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Infectious Diseases Categories of Infectious Agents

P. B. Casuela, Jr. MD, FSP  Prions – composed only of a modified host protein that
can cause transmissible spongiform encephalopathy
Inflammation – tissue reaction to injury of whatever etiology  Viruses – obligate intracellular parasites that are
Infection – tissue reaction to injury due to microbiologic agents dependent on host cell metabolism for their replication
- Classified by the nucleic acid content of the core
Importance of Infectious Diseases (DNA or RNA) and by the shape of their protein
1. They are major causes of morbidity and mortality coat or capsid
2. Greater transmission (vertical or horizontal) than any  Bacteriophages, Plasmids, Transporons – mobile genetic
other disease. elements that encode bacterial virulence factors
3. Versatile diseases evolving and adapting through - Can infect bacteria and incorporate themselves
time. in their genome --> converting to virulent one or
4. Some are self-limiting and requires no specific an antibiotic-resistant one
treatments. - Exchange of these elements between strains &
5. Many are preventable. species endow survival advantage
6. Association with congenital diseases:  Bacteria – prokaryotes that lack nuclei and ER
Varicella (German measles) - multiple - Relatively rigid cell wall, classifiable as gram (-)
congenital anomalies or Gram (+)
Syphilis - Bacteria synthesize their own DNA, RNA and
HIV proteins, but depend on the host for favorable
7. Association with neoplastic conditions conditions
Enterobacter pylori – gastric CA - Second to viruses as most frequent & diverse
Herpes (Type 2) genitalis virus and HPV – class of human pathogen
squamous cell carcinoma of the cervix  Chlamydiae, Rickettsia and Mycoplasmas – similar to
Ebstein-Barr virus – Nasopharyngeal CA bacteria in that they divide by binary fission and are
Burkitt’s lymphoma susceptible to antibiotics but lack:
S. japonicum ,Aspergillus flavus: Hepatocellular CA - Cell wall – Mycoplasma
S. hematobium: urinary bladder transitional cell CA - ATP synthesis – Chlamydia
Clonorchis sinensis & Opistorchis felineus -  Transmitted by insect vectors - Rickettsia
cholangiocarcinoma  Fungi – possess thick, ergosterol-containing cell walls and
grow as perfect, sexually producing forms in vitro and as
Epidemiology – Branch of medicine dealing with the incidence imperfect forms in vivo, which include budding yeasts and
and prevalence of diseases in large populations and with hyphae
detection of the source of epidemics of infectious disease. - Classified as: Dermatophytes Systemic
Incidence Rate – occurrence in 100,000 population per given Subcutaneous Opportunistic
time  Protozoa – parasitic, single-celled organisms endowed
Prevalence – widespread; of wide extent or occurrence with motility, pliable plasma membranes and complex
Endemic – belonging exclusively or confined to a particular place. cytoplasmic organelles
Epidemic – affecting many persons at the same time and - Classified as: Flagellates Blood-borne
spreading from person to person in a locality where the diseas Intestinal
is not permanently prevalent.  Helminths – parasitic worms that are highly differentiated
Pandemic – prevalent throughout an entire country , continent, multicellular organisms
or the whole world. - With complex life cycles; most alternate
between sexual reproduction in definitive hosts
General Principles of Microbial Pathogenesis and asexual reproduction in intermediate hosts
Pathology deals with host response to different infectious  Ectoparasites – arthropods (lice, ticks, bedbugs, fleas) that
agents, the different classes of agents, their mode of attach and live on the skin
transmission, how they cause disease, and possible outcome - Can be vectors for other pathogens
(biologic behavior).
Transmission and Dissemination of Microbes
The Triad  Hosts Barriers to Infection
Patient: Age - 1 – intact host skin, mucosal surfaces & their
Physiology secretory-excretory products
Genetics - Respiratory tract – mucociliary blanket of upper air
Immune state passages, cough reflex, alveolar macrophage
Malnutrition - GIT – acid gastric juice, viscous mucous layer covering
the gut, lytic pancreatic enzymes & bile detergents,
Environment: Infectious Agent: secreted IgA antibodies
Extraneous factors “Koch’s Postulate” - GUT – regular flushing of the urinary tract with urine
Sanitation Pathogenicity/Virulence serves as a defense against invading microorganisms,
Climate and temperature Tropism vagina with low pH is protective
- Skin – dryness and constant shedding of impermeable
keratinized epithelium and competition from
commensal bacteria || 1st semester, AY 2011-2012

 Spread and Dissemination of Microbes
- Some microorganisms proliferate locally at site
of infection
- Others penetrate the epithelial barrier & spread
to other sites via the lymphatics, the blood, or
- Major manifestations of infectious disease may
arise at sites distant from those of microbe entry
- Placental-fetal route is an important mode of
 Release of Microbes from the Body
- In transmission of disease, exit of the organism
in the host’s body is as important as its entry
- Depends on the location of the infection: skin
shedding, coughing, sneezing, voiding in
urine/stool, through insect vectors
Mode of transmission:
Respiratory, fecal-oral, sexual routes, direct contact,
through blood & blood products, through vertebrate &
invertebrate vector, zoonotic transmission

