Infectious Diseases

dr. Gunawan Arsyadi, SpPA (K), SpF

Overview of infectious disease
 The most feared disease of human because of
their ability to affect large number of health
people over a short period
 Plaque killed about 10% of the population in
London in 1665.
 The only infectious disease succesfully
eradicated from the world is smallpox
 While many causes of old epidemics have been
controlled, new epidemics have emerged
Infection
The entry and multiplication of an infection
agent in an host.
A. No Disease : Immune system not activated
B. Subclinical infection
No clinical apparent disease but  evidence of
immune respons against the agent
c. Clinical infection: Tissue damage of occurs,
immune system activated.
Infection of the bloodstream
 Infectious agents enter the lymphatics and the bloodstream
from any infected tissue.
A. Transient Bacteremia
- Small numbers of microorganism in the bloodstream
- No multiply, since they are rapidly removed by the body’s
defence mechanism
- Common in person with infected gum & teeth
- Maybe manifest in:
* Immunocompromised host
* Cardiac valve disease cardiac prothese
* Infection in an internal organ
Infection of the bloodstream
B. Severe bacteremia
- Serious infection in which large and increasing

numbers of microorganisms have

overwhelmed the body’s defence mechanism
- Associated with toxemia (bacterial toxins
present in the bloodstream)
- High fever, chills, tachycardia & hypotension
 death
Classification of infectious agents
A. Clasification According to Pathogenicity
Pathogenicity : Ability to cause disease
• Low-grade  cause disease only in
immunocompromised hosts (opportunistic
infections)
• High – grade / virulent  cause disease in
normal people
Infectivity: Ability of an infectious agents to
estables it self in tissue
Classification of infectious agents
B. Clasification Acording to Site of
Multiplication
1. Obligate Intracellular Organism
- Can grow & multiply only in host cells &
require the metabolic apparatus of host
cells for growth
- Culture of such organisms require living
cells system eg. embryonal eggs
Classification of infectious agents
B. Clasification Acording to Site of Multiplication
2. Facultative Intracelluler Organism
- The microorganisms are capable of both
extracellular & intracellular growth &
multiplication
- Can be culture on artificial media
3. Extracelluler Organism
- The organisms multiply outside cells
- Most can be cultured on articial media (except
protozoa, metazoa & treponema pallidum)
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
I Obligate Intacellular Organisms
A. Cell Necrosis
a. Acute necrosis : Replication of the agent is
accomponied by a lethal abnormality in cell function.
* Hepatitis virus
* Polio
b. Chronic necrosis
* Hepatitis B & C virus
* HIV
B. Cell Swelling
- Sublethal injury
- Diffuse swelling in acute viral hepatitis
- Endothelial cell swelling that may lead to thrombosis
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
I. Obligate Intacellular Organisms
C. Inclusion Body Formation
- Visible on light microscopy
- The are composed either of assembled
viral particles or of remnants of viral nucleid
acid synthesis
- Ocurr in the nucleous/ cytoplasm
- Aid in the diagnosis of specific viral infection
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
I. Obligate Intacellular Organisms
D. Giant Cell Formation
- Mulinucleated giant cells
- Measles:  Wharthin – Finkeldey giant cell
* Lung
* Lymphoid Tissue
* Appendix
* Tonsil
- Herpes Zoster/ Herpes Symplex
* Stratified squamous epithelial cells
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
I. Obligate Intacellular Organisms
E. Latent Viral Infection
Virus can remain latent in the infected cells, often for the
lifetime of the host.
1. Reactivation
* Stress
* Trauma
* Coexsistent disease
* Immune deficiency
2. Oncogenesis (Production of Neoplasm)
- Some virus are thought to cause neoplasm in
animals & humans
- Ebstein – Barr Virus  Burkitt’s Lymphoma,
Nasopharyngeal Carsinoma
- HTLV – 1  Japanese T Cell Lymphoma
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
II. Facultative Intracellular Organisms
- Tissue damage (mycobacterium & fungi)
- Granuloma formation (mycobacterium
tuberculosis, treponema pallidum)
- Delayed hypersensitivity responsible for
caseous necrosis
 TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
III. Extracellar Organism
A. Release of Locally Acting Enzymes
- Virulent organism  enzym liberated into
tissue breakdouwn various subtrate molecule
- Staphylococcus Aureus Coagulase  convert
fibrinogen into fibrin bacterium to become
coated by fibrin increase its ability to resist
phagocytosis
- Streptoccocus pyogenes hyaluronidase degrades
hyaluronic acid facilitates the spread of infection.
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
III. Extracellular Organism
B. Production of Local Vasculitis
Highly virulent organisms eg anthrax,
aspergillus, mucor infect & cause
thrombosis of local small vessels & cause
ischemic necrosis in / and arround the area of
infection
 TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
III. Extracellular Organism
C. Production of Remotely Acting Toxins
- Cause cell injury far removed from the point of infection.
1. Endotoxin
- Are lipopolysaccharide components of the cell walls of gram
negative bacteria released into bloodstream after the death &
lysis of bacteria.
- Cause generalized vascular dilatation  shock, endothelial cell
damage
- Endotoxin induced macrophages TNF  vasodilatation of
blood vessels
- Endotoxin  indused macrophages IL-1 fever
- Relatively heat stable
TISSUE DAMAGE CAUSED BY
INFECTIOUS AGENTS
III. Extracellular Organism
C. Production of Remotely Acting Toxins
2. Exotoxin
- Often proteins secreted by living bacteria  come in the
bloodstream
- Highly antigenic inducing promotion of specific
antibodies
- Heats labile, destroyed by cooking/heating above 600 C
3. Enterotoxin
- Exotoxins that act on intestinal mucosal cells the toxins
attach to surface receptors on intestional mucosal cells
cause structural damage or fuctional alteration (V. cholerae).
TISSUE REACTION CHANGES CAUSED BY
INFECTION
INFECTIOUS AGENT

