
< 50 species cause > 90 % fungal
infection
Breaking down and recycling organic
matter
Contributing to food production
Contribute to medicine; antibiotics:
penicillin, immunosuppressive:
cyclosporine
Eukaryote model by geneticist &
molecular biologist
Phytopathogens  economic loss.
VIRUSES
Electron microscope of Coronavirus,
never before seen in humans (WHO)
 Paramyxovirus Coronavirus

Larger glycoprotein (HN, H, G) Peplomeric glycoprotein

(viral attachment protein) E2
Smaller glycoprotein Transmembrane
(fusion [F]) glycoprotein
E1
Lipid bilayer Lipid bilayer

RNA
Nucleocapsid

Matrix (M) Nucleoprotein N

protein
 HIV VIRUS

Gp 40

Gp 120

CD4 receptor
of host cell

KONAS 03
Life cycle of Virus
DNA virus replication
RNA virus replication
Lytic & lysogenic cycle
DEFENCE SYSTEM
IMMUNE SYSTEM
IMMUNE SYSTEM

INNATE = NATURAL = NON SPECIFIC =

FACTORY PREPROGRAMMED
Genetic, Intact epithelium / mucous
membrane, bacterial flora, lysozym, etc.

ADAPTIVE = SPECIFIC = ACQUIRED

IMMUNITY = USER PROGRAMMABLE
In respons to stimuli : microbes, foreign
protein, non self antigen
DEVELOPMENT OF IMMUNE SYSTEM

STEM CELL

H B CELL T CELL
C
M Plasma
cell
T CELL
M
IIgG, IgM, IgA,
Cytokine
I
IgE, IgD
DEVELOPMENT OF IMMUNE SYSTEM

Antigen

APC

Th 0
Th1 Th2
IFN-, No, TGF- IL4, IL5, IL9
IL2, 3,10,13, GM-CSF IL2,3,10,13,GM-CSF
D.T.H ATOPY
DEVELOPMENT OF IMMUNE SYSTEM

STEM CELL

Ag
B CELL T CELL

TH
Plasma T CELL
cell
TS

IgG, IgM, IgA,

IgE, IgD Cytokine
NORMAL FLORA
Indegenous flora
Human body :
1. Sites with normal flora :
a. Function : - part of innate immunity
- contribute to body normal function
b. If disturb  dysfunction
causes a diseases
c. Skin, Resp. tract, GI tract, GU tract, etc
2. Steril sites :
e.g. Blood, CNS, eye, soft tissue, bone marrow, etc.
Normal Flora:
1. Resident Flora = commensals
- relatively constant: type and dominance
- if disturbed  it will return
2. Transient Flora  non pathogenic
- varies

Type and distribution depend on: temperature,

humidity, nutrients, inhibitors  specific for
certain locations.
Function of Normal Flora:
1. Maintain normal function & health
2. As “bacterial interference” for
pathogenic: occupy the sites, produce
inhibitors.
3. Stimulate immunology
4. Source of infection  if displaced to
other normal site, e.g: during
operation.
5. Carcinogenic ?
 STERIL SITES
Brain and spinal cord are protected by skull and
spinal column.

Skull
Dura mater
Arachnoid mater
Subarachnoid space : CSF
Pia mater

Brain

Blood brain barrier / blood CSF barrier :

Capillary endothelial cells resting on a basement membrane.
Tight junction between these cells  unable to cross.
 Ciliated Viral infection 
pseudostratified disrupt function
columnar  bacteria enter
epithelium with the steril site
DEFENCE mucus
IMMUNO
SYSTEM COMPRO
MISE OF
DEFENCE
Alveolar Bronchi SYSTEM
macro- olar
phage carcino
ma

Cough Trauma or
reflex abdomnal
surgery 
disturb
reflex
Normal Flora
Normal Flora
AGENT
 NON VIRAL MENINGITIS
PATHOGEN TREATMENT PREVENTION
N meningitidis Penicillin Rifampicin prophylaxis for close
( or chloramphenicol ) contact
Polysaccharide vaccine (poor
protection against group B)
H influenzae Ampicillin or chloramphenicol Rifampicin prophylaxis for close
or cefotaxime contact
Vaccine
Str pneumoniae Penicillin Prompt treatment of OMA & resp.
( or chloramphenicol ) infection
Polyvalent (23 serotypes)
polysaccharide vaccin
E coli, Gr B strep, Gentamycin & penicillin or No vaccin available
L monocytogenes, chloramphenicol
S epidermidis
M tbc INH & rifampicin & BCG vacc, INH prophylax for
pyrazinamide ± streptomycin caontacts
C neoformans Amphotericin B & flucytosine No vaccine available
 Bacterial meningitis-virulence factor for major pathogens

Virulence Bacterial pathogen

factor
Capsule N meningitidis H influenzae S pneumoniae
+ + +
IgA + + +
protease

Pili + + -

Endotoxin + + -

OMPs ? + -
 CAPSULES : important virulence factors
Pathogen Capsule Important type Vaccine

N meningitidis polysaccharide A,B,C,Y,W-135 Good for A&C

Poor for B

H influenzae polysaccharide b New vaccine

available for < 1
year old
S pneumoniae polysaccharide many Pneumovax:23-
valent
most common
type
Gr B streptococcus Polysaccharide rich in (Ia,Ib,II) III in
E coli sialic acid meningitis
KI in meningitis
 Bacterial meningitis – Clinical Features

Patogen Host Important Mortality Sequelle

clinical features (as % of (as % of
treated treated
cases) cases)
N meningitidis Children & Acute onset (6- 7 – 10 <1
adolescence 24 h) skin rash

H influenzae Children < 5 yrs Onset often less 5 9

acute (1-2 days)

S pneumoniae All ages but Acute onset 20 - 30 15 - 20

especially may follow
children < 2 yrs pneumonia &/or
and eldery septicaemia n
eldery
KOCH’S POSTULATES
TRANSMISSION
Routes of transmission
 Lecture Topic Lecturer

Overview of Infectious Agent Prof. Dr. dr. Winarto, DMM, SpMK, SpM(K)

Microbiological Diagnosis Prof. Dr. dr. Winarto, DMM, SpMK, SpM(K)

Virology Dr Purnomo Hadi, M.Si.

Agent Penyebab Infeksi Dr Purnomo Hadi, M.Si.

Molecular Pathogenesis Prof. Dr. dr. Winarto, DMM, SpMK, SpM(K)

5 x 2 jam kuliah = 10 jam kuliah 

1 SKS