How microorganisms cause disease

 Infectious agent can contact or enter host cells and
directly cause cell death
 May release toxins, enzymes Viruses once inside the host cells can
 Can induce host cellular responses (though directed kill &/or cause tissue damage thru:
against the invader) cause additional tissue damage, 1. Inhibit host cell DNA, RNA or protein synthesis
usually immune-mediated 2. Viral proteins may insert into the host cell’s plasma
membrane & directly damage its integrity/ promote
Mechanisms of Viral Injury cell fusion
Viruses can directly damage host cells by entering them and 3. May lyse host cells
replicating at the host’s expense 4. May manipulate programmed cell death (apoptosis)
5. Viral proteins on the surface of the host cells
Tissue tropism
recognized by the immune system will cause
- Predilection of viruses for certain cells and not others
lymphocytic attack
6. May damage cells involved in host antimicrobial
Factors that determine tissue tropism:
defense, leading to secondary infections
1. Host cell receptors for the virus (major)
7. Viral killing of one cell type may cause the death of
2. Cellular transcription factors that recognize viral
enhancer & promoter sequences other cells that depend on them
3. Anatomic barriers 8. Some can cause proliferation & transformation
4. Local temperature, pH, host defenses of cells resulting in cancer || 1st semester, AY 2011-2012

Mechanisms of Bacterial Injury Spectrum of Inflammatory Responses To Infection
1. Bacterial Virulence – depends on the ability of the 1. Suppurative Inflammation (Neutrophils)
bacteria to adhere to host cells, invade cells and - Caused by “pyogenic” bacteria, mostly
tissues, or deliver toxins extracellular gram positive cocci and
o Pathogenic bacteria have virulence genes gram-negative rods
that encode proteins that confer these - Secondary to/increased by vascular permeability
properties – grouped together in clusters and leukotaxis of neutrophils attracted by
called “pathogenicity islands” bacterial peptides, which contains N-formyl
o Increase in concentration in tissues of methionine residues
bacteria will increase virulence factors - Follows the path of acute inflammation
2. Bacterial Adherence to Host Cells  Vascular events
o Adhesins – bacterial surface molecules that  Cellular events
bind - Recruitment of leukocytes into the site of
o Fibrillae – covering the surface of Gram(+) infection
organism, S. pyogenes  composed of  Chemotaxis – emigration of
lipoteichoic acids and M protein, protein F neutrophils towards the site of
o Fimbriae or pili – filamentous proteins on inflammation
the surface of Gram (-) bacteria, tip  Chemoattractant - most common
determine exogenous agent are bacterial
3. Virulence of Intracellular Bacteria products
Facultative intracellular bacteria infect either • Peptides that contains
epithelial cells, macrophages or both N-formylmethionine terminal
- Bacteria may reproduce within the amino acid and some
phagolysomes or cytosol chemoattractant.
4. Bacterial endotoxin is a lipopolysaccharide that • Binds to specific
induces fever via host lymphokines, including tumor transmembrane G
necrosis factor and interleukin-1. protein-coupled receptor on
5. Bacterial exotoxins are composed of a binding part the surface of leukocytes.
and a catalytic part, which ADP-ribosylates and o Initiates reaction
inactivates host proteins or degrades host proteins within leukocytes
with the end result
Immune Evasion by Microbes of the leukocytes
migrating towards
Microbes avoid the host immune response by: the stimulus
 Remaining inaccessible within the lumen of the small - Leukocytes infiltration varies with the age of
intestine or rapidly entering host cells inflammatory response and the type of stimulus.
 Producing a capsule that covers antigens and  Leukocytes 6 – 24 hours. Apoptosis
prevents phagocytosis and disappear after 24 to 48 hours
 Changing their surface antigens  Neutrophils first appear because they
 Infecting lymphocytes and damaging the host are numerous in the circulation
immune system  Respond more rapidly to chemokines
 Attached more firmly to the adhesion
Special Techniques for Diagnosing Infectious Agents molecule
 Some can be directly observed in hematoxylin and - Disappear after 48 hours
eosin-stained sections - Exceptions – like pseudomonas – continuous
 Best visualized after special stains that identify recruitment of neutrophils for several days
organisms based upon particular characteristics of
their cell walls or coat. Recognition of microbes
 Cultures of lesional tissues are performed to separate  Activation of leukocytes at the site of inflammation by:
organisms and determine drug sensitivity o Recognition of the offending agents, which
delivers the signal
Gram stain Most bacteria (Gram (-); (+) o Activate the leukocytes to ingest and
Acid fast stain Mycobacteria, Nocardia destroys the offending agents
(modified) o Amplify the inflammatory reaction
Silver stains Fungi, Legionella, Pneumocystis  Receptors for microbial products –
Periodic acid-Schiff Fungi, amoebae (TLRs) Toll-like receptors
Mucicarmine/india ink Cryptococci  Response to:
Giemsa Campylobacteria, Leishmania, o Bacterial lipopolysaccharide
malaria, Herpes o Bacterial proteoglycans and lipids
Antibody probes Viruses, ricketssiae o Unmethylated CpG nucleotide
Culture All classes  G protein-coupled receptors
DNA probes Viruses, bacteria, protozoa o Found in neutrophils, macrophages and
other leukocytes
o Attracted by N-formylmethionyl || 1st semester, AY 2011-2012