INFLAMMATORY REACTION IMMUNE RESPONS

NEUTRALISATION OF
INFECTIOUS AGENT

TISSUE DAMAGE TISSUE DAMAGE

TISSUE NECROTIC

DEATH
ACUTE INFLAMMATION

  DOLOR
  RUBOR
  CALOR
  TUMOR
EKSOGEN
PYROGEN
ENDOGEN (*INTERLEUKIN)
EXTRACELLULAR ORGANISM
• Commonly bacteria
• Body reaction: neutrophil

Neutrophylia
• Chemotactic factor activity at infection site.
INTRACELLULAR ORGANISM
• Rarely ---- acute inflammation
• Acute inflammation (for ex: Typhoid Fever)
 Infiltration of macrophage
 A few neutrophil
OBLIGATE INTRACELLULAR ORGANISM
• Lymphocyte, plasma cell, macrophage
• A few of neutrophyle
• No chemotactic factor
Immune respons
 Epitheloid Granuloma

1. Mycobacteria
2. Fungi:
• Coccidiodes immitis
• Histoplasmosis capsulare

3. Species Brucella
4. Treponema Pallidum
Gumma
Suppurative Inflammation
 Acute inflammatory complication

Liquifaction necrotic
 Acute and Chronic
A. Acute suppurative
Phagocyte resistent bacteria
 S. aureus
 Klebsiella
 Pseudomonas
 Pneumococcus tipe 3
B. Chronic suppurative
 Persisten acute suppurative inflammation
 Infection: Filamentous bacteria, fungi
 Progressif, multiple abcess, fibrosis
Chronic Inflammation
A. Granumatous chronic inflammation
• Epitheloid granuloma: Spesific body respons due to
facultative intracellular organism multiplication in
macrophage
• Tcell mediated: Hypersensitivity reaction type
IV
• Activated Tcell: Lymphokine
macrophage acummulation & activation
• Delayed hypersensitivity: Caseous necrosis
Chronic Inflammation
B. Chronic inflammation with macrophage
proliferation
• cell-mediated immune respons deficiency
• No production of T-cell lymphokines: epitheloid
granuloma is not forming
• Intracelluler facultative organism
 Mycobacterium tbc, leprae
 Atypical mycobacterium
 Klebsiella rhinoscleromatis
 Leishmania species
• Non immune phagocytosis is not efective to destroy
bactery
Chronic Inflammation
C. Chronic inflammation with
lymphocyte and plasma cells
• Body reaction due to persisten
infection cause by obligate
intracellular organism (chronic
viral hepatitis)
• Humoral and cellular immune
respons combination.
Chronic Inflammation
C. Mixed type of suppurative and
granulomatous inflammation
• Deep fungal infection
• Stellate granuloma: found neutrophil in
the central of epitheloid granuloma
 Lymphogranuloma venerum
(Chlamidia trachomatis)
 Cat-scratch disease (Atypia felis)
 Tularemia (Francisella tularesis)
 Glanders (Pseudomonas mallei)
 Meliodosis (Pseudomonas
pseudomallei)