MIKROBIOLOGI

DASAR
dr. ELITA DEVINA, Sp.MK
LAB.MIKROBIOLOGI KLINIK RSUD SIDOARJO
PELATIHAN PPI DASAR 2017
SARS CoV-2003
Avian Influenza 2005
H1N1 Swine Flu-2009
H7N9 Influenza-2013
Ebola Hemorrhagic Fever-2014
MERS-CoV 2012-2014
Talaro and Chess, 2015
Evolutionary Timeline

Talaro and Chess, 2015

 Size comparison of viruses
with a yeast cell and Bacteria

Talaro and Chess, 2015

Leeuwenhoek

Talaro and Chess, 2015

Fransisco Redi’s Experiment
Abiogenesis
Theory
 Pasteur and Theory of Germ

“Generatio Spontanea Theory”

Talaro and Chess, 2015

 Koch’s Postulate

Baumann, 2015 Talaro and Chess, 2015

VIRUS
Three main properties of viruses :

 smallsize: the smallest known infective agents

(20 nm – 300 nm); bacteria: 1000 nm; erythrocytes:
7500 nm.
 genome: contain only one kind of nucleic acid
(DNA or RNA).
 metabolically inert: no metabolic activity outside
susceptible host cells; do not possess active
ribosomes/ protein-synthesizing apparatus, although
some viruses contain enzymes.
VIRUS STRUCTURE:
Consist of nucleic acid/ genome, surrounded by a protein coat

 Virion: the intact virus particle

 Capsid: the protein coat
 Capsomeres: the protein structural units of capsid
 Nucleic acid genome: either DNA or RNA
 Envelope: some virus particles are surrounded by a lipoprotein envelope;
containing viral antigens
Talaro and Chess, 2015
 Virus
Replication

Talaro and Chess, 2015

VIRUS DISEASES
Most are mild & the viruses makes a complete recovery;
many are silent in the body without causing any symptoms,
which sometimes cause severe disease in an unusually
susceptible patient. Few viral diseases are severe with high
mortality.

Viruses enter the body through 4 main ways:

 Inhalation: via respiratory tract.
 Ingestion: via gastrointestinal tract.
 Inoculation: through skin abrasions, mucous membranes
(e.g. sexual); transfusion; injections; transplants; via the
bite of an arthropod.
 Congenital: i.e. from mother to fetus.
Inge Lusida, Viruses
EFFECTS OF VIRUSES ON CELLS
1. Death: the infection is lethal; causes a cytopathic effect (CPE)
which kills the cell; e.g. multinucleated giant cells/ syncitia,
inclusion bodies.
2. Transformation: the cell is not killed, but is changed from a
normal cell to a malignant or cancerous cell.
3. Latent infection: virus remains within the cell in a potentially
active state, but produces no obvious effects on the cell’s
functions.
4. Haemadsorption: some viruses have haemaglutinin in their
outer coats adheres to erythrocytes
agglutination
Cytopathic changes in cells and
cell cultures infected by viruses

Talaro and Chess, 2015

Effect of Physical and Chemical Agents on Viruses

 Heat: most are inactivated at 56oC for 30 min or 100oC for a

few seconds.
 Cold: stable at low temperatures, can be stored at -70oC
for years.
 Drying: variable
 Ultraviolet: inactivates viruses
 Chloroform, ether and other organic solvents: enveloped
viruses are inactivated; those without envelopes are resistant
 Oxidizing & reducing agents: viruses are inactivated by
formaldehyde, chlorine, iodine & hydrogen peroxide
 (Effect of Physical and Chemical Agents on Viruses)

 Phenols: most viruses are relatively resistant.

 Virus desinfectants: the best are hypochlorite solution &
glutaraldehyde.
corrosive

Sensitization & irritation to users

 Virus HAI’s
– Adenoviral pharyngitis
– Influenza virus
– Parainfluenza virus
– Hepatitis A virus
– Hepatitis B virus
– Hepatitis C virus
– HIV
BACTERIA
Morphology of Bacteria

Talaro and Chess, 2015

Bacterial Structures
Bacteria Cell Wall

Madigan, et al, 2015

Endospore Formation
Pili /Fimbriae
 Plasmid
(mobile genetic material)

Mechanism of
Bacterial Transfer Gene
Reproduction of Bacteria
 Flemming
and Antibiotic

Baumann, 2015; Talaro and Chess, 2015

DEFINISI

FLORA NORMAL
KONTAMINASI
KOLONISASI
INFEKSI
PATHOGEN
PATHOGEN POTENSIAL
OPPORTUNISTIC PATHOGEN
PATHOGENITAS
Di alam lingkungan sekitar kita dihuni :
5 x 10³º sel mikroorganisme.