o Also recognizes chemokines, C5a Characteristic nuclear changes
o Bindings of these ligands to G protein - Multinucleation
couple receptor induces migration of - Molding of nuclei
leukocytes from blood also activation of - Margination of chromatin
respiratory burst
 Receptors for opsonins- coating of microbes to target Formation of Inclusion Bodies
it for phagocytosis  Alteration of cytoskeleton organization by virus
o C3 – also potent opsonin infection
 Binds to microbes and phagocytes o Normal cells have networks of
 Expresses a receptor called Type 1 microtubules, and intermediate filaments
complement receptor (CR1) throughout the cytoplasm. Infection with
o Receptors for cytokines – leukocytes reovirus causes a perinuclear aggregation of
expresses receptors for cytokines that are microtubules, and infection with
produced in response to microbes. cytomegalovirus causes a modification of
o Interferon-γ – secreted by natural killer cells intermediate filaments proteins, including
reacting to microbes and by antigen their relocation into the nuclear and
activated T-lymphocytes during adaptive cytoplasmic inclusion bodies.
immune response
 Major macrophage-activating
 Furuncle or boils – recurrent, most frequent in moist
hairy areas

2. Mononuclear and granulomatous Inflammation

- Induced by viruses, intracellular bacteria,
spirochetes, intracellular parasites, or helminths
- Includes mostly lymphocytes or macrophages,
depending upon the characteristics of the
organism and the host plasma cells – syphilis

 Stages of Transformation: Transformation involves at

Syphillis with plasma cell infiltrates least two processes: first, the cell gains the capacity
for unlimited cell division (immortalization), and
3. Cytopathic-Cytoproliferative Inflammation second, the immortalized cells acquire additional
- characterized by virus-mediated damage to heritable genetic changes by which the cell is able to
individual host cells in the absence of host produce a tumor in an appropriate host.
inflammatory response  Mechanisms of Oncogenic Transformation: There are
- may show inclusion bodies (CMV), polykaryons, two general patterns by which cell transformation
blisters and warty changes may be accomplished: 1) the tumor virus may
- Polykaryon – cell to cell fusion. Mechanism is introduce and express a so-called transforming gene
poorly understood in the cells or 2) the tumor virus may alter the
expression and (or) coding capacity of preexisting
cellular genes. After development of a malignant
phenotype the relevant segment(s) of the viral
genome may or may not be retained in the
transformed cells, depending on the mechanism of
transformation. These mechanisms are not mutually
exclusive, and both may occur in the same cell. || 1st semester, AY 2011-2012

Common Infectious Diseases Involving Different Organs

 Furuncle
 Carbuncle
 Exanthematous diseases
 Herpes
 Tinea
Development and progression of viral cytopathology
 Leprosy (Hansen’s disease)
Human embryo skin muscle cells were infected with human
cytomegalovirus and stained at selected times to demonstrate
(A) uninfected cells, (B) late virus cytopathic effects (nuclear
 Viral and bacterial meningitis/encephalitis/
inclusions, cell enlargement), (C) cell degeneration, and (D) a
focus of infected cells in a cell monolayer (i.e., a plaque),
 Rabies
hematoxylin and eosin stain.
 Tetanus
4. Necrotizing Inflammation  Abcess
- Caused by uncontrolled viral infection (eg  Poliomyelitis
fulminant hepatitis B infection), secreted
bacterial toxins (Clostridium perfringes), or Head & Neck:
contact- mediated cytolosis of host cells by  Conjunctivitis
protozoa (E. histolytica)  Mumps
- Results in severe tissue necrosis in the absence
of inflammatory infiltrates Respiratory:
 Pneumonia
 Tuberculosis
 Diphtheria
 Bronchitis

 Viral myocarditis

 Acute gastro-enteritis
 Diarrheal diseases
o Cholera
o Viral
o E. coli
o Bacillary dysentery
 Infectious ulcerative diseases
Tissue necrosis o Typhoid fever
o TB enteritis
 Caused by toxins: o Amebiasis
 E.g , α-toxin of C. Perfringens –
o Has phospholipase C that degrades lecithin Hepato-Biliary:
 Cause myonecrosis  Hepatitis
o Has spingomyelinase – nerve sheath  Abscess
damage  Schistosomiasis
 HBV – massive apoptosis
o Cause fulminant hepatitis GUT:
 E. Histolytica – cytotoxic to epithelial cells,  UTI,
neutrophils and macrophages  STD (Gonorrhea, Chlamydia, Trichomosiasis, Syphilis,
o Adherence to target cells Tuberculosis, HIV, HPV)
o Complement mediated
5. Chronic Inflammation and Scarring  Dengue H. fever
- Caused by certain acute infections (Gonococcal  Malaria
salpingitis) or chronic infections
- May be severe despite a paucity or organisms
present (M. tuberculosis) || 1st semester, AY 2011-2012