Pharmaceutical Microbiology and Parasitology CONTENT 1

LET’S BEGIN!
UNIT 1: Introduction to Microbiology

Intended Learning Outcomes
At the end of the unit, you are expected to:
1. Identifying the events and people involved in the development
of microbiology;
2. Describe the history of microbiology; and
3. Describe the various applications of microbiology in pharmacy
practice
Introduction
It is more or less a gospel truth that in science the ultimate credit,

glory, and fame goes to the one who actually succeeds to convince the
world, and not to the one who first had conceived the original concept and
idea. Hence, in the development of microbiology the most popular and
common names are invariably of those researchers/scientists who not only
convinced the world in general, but also developed a tool or a specific
technique or an idea (concept) which was virtually adopted or who
expatiated their observations/findings rather vividly or astronomically that
the science grew and prospered in particular.
Unlocking of Difficulties
To attend the following intended learning outcomes for the first

lesson of the course, you need to fully understand the following essential
knowledge that will be laid down in the succeeding pages. Please note that
you are not limited to exclusively refer to these resources. Thus, you are
expected to utilize other books, research articles and other resources such
as e-journals and various pharmacy mobile applications.
Key Terms:
 MICROBIOLOGY – the study of microbes
 MICROSCOPE – an optical instrument that permits one to observe a
small object by producing an enlarged image of the object.
 MICROSCOPIC- it is used to describe a very small object that can only
be seen using a microscope.
 MICROORGANISMS – it refers to a very small organisms that are
microscopic.
1
Lecture Notes
Did you know that there are people in the past which led to the
development of microbiology?
Let`s find out
key events and contribution of
important historical personalities in microbiology with the development of
current medical practice and application
.
The Microscope
The evolution of microscope gathered momentum in the year 1674, when a
Dutch cloth merchant Anton van Leeuwenhoek first of all had a glimpse at a
drop of lake-water via a lens made of glass that he had ground himself.
Through this simple device using a magnifying lens Leeuwenhoek first and
foremost ever had an ‘amazing sight’ of the most fascinating world of the
microbes.
Figure 1: Anton Van Leeuwenhoek & his 1st observation on microbes

(From: https://www.famousscientists.org/antonie-van-leeuw)
The earlier observations of microorganisms were made duly by several
researchers chronologically as given below:
Roger Bacon (1220–1292): first ever postulated that a disease is caused by
invisible living creatures.
Girolamo Fracastoro (1483–1553) and Anton von Plenciz (1762): these two
reseachers also made similar observations, assertions, and suggestions but
without any experimental concrete evidences/ proofs.
Athanasius Kircher (1601–1680): made reference of these ‘worms’ that are
practically invisible to the naked eyes and found in decaying meat, milk,
bodies, and diarrheal secretions. Kircher was, in fact, the pioneer in
pronouncing the cognizance and significance of bacteria and other
microbes in disease(s).
Anton van Leeuwenhoek (1632–1723): initiated the herculian task of
‘microscope making’ through his inherent hobby of ‘lens making’.
2
Figure 2: Leeuwenhoek`s 1st Microscope
(https://www.researchgate.net/figure/Original-Antonie-van-
LeeuwenhoekMicroscope-property-of-the-Utrecht-
Universitymuseum_fig39_254858295)
Spontaneous Generation vs. Biogenesis
SPONTANEOUS GENERATION – the idea that life can arise spontaneously
from nonliving material and also known as abiogenesis.
BIOGENESIS – life can only arise from preexisting life.
John Needham (1713-1781): Precisely in the year 1749, while
experimenting with raw meat being exposed to hot ashes, he observed
meticulously the appearance of organisms that were not present at the
initial stages; and, therefore, inferred that the bacteria virtually originated
from the raw meat itself.
Figure 3: Needham`s Experiment

(https://microbenotes.com/experiments-in-support-and-
againstspontaneous-generation)
Lazaro Spallanzani (1729-1799): actually boiled ‘beef broth’ for a duration
of 60 minutes, and subsequently sealed the flasks tightly. After usual
incubation for a certain length of time, practically no microbes appeared.
However, Needham never got convinced with Spallanzani’s findings, and
vehemently insisted that ‘air’ happened to be an essential component to
the process of spontaneous generation of the microbes, and that it had
been adequately excluded from the flasks by sealing them precisely by the
later.
3
Figure 4: Spallanzani`s Experiment
(https://sites.google.com/site/pl99323/genetics1/spallanzani)
Franz Schulze (1815-1873) and Theodor Schwann (1810–1882): these two
scientists independently fully endorsed and justified the earlier findings of
Spallanzani by allowing air to pass through strong acid solutions into the
boiled infusions, and by passing air into the flasks via red-hot tubes
respectively. In neither instance did microorganisms appear.
H. Schröder and T. von Dusch (1850): carried out a more logical and
convincing experimental design by passing air via cotton fibers so as to
prevent the bacterial growth; and thus, it ultimately initiated and gave rise
to a basic technique of ‘plugging’ bacterial culture tubes with ‘cotton plugs’
(stoppers), which technique being used still as to date.
Figure 5: Schröder & Dusch Experiment

(http://bpharmmicrobiologynotes.blogspot.com/2018/01/1220-
1292roger-bacon-postulated.html)
Felix Archimede Pouchet (1800–1872): revived once again the concept and
ideology of spontaneous generation via a published comprehensive and
extensive research article thereby proving its occurrence.
Pasteur (1822–1895) carried out a number of experiments that virtually
helped in concluding the on-going argument once for all time. Pasteur
designed a flask having a long and narrow gooseneck outlet. Thus, the
nutrient broths were duly heated in the above specially–designed flask,
whereby the air — untreated and unfiltered — may pass in or out but the
germs settled in the ‘very gooseneck’ ; and, therefore, practically no
microbes ultimately appeared in the nutrient broth (solution).
4
Figure 6: Pasteur`s Experiment on Spontaneous Generation
(https://www.pinterest.ph/pin/10625749100522034/)
John Tyndall (1820-1893): conducted finally various well planned
experiments in a specifically designed box to establish and prove the fact
that ‘dust’ actually contained and carried the ‘microbes’ (i.e., germs). He
subsequently demonstrated beyond any reasonable doubt that in a
particular situation whereby absolutely no dust was present, the sterile
nutrient broth could remain free of any sort of microbial growth for an
indefinite length of time.
Fermentation
- An anaerobic biochemical pathway in which substances are broken
down and energy and reduced compounds are produced; oxygen does
not participate in the process.
- It is also a process of growing microorganisms (microbes) to produce
various chemicals or pharmaceutical compounds.
Figure 7: Fermentation process

(https://ragingalcoholic.com/alcohol-fermentation/)
The Germ Theory
Germ theory, in medicine, the theory that certain diseases are caused by
the invasion of the body by microorganisms, organisms too small to be
seen except through a microscope.
Later on various other scientists supported and proved the aforesaid ‘germ
theory’ in one way or the other as stated under:
Girolamo Fracastro (1483–1553): advocated that certain diseases might be
caused by virtue of invisible organisms transmitted from one subject to
another.
Plenciz (1762): stated that the living microbes (or agents) are the ultimate
cause of disease but at the same time aired his views that different germs
were responsible for different ailments.
5
Oliver Wendell Holmes (1809–1894): suggested that puerperal fever** was
highly contagious in nature; besides, it was perhaps caused by a germ
carried eventually from one mother to another either by midwives or
physicians.
Ignaz Philipp Semmelweis (1818–1865): pioneered the usage of antiseptics
specifically in the obstetrical practices.
Joseph Lister (1890) made known in England the importance of antisepsis,
which was subsequently fully appreciated by the medical profession.
Robert Koch (1843–1910): discovered the typical bacilli having squarish
ends in the blood sample of cattle that had died due to anthrax.
Figure 8: Bacillus anthracis shape

(http://textbookofbacteriology.net/Anthrax.html)
Contributors of Medical Microbiology
Edwin Klebs (1883) and Frederick Loeffler (1884): discovered the
diphtheria bacillus, Corynebacterium diphtheriae; and showed that it
produced its toxins (poisons) in a laboratory flask.
Figure 9: Corynebacterium diphtheria

(http://textbookofbacteriology.net/diphtheria.html)
Emil von Behring and Shibasaburo Kitasato: devised an unique technique
of producing immunity to infections caused by C. diphtheriae by injecting
the toxins into healthy animals so that an antitoxin**** gets developed.
-They also cultivated (grown) the microorganism responsible for causing
tetanus (lockjaw), Clostridium tetani; and Behring prepared the
corresponding antitoxin for the control, prevention, treatment, and
management of this fatal disease.
6
Figure 10: Clostridium tetani
(https://microbeonline.com/clostridium-tetani-properties-
pathogenesisdiagnosis/)
De Salmon and Theobald Smith: proved amply that immunity to a plethora
of infectious diseases may be produced quite effectively and efficiently by
proper timely inoculation with the killed cultures of the corresponding
microorganisms.
Elie Metchnikoff: described for the first time the manner certain specific
leukocytes (i.e., white blood cells) were able to ingest (eat up) the
diseaseproducing microorganisms present in the body. He baptized these
highly specific defenders and crusaders against bacterial infections known
as phagocytes (‘eating cells’), and the phenomenon is termed as
phagocytosis.
Figure 11: Leukocytes

(https://socratic.org/questions/what-is-the-difference-between-
aleukocyte-and-a-lymphocyte)
Metchnikoff’s Theory: Based of the aforesaid explanations Metchnikoff put
forward a theory that — ‘the phagocytes were the body’s first and most
important line of defense against a variety of infection’.
Figure 12: Phagocytosis

(https://www.tempobioscience.com/blog/?p=699)
Paul Ehrlich: (Robert Koch’s brilliant student) describe the concept of the
following:
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(a) Antibody: The logical explanation of immunity based upon certain
antibodies in the blood, and
(b) Chemotherapy and Antibiotics: Both these aspects virtually opened the
flood gates to the enormous future developments in combating the
growth and destruction of pathogenic bacteria.
Figure 13: Antibodies

(https://www.sciencenewsforstudents.org/article/what-are-
antibodiesexplainer)
Example: Arsphenamine (Salvarsan®): A light yellow organo-metallic
compound (powder) containing about 30% Arsenic (As), was formerly used
in the treatment of syphilis. The two decades stretching from 1880–1900
proved to be indeed a golden era for the ‘science of microbiology’ to step
into adolescence from the stage of infancy.
Figure 14: Salvarsan

(https://wellcomecollection.org/works/dpmpdvds)
Focus Questions
Guide questions for Unit 1 discussions:

1. What is the significance of microscope in the development of
microbiology?
2. What is there a need to study microbiology in the field of pharmacy?
Related Readings
To appreciate and further understand the above discussion, kindly read the
research article on “Technological Microbiology: Development and
Applications” by Vitorino & Bessa (2017) through
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423913/
8
Learning Assessment
Learning assessment will be served as your assignment and quiz and will be
given via Schoology at the end of the week after our virtual consultation.
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UNIT 2: Prokaryotes and Eukaryotes

1. Differentiate prokaryotic from eukaryotic cells;
2. Describe the cell structures & characteristics of pathogenic
and non-pathogenic microorganisms; and
3. Describe the characteristics of cellular and Acellular
microorganisms.
Introduction
Microorganisms or microbes are microscopic organisms that exist as

unicellular, multicellular, or cell clusters. Microorganisms are widespread in
nature and are beneficial to life, but some can cause serious harm. They can
be divided into six major types: bacteria, archaea, fungi, protozoa, algae,
and viruses.
To attend the following intended learning outcomes, the lesson of

the course, you need to fully understand the following essential knowledge
that will be laid down in the succeeding pages. Please note that you are not
limited to exclusively refer to these resources. Thus, you are expected to
utilize other books, research articles and other resources such as e-journals
and various pharmacy mobile applications.
Key Terms:
 CELLS – smallest unit of living structure capable of independent
existence.
 CELLULAR MICROBES – also called microorganisms and can be
either unicellular or multicellular and divided into two broad
categories, based on their cell type: prokaryotic or eukaryotic.
 ACELLULAR MICROBES – also called infectious particles that is
not composed of cells.
9
Lecture Notes
Can you determine ifcertain

a microorganism is prokaryotic or
eukaryotic? Let`s find out their characteristics and features.
Table 1: DISTINGUISHING FEATURES OF PROKARYOTES & EUKARYOTES

CHARACTERISTIC EUKARYOTES PROKARYOTES
SIZE Normally >10µm Typically 1-5 µm
LOCATION OF Within a true nucleus In the cytoplasm,
CHROMOSOMES separated from the usually attached to
cytoplasm by a nuclear the cell membrane
membrane
NUCLEAR DIVISION Exhibit mitosis & meiosis Mitosis & meiosis are
absent
NUCLEOLUS Present Absent
REPRODUCTION Asexual or sexual Normally asexual
reproduction reproduction
CHROMOSOME No. >1 1
MITOCHONDRIA & May be present Absent
CHLOROPLASTS
CELL MEMBRANE Sterols present Sterols absent
COMPOSITION
CELL WALL Cell Walls (When Walls usually contain
COMPOSITION present) usually contain peptidoglycan
cellulose or chitin but not
peptidoglycan
RIBOSOMES Cytoplasmic ribosomes Ribosomes are usually
are 80S 70S
FLAGELLA Structurally complex Structurally simple
PILI Absent Present
FIMBRIAE Cilia Present
STORAGE Poly-β-hydroxybutyrate Poly-
COMPOUNDS absent βhydroxybutyrate
often present
10
Figure 1: Acellular & Cellular Microorganism
(Mosley, 2020)
EUKARYOTIC CELL STRUCTURE:
Figure 2: Eukaryotic Cell structure

(https://biologydictionary.net/eukaryotic-cell/)
• Cell Membrane
- referred to as the plasma, cytoplasmic or cellular membrane.
- composed of large molecules of proteins and phospholipids.
- It regulates the passage of nutrients, waste products and
secretions into and out of the cell (Selective permeability).
• Nucleus
- controls the functions of the entire cell and can be thought of as
the “commander center” of the cell.
- It has three components:
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1. Nucleoplasm - the gelatinous matrix or base material of the
nucleus.
2. Chromosomes - are embedded or suspended in the
nucleoplasm.
3. Nuclear membrane - serves as the “skin” around the nucleus
that contains holes through which large molecules can enter
and exit the nucleus.
• Eukaryotic chromosomes consists of linear DNA molecules and
proteins.
• Genes
 are located along the DNA molecules  described as “beads on
the string”.
 Each gene contains the genetic information that enables the cell
to produce one or more gene products.
 Most gene products are proteins but some genes code for the
production of two types of RNA: (1) ribosomal ribonucleic acid
(rRNA) & (2) transfer ribonucleic acid (tRNA).
• Cytoplasm
- a semifluid, gelatinous, nutrient matrix,
- Inside the cytoplasm is where the insoluble storage granules &
various type cytoplasmic organelles such as ER, ribosomes,
mitochondria & other membrane bound vacuoles.
- It is where most of the cell`s metabolic reactions occur. - the
semifluid portion of cytoplasm is called cytosol.
• Endoplasmic Reticulum (ER)
- is a highly convoluted system of membranes that are
interconnected and arranged to form a transport network of
tubules and flattened sacs within cytoplasm.
a.) Rough ER
 the rough appearance is caused by the many ribosomes
attached to the outer surface of the membranes. 
synthesis, secretion or storage of proteins.
b.) Smooth ER
 ER to which ribosomes are not attached is called Smooth
ER.
 makes lipids and modifies the structure of some
carbohydrates
12
Figure 3: Endoplasmic Reticulum
(Davidson, 2015)
• Ribosomes
 Contain mainly of rRNA & play an important role in protein
synthesis.
 Cluster of ribosomes are called polyribosomes & polysomes.
 Each eukaryotic ribosomes is composed of 2 subunits- a large
subunit (60S) and a small subunit (40S) that are produce in the
nucleus.
 The subunits are then transported to the cytoplasm where
they remain separate until such time as they join together with
an mRNA molecule to initiate protein synthesis.
• Golgi Complex
 Also known as Golgi apparatus or Golgi body which connects or
communicates with the ER.
 It completes the transformation of newly synthesized proteins
into mature, functional ones, and packages them into small,
membrane-enclosed vesicles for storage within the cell or
export outside the cell.
• Lysosomes
 Small vesicles that originate at the Golgi complex.
 They contain lysozyme & other digestive enzymes that break
down foreign material taken into the cell by phagocytosis.
 These enzymes also aid in breaking down worn out parts of the
cell and may destroy the entire cell by a process called
autolysis.  Peroxisomes
 Are membrane-bound vesicles in which hydrogen peroxide is
both generated and broken down.
 It contains the enzyme catalase, which catalyzes the
breakdown of hydrogen peroxide into water and oxygen.
• Mitochondria
 powerhouse of the cell
 energy is released from organic molecules by the process of
cellular respiration
 convert stored energy into energy to power the cell (ATP)
• Plastids
13
 Are membrane–bound structures containing various
photosynthetic pigments, they are site of photosynthesis.
• Cytoskeleton
 It contains three types of cytoskeletal fibers are microtubules,
microfilaments, and intermediate filaments.
 It serves to strengthen, support & stiffen the cell, and give the
cell its shape.
• Cell Wall
 Provides rigidity, shape and protection
 Cell wall of algae contains polysaccharide called “cellulose”
(which are not found in cell wall of any microorganisms)
 Cell wall of fungi contains polysaccharide called “Chitin”
• Flagella
 Organelles for locomotion
 Flagellated protozoa are called flagellates
 The whipping motion of the flagella enables flagellated cells to
swim through liquid environments.
• Cilia
 Also an organelles for locomotion, but tend to be shorter
(more hair-like), thinner, & more numerous than flagella.
 Unlike flagella, it tend to beat with a coordinated, rhythmic
movement.
PROKARYOTIC CELL STRUCTURE

• Cell Membrane
 Enclosing the cytoplasm of a prokaryotic cell is the cell
membrane which has similar structure & function to the
eukaryotic cell membrane.
 Inward foldings of the cell membranes is called “Mesosomes”
where cellular respiration takes place in bacteria.
Figure 4: Prokaryotic Cell

(https://courses.lumenlearning.com/microbiology/chapter/
uniquecharacteristics-of-prokaryotic-cells/)
14
• Chromosome
 Prokaryotic chromosome usually consists of a single, long
supercoiled, circular DNA molecule which serves as the control
center of bacterial cell.
 Capable of duplicating itself, guiding cell division & directing
cellular activities.
• Cytoplasm
 The semiliquid cytoplasm of prokaryotic cells consists of water,
enzymes, dissolved oxygen, waste products, essential
nutrients, proteins & subunits.
 Cytoplasmic granules may contain starch, lipids, sulfur, iron, or
other stored substances.
• Bacterial Cell Wall
 Rigid exterior cell wall that defines the shape of bacterial cells.
 The main constituent of most bacterial cell walls is a complex
polymer known as “Peptidoglycan”.
 Gram (+) bacteria have a thick layer of peptidoglycan
combined with teichoic acid & lipoteichoic acid
 Gram (-) bacteria have thin layered of peptidoglycan covered
with a complex layer of lipid macromolecules.
 Some bacteria lose their ability to produce cell walls,
transforming into tiny variants of the same species , referred to
as L-form or Cell wall-deficient (CWD) bacteria.
• Glycocalyx
 Slimy, gelatinous material produced by the cell membrane &
secreted outside of the cell wall.
Figure 5: Peptidoglycan Structure of Gram (+) & Gram (-) bacteria

(https://www.sigmaaldrich.com/technical-
documents/articles/biology/glycobiology/peptidoglycans.html)
2 Types of Glycocalyx:
15
1. “Slime layer” which is not highly organized & not firmly
attached to the cell wall. Slime layers enable certain
bacteria to glide or slide along the solid surfaces & seem
to protect bacteria from antibiotics & desiccation such
as the genus Pseudomonas.
2. “Capsule” is highly organized & firmly attached to the
cell wall which is useful in differentiating among
different types of bacteria within a particular species.
Encapsulated bacteria produce colonies on nutrient agar
that are smooth, mucoid & glistening referred to as
“S-colonies” and Non-encapsulated bacteria tend to
grow as dry, rough, colonies called “R-colonies”.
• Flagella
 Are thread-like, protein appendages that enable bacteria to
move.
 Flagellated bacteria are said to be motile and nonflagellated
bacteria are nonmotile.
 Types of flagella:
 Peritrichous bacteria- bacteria possessing flagella over
the entire surface.
 Lophotrichous bacteria- bacteria with a tuft of flagella at
one end
 Amphitrichous bacteria- those having one or more
flagella at each end.
 Monotrichous bacteria- possessing a single polar
flagellum.
• Pili
 Also known as fimbriae, are hair-like structures often observed
on gram negative bacteria
 Composed of polymerized protein molecules called pilin.
 It enable bacteria to anchor themselves to surfaces.
• Spores
 Few genera of bacteria such as Bacillus and Clostridium are
capable of forming spores as a means of survival when their
moisture or nutrient is low.
 Bacterial spores are referred to as endospores and the process
which they are form is called sporulation.
16
Figure 6: Bacterial Cell Anatomy
(https://microbiologynotes.com/differences-between-flagellaand-
pili/)
CELLULAR MICROBES
Eukaryotes:
Algae
Algae, also called cyanobacteria or blue-green algae, are unicellular or
multicellular eukaryotes that obtain nourishment by photosynthesis.
They live in water, damp soil, and rocks and produce oxygen and
carbohydrates used by other organisms. It is believed that cyanobacteria
are the origins of green land plants.
Figure 7: Algae
(https://asa.com/news/2019/03/11/could-algae-save-the-world/)
Protozoa
 Protozoa are unicellular aerobic eukaryotes.
 They have a nucleus, complex organelles, and obtain
nourishment by absorption or ingestion through specialized
structures.
 They make up the largest group of organisms in the world in
terms of numbers, biomass, and diversity.
 Their cell walls are made up of cellulose.
 Protozoa have been traditionally divided based on their mode of
locomotion:
 flagellates produce their own food and use their whip-like
structure to propel forward,
 ciliates have tiny hair that beat to produce movement,
 amoeboids have false feet or pseudopodia used for feeding and
locomotion, and
 sporozoans are non-motile.
 They also have different means of nutrition, which groups them
as autotrophs or heterotrophs.
17
Figure 8: Protozoa
(https://microbiologysociety.org/why-microbiology-matters/what-
ismicrobiology/protozoa.html)
Fungi
 Fungi (mushroom, molds, and yeasts) are eukaryotic cells (with a
true nucleus).
 Most fungi are multicellular and their cell wall is composed of
chitin.
 They obtain nutrients by absorbing organic material from their
environment (decomposers), through symbiotic relationships
with plants (symbionts), or harmful relationships with a host
(parasites).
 They form characteristic filamentous tubes called hyphae that
help absorb material.
 The collection of hyphae is called mycelium. Fungi reproduce by
releasing spores.
Figure 9: Fungi
(https://www.nature.scot/plants-animals-and-fungi/fungi)
Prokaryotes:
Archaea or Archaebacteria:
 differ from true bacteria in their cell wall structure and lack
peptidoglycans.
 They are prokaryotic cells with avidity to extreme environmental
conditions. Based on their habitat,
 all Archaeans can be divided into the following groups:
 methanogens (methane-producing organisms),
 halophiles (archaeans that live in salty environments),
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 thermophiles (archaeans that live at extremely hot
temperatures),  and psychrophiles (cold-temperature
Archaeans).
 Archaeans use different energy sources like hydrogen gas, carbon
dioxide, and sulphur.
 Some of them use sunlight to make energy, but not the same way
plants do.
 They absorb sunlight using their membrane
pigment, bacteriorhodopsin.
 This reacts with light, leading to the formation of the energy
molecule adenosine triphosphate (ATP).
Figure 10: Archaea

(Amazon, 2020)
ACELLULAR MICROBES
Viruses
 Viruses are noncellular entities that consist of a nucleic acid core
(DNA or RNA) surrounded by a protein coat. Although viruses are
classified as microorganisms, they are not considered living
organisms. Viruses cannot reproduce outside a host cell and
cannot metabolize on their own. Viruses often infest prokaryotic
and eukaryotic cells causing diseases.
Figure 11: Virus

(https://www.nationalgeographic.org/encyclopedia/viruses/)
Prions
 Prions are infectious agents that appear to behave like other
infectious organisms, yet they lack any of the most fundamental
features of organisms.
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 They lack any genetic material (DNA or RNA).
 A prion is a type of protein that can trigger normal proteins in the
brain to fold abnormally.
 Prion diseases can affect both humans and animals and are
sometimes spread to humans by infected meat products.
 The most common form of prion disease that affects humans is
Creutzfeldt-Jakob disease (CJD).
Figure 12: Prions

(https://www.mcgill.ca/oss/article/health-you-asked/what-are-prions)
Focus Questions

1. What are the unique characteristics of acellular and cellular microbes?
2. What are the significance of microorganisms in our ecosystem?
Related Readings
In order to appreciate and further understand the above discussion, kindly

read the article “Pathogenic and Non-Pathogenic Microorganisms in the
Rapid Alert System for Food and Feed” by Marcin Pigłowski (2019) through
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6388125/.
Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT II - - - - - - - - - - - - - - - - - - -
UNIT 3: Microbial Growth and Metabolism

1. Describe the process of microbial growth and metabolism; and
2. Determine the growth requirements of microorganisms.
20
Introduction
Microbial metabolism is the means by which a microbe obtains the

energy and nutrients (e.g. carbon) it needs to live and reproduce. Microbes
use many different types of metabolic strategies and species can often be
differentiated from each other based on metabolic characteristics.
To attend the following intended learning outcomes the lesson of the

course, you need to fully understand the following essential knowledge that
will be laid down in the succeeding pages. Please note that you are not
Key Terms:
 NUTRIENTS- refers to the various chemical compounds that
organisms including microorganisms use to sustain life.
 METABOLISM – refers to all the chemical reactions that occur
within any cell.
 CATABOLISM – involves breaking of chemical bonds and the
release of energy
 ANABOLISM – involves the formation of bonds which require
energy.
Lecture Notes
Did you know that microorganisms also need nutrients to sustain

their life? Let`s find out their growth and metabolism.
BACTERIAL METABOLISM
 Metabolism refers to all the biochemical reactions that occur in a cell
or organism.
 The study of bacterial metabolism focuses on the chemical diversity
of substrate oxidations and dissimilation reactions (reactions by
which substrate molecules are broken down), which normally
function in bacteria to generate energy
• Heterotrophic Metabolism
 Heterotrophic metabolism is the biologic oxidation of organic
compounds, such as glucose, to yield ATP and simpler organic (or
inorganic) compounds, which are needed by the bacterial cell for
biosynthetic or assimilatory reactions.
• Respiration
21
 Respiration is a type of heterotrophic metabolism that uses
oxygen and in which 38 moles of ATP are derived from the
oxidation of 1 mole of glucose, yielding 380,000 cal. (An additional
308,000 cal is lost as heat.)
• Fermentation
 In fermentation, another type of heterotrophic metabolism, an
organic compound rather than oxygen is the terminal electron (or
hydrogen) acceptor. Less energy is generated from this
incomplete form of glucose oxidation, but the process supports
anaerobic growth.
• Krebs Cycle
 The Krebs cycle is the oxidative process in respiration by which
pyruvate (via acetyl coenzyme A) is completely decarboxylated to
CO2. The pathway yields 15 moles of ATP (150,000 calories).
• Glyoxylate Cycle
 The glyoxylate cycle, which occurs in some bacteria, is a
modification of the Krebs cycle. Acetyl coenzyme A is generated
directly from oxidation of fatty acids or other lipid compounds.
• Electron Transport and Oxidative Phosphorylation
 In the final stage of respiration, ATP is formed through a series of
electron transfer reactions within the cytoplasmic membrane that
drive the oxidative phosphorylation of ADP to ATP. Bacteria use
various flavins, cytochrome, and non-heme iron components as
well as multiple cytochrome oxidases for this process.
• Mitchell or Proton Extrusion Hypothesis
 The Mitchell hypothesis explains the energy conservation in all
cells on the basis of the selective extrusion of H+ ions across a
protonimpermeable membrane, which generates a proton motive
force. This energy allows for ATP synthesis both in respiration and
photosynthesis.
• Bacterial Photosynthesis
 Bacterial photosynthesis is a light-dependent, anaerobic mode of
metabolism. Carbon dioxide is reduced to glucose, which is used
for both biosynthesis and energy production. Depending on the
hydrogen source used to reduce CO2, both photolithotrophic and
photoorganotrophic reactions exist in bacteria.
• Autotrophy
 Autotrophy is a unique form of metabolism found only in bacteria.
Inorganic compounds are oxidized directly (without using
sunlight) to yield energy (e.g., NH 3, NO2–, S2, and Fe2+). This
metabolic mode also requires energy for CO 2 reduction, like
photosynthesis, but no lipid-mediated processes are involved.
22
This metabolic mode has also been called chemotrophy,
chemoautotrophy, or chemolithotrophy.
• Anaerobic Respiration
 Anaerobic respiration is another heterotrophic mode of
metabolism in which a specific compound other than O2 serves as
a terminal electron acceptor. Such acceptor compounds include
NO3–, SO42–, fumarate, and even CO2 for methane-producing
bacteria.
• The Nitrogen Cycle
 The nitrogen cycle consists of a recycling process by which
organic and inorganic nitrogen compounds are used
metabolically and recycled among bacteria, plants, and
animals. Important processes, including ammonification,
mineralization, nitrification, denitrification, and nitrogen
fixation, are carried out primarily by bacteria.
MICROBIAL GROWTH
Microbial Growth:
 Refers to an increase in cell number, not in cell size.
 Bacteria grow and divide by binary fission, a rapid and
relatively simple process
THE POPULATION GROWTH CURVE:

In a closed growth system, a bacterial population usually exhibits a
predictable pattern of growth - its growth curve - that follows several
stages or phases:
1. The lag phase
 During the lag phase growth is relatively flat and the population
appears either not to be growing or growing quite slowly During this
phase the newly inoculated cells are adapting to their new
environment and synthesizing the molecules they will need in order
to grow rapidly.
2. The exponential growth phase (also called the logarithmic or log phase)
 This is the phase where the population increases geometrically as
long as there is sufficient food and space for growth.
3. The stationary growth phase

 Here the population grows slowly or stops growing because of
decreasing food, increasing waste, and lack of space. The rate of
replication is balanced out by the rate of inhibition or death.
4. The decline or death phase

 Here the population dies exponentially from the accumulation of
waste products. Although the rate of death depends on the degree of
23
toxicity and the resistance of the species and viable cells may remain
for weeks to months.
Figure 1: Logarithmic growth of bacteria

(https://www.researchgate.net/figure/A-typical-bacterial-growth-
curveconsisting-of-lag-phase-exponential-or-log-phase_fig3_327558675)
REQUIREMENTS FOR GROWTH
Physical Requirements:
1. Temperature:
Microbes are loosely classified into several groups based on their
preferred temperature ranges.
A. Psychrophiles: “Cold-loving”. Can grow at 0oC.
Two groups:
 True Psychrophiles: Sensitive to temperatures over 20oC.
Optimum growth at 15oC or below. Found in very cold
environments (North pole, ocean depths). Seldom cause
disease or food spoilage.
 Psychrotrophs: Optimum growth at 20 to 30oC. Responsible for
most low temperature food spoilage.
B. Mesophiles: “Middle loving”. Most bacteria.

 Include most pathogens and common spoilage organisms.
 Optimum temperature commonly 37oC.
 Many have adapted to live in the bodies of animals.
C. Thermophiles: “Heat loving”.

 Optimum growth between 50 to 60oC.
 Many cannot grow below 45oC.
 Adapted to live in sunlit soil, compost piles, and hot springs
2. pH:
 Most bacteria prefer neutral pH (6.5-7.5). 
Molds and yeast grow in wider pH range, but
 prefer pH between 5 and 6.
24
 Acidity inhibits most microbial growth and is
used frequently for food preservation (e.g.:
pickling).
Organisms can be classified as:

A. Acidophiles: “Acid loving”.
 Grow at very low pH (0.1 to 5.4)
 Lactobacillus produces lactic acid, tolerates mild acidity.
B. Neutrophiles:
 Grow at pH 5.4 to 8.5.
 Includes most human pathogens.
C. Alkaliphiles: “Alkali loving”.

 Grow at alkaline or high pH (7 to 12 or higher)  Vibrio cholerae
and Alkaligenes faecalis optimal pH 9
3. Osmotic Pressure:
Cells are 80 to 90% water.
A. Hypertonic solutions:
 High osmotic pressure
 removes water from cell, causing shrinkage of cell 
membrane (plasmolysis).
 Used to control spoilage and microbial growth.
B. Hypotonic solutions:
 Low osmotic pressure causes water to enter the cell. cell wall
 Cell wall prevents excessive entry of water. Microbe may
 lyse or burst if cell wall is weak.
Focus Questions

1. What are the significance of metabolism to microorganism?
2. What are the factors that affects the growth of microorganisms?
Related Readings

read the article “Predicting Microbial Growth in a Mixed Culture From
Growth Curve Data” by Ram et al., (2019) through
https://www.pnas.org/content/116/29/14698.
25
Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT III - - - - - - - - - - - - - - - - - - -
UNIT 4: Microbial Control

1. Describe the basic concept of microbial
control;
2. Determine the Physical methods of microbial control; and
3. Determine the Chemical methods of microbial control.
Introduction
In certain environments, it is necessary to control the growth of

microbes especially in hospitals, nursing homes and other healthcare
institutions to avoid the risk of transmission of diseases cause by microbes.
Moreover, Kaiser (2020) stated that control of microorganisms is essential
in order to prevent the transmission of diseases and infection, stop
decomposition and spoilage, and prevent unwanted microbial
contamination. Microorganisms are controlled by means of physical agents
and chemical agents.
This unit will focus on the concepts of microbial control which

includes the physical and chemical methods of controlling the growth of
microorganism.

Key Terms:
 STERILIZATION – the process of destroying all living organisms and
viruses. A sterile object is one free of all life forms, including bacterial
endospores, as well as viruses.
26
 DECONTAMINATION – is the treatment of an object or inanimate
surface to make it safe to handle.
 DISINFECTANT – agents used to disinfect inanimate objects but
generally to toxic to use on human tissues.
 ANTISEPTIC – agents that kills or inhibits growth of microbes but is
safe to use on human tissue.
Lecture Notes
Did you know that there are methods or ways on how to control
microbial growth? Let`s find out the efficiency of these methods in
controlling microbial growth.
I. INHIBITING THE GROWTH OF MICROBES

 STERILIZATION
 Involves the destruction or elimination of all microbes
including cells, spores and viruses.
 In healthcare facilities, sterilization of objects can be
accomplished by physical or chemical methods.
 DISINFECTION
 Describes the elimination of most or all pathogens (except
bacterial spores) from nonliving objects.
 In healthcare settings, objects usually are disinfected by liquid
chemicals or wet pasteurization.
 Pasteurization- methods of disinfecting liquids.
 DISINFECTANTS
 Chemicals used to disinfect inanimate objects, such as bedside
equipment and operating rooms.
 Do not kill bacterial spores
 Not used on living tissue because they are strong chemical
substances
 ANTISEPTIC
 are solutions used to disinfect skin and other living tissues.
 SANITATION
 The reduction of microbial populations to levels considered safe by
public health standards.
II. MICROBICIDAL AGENTS

 The suffix –cide or –cidal refers to “Killing”
27
 General terms such as Germicidal agents (Germicides), Biocidal
agents(Biocides), and Microbicidal agents (Microbicides)
 Bactericidal agents (Bactericides) specifically kill bacteria, but not
necessarily bacterial endospores.
 Sporicidal agents are required to kill bacterial endospores.
 Fungicidal agents (fungicide) kills fungi including fungal spores.
 Algicidal agents (algicides) used to kill algae in swimming pools and
hot tubs.
 Viricidal agents destroy viruses
III. MICROBISTATIC AGENTS

 Microbistatic agents is a drug or chemical that inhibits reproduction
of microorganisms, but does not necessarily kill them.
 Bacteriostatic agents is one that specifically inhibits the metabolism
and reproduction of bacteria.
 Freeze-drying (Lyophilization) and Rapid Freezing (using liquid
nitrogen) are microbistatic techniques to preserve microbes for
future study.
 Lyophilization is a process that combines dehydration (drying) and
freezing.
 Lyophilized materials are frozen in a vacuum, the container is then
sealed to maintain the inactive state.
 Freeze drying is widely used in industry to preserve foods, antibiotics,
antisera, microorganisms and other biological materials.
IV. ASEPTIC AND ASEPSIS TECHNIQUE

 Sepsis refers to the presence of pathogens in blood or tissues 
Asepsis refers to the absence of pathogens.
 Aseptic techniques are used to eliminate and exclude pathogens.
It includes sterilization of surgical equipment and hand hygiene,
use of sterile gloves, masks (PPE)
 Antisepsis is the prevention of infection
 Antiseptic technique develop by Joseph Lister, refers to the use of
antiseptic such as carbolic acid (phenol) to cleanse surgical
wounds and equipment.
V. USING PHYSICAL METHODS TO INHIBIT MICROBIAL GROWTH

1. HEAT
 The most practical, efficient and inexpensive method of
sterilization of those inanimate objects and materials that can
withstand high temperatures.
 Temperature & Time  to factors that determine the
effectiveness of heat for sterilization.
28
 The higher the temperature, shorter the time required to kill
microorganism.
 Thermal Death Point (TDP) the lowest temperature that will kill
specified period.
 Thermal Death Time (TDT)  the length of time necessary to
sterilize a pure culture at a specified temperature.
 Dry Heat  Baking in a thermostatically controlled oven provides
effective sterilization of metals, glassware, powders, oils & waxes.
(1600C o 1650C) for 2 hours or (1700C to 1800C) to for 1 hour.
 Incineration is an effective means of destroying contaminated
disposable materials.
 Moist Heat – heat applied in the presence of moisture, as in
boiling or streaming, is faster and more effective than dry heat.
 AUTOCLAVE is like a large metal pressure cooker that uses steam
under pressure to completely destroy all microbial life.
Autoclaving at a pressure of 15psi, at a temperature of 121.50C.
2. COLD
 Most microorganisms are not killed by cold temperatures but their
metabolic activities are slowed and inhibit their growth.
 Slow freezing cause ice crystals to form within cells and may rupture
the cell membranes and cell walls of some bacteria.
 Rapid Freezing, using liquid nitrogen is a good way to preserve foods,
biologic specimens and bacterial cultures.
 Note: Refreezing of thawed foods is unsafe practice (if the endospore
of Clostridium botulinum or Clostridium perfringes were present-
food poisoning)
3. RADIATION
 UV lamp (germicidal lamp) is useful for reducing number of
microorganisms in the air. It contains low pressure mercury vapor
tube.
 UV radiation that has a wavelength of 260nm causes thymidine
dimers resulting in the inability of bacterial DNA to be replicated.
(Generally bactericidal but not sporicidal)
 Ionizing radiation of 1nm or less (gamma ray) causes free radical
formation that damage proteins, DNA & lipids (Both Bactericidal and
sporicidal).
 Many biologic materials such as sera, antisera, toxins, and vaccines
are sterilized with UV rays.
4. FILTRATION
29
 Filters with tiny pore (Micropore filters) are used in laboratories to
filter bacteria and viruses out of liquids.
 A cotton plug in a test tube, flask or pipette is a good filter for
preventing the entry of microorganisms.
 High Efficiency Particulate Air (HEPA) Filters are used to protect
workers from contamination. It is also located in operating rooms
and patient rooms to filter the air that enters or exits the room.
5. GASEOUS ATMOSPHERE
 In limited situations, growth of microorganisms are inhibit by altering
the atmosphere in which they are located.
 Aerobes and microaerophiles require oxygen  killed by placing
them in an atmosphere of devoid oxygen.
 Conversely, obligate anaerobes  can be killed by placing them in an
atmosphere containing oxygen.
 Example: Gas gangrene caused by various anaerobes in the genus
Clostridium  place the patient in hyperbaric (Increased pressure)
oxygen chamber  As a result of pressure, oxygen is forced into the
wounds and kill the Clostridia.
VI. USING CHEMICAL METHODS TO INHIBIT MICROBIAL GROWTH

1. Alcohols
 Functionally act as “liquid desiccants”
 Rapid, broad spectrum antimicrobial activity against vegetative
bacteria, viruses and fungi but are not sporicidal
2. Aldehydes
 Glutaraldehyde or formaldehyde are used for low temperature
disinfection & sterilization of surgical tools
 Normally used as a 2% solution to achieve sporicidal activity
 Bactericidal & sporicidal
3. Biguanides
 Chlorhexidine- widely used in hand washing and oral products
 Disinfectant and preservative
 Mycobacteria are highly resistant in general
4. Bisphenols
 The Bisphenols are widely used as antiseptic soaps
 Have low activity against Pseudomonas aeroginosa and molds.
 Triclosan and hexachlorophene bactericidal & sporostatic
5. Halogen-Releasing Agents
30
 Chlorine-releasing agents such as Sodium hypochlorite, chlorine
dioxide and sodium dichloroisocyanurate  oxidizing agents that
destroy the cellular activity of proteins.
 Hypochlorous acid (active compound)
 Iodine  bactericidal and sporicidal
6. Heavy Metal Derivatives

 Silver Sulfadiazine – broad spectrum antibacterial agents