Di dalam tubuh manusia :

tubuh manusia juga dihuni oleh
mikroorganisme.
DEFINISI

FLORA NORMAL PADA TUBUH MANUSIA

FLORA NORMAL : mikroba yang hidup pada kulit dan selaput lendir
manusia dalam keadaan normal / sehat

Ada 2 kelompok mikroba :

1. RESIDENT FLORA (FLORA TETAP) :
mikroba yang secara normal menetap pada bagian tubuh tertentu

2. TRANSIENT FLORA (FLORA SEMENTARA) :

mikroba non pathogen atau potensial pathogen yg tinggal di kulit atau
selaput lendir selama kurun waktu tertentu yg berasal dari lingkungan

Bila resident flora berubah, maka transient flora dapat membentuk

kolonisasi, berkembang biak dan menimbulkan penyakit
MENGAPA MEREKA MENGUNTUNGKAN HOST ?

- Menghalangi tumbuhnya organisme lain

“MENJAGA KESEIMBANGAN”
–Memecah protein
–Mencerna makanan
–Stimulasi pembentukan antibodi
–membentuk vit.K dan B

Kulit : 1 cm² mengandung 3 juta bakteri.

Kolon : mengandung bermacam bakteri yang jumlahnya tidak
terhitung
The origins of
microbiota
in newborns

Talaro and Chess, 2015

The Human Microbiome
A Superorganism

Talaro and Chess, 2015

Normal Skin Microflora
DEFINISI

KOLONISASI:
- MIKROBA (+) → MINGGU → BULAN → TAHUN
- Tidak ada luka, tidak invasi jaringan

Bacterial interactions with mucous membranes

BIOFILM FORMATION

Talaro and Chess, 2015

Biofilms Formation

Talaro and Chess, 2015

DEFINISI

PATHOGEN:
ORGANISME YG MENYEBABKAN SAKIT PADA
SUSCEPTIBLE HOST

PATHOGEN POTENSIAL:
FLORA NORMAL, tapi pada keadaan tertentu dapat
mengalahkan pertahanan tubuh host dan
menyebabkan sakit

OPPORTUNISTIC PATHOGEN:
- NORMAL HOST TAK SAKIT
- HOST DENGAN SISTEM IMUN ↓ → SAKIT
DEFINISI

INFEKSI:
Proses masuknya organisme ke dalam host, invasi dan
multiplikasi
- LUKA / INVASI → JARINGAN RUSAK OLEH
MIKROBA

PENYAKIT INFEKSI :
Manifestasi klinis dari kerusakan atau gangguan
struktur dan fungsi sel dan jaringan akibat proses
infeksi.
(+ symptoms, + signs, + syndromes)
DEFINISI

PATHOGENITAS:
KEMAMPUAN KUMAN MENYEBABKAN SAKIT

= FAKTOR VIRULENSI:
- TOXIN
- INVASIVENESS (kemampuan kuman untuk
masuk & menyebar dalam tubuh host)
- KECEPATAN REPLIKASI KUMAN &
KEMAMPUAN MEMBENDUNG PERTAHANAN
HOST
Stages in the course of infection
and disease

Talaro and Chess, 2015

 Ten most common pathogens
that account for 84% of all HAIs (n=33.848)
• Coagulase-negative staphylococci (15%)
• Staphylococcus aureus (15%)
• Enterococcus species (12%)
• Candida species (11%)
• Escherichia coli (10%)
• Pseudomonas aeruginosa (8%)
• Klebsiella pneumoniae (6%)
• Enterobacter species (5%)
• Acinetobacter baumannii (3%)
• Klebsiella oxytoca (2%)
Infect Control Hosp Epidemiol 2008; 29:996-1011
Talaro and Chess, 2015
 Associations
between microbes and humans

Talaro and Chess, 2015

 VID-20170206-
“Let’s watch the WA0021.mp4
movie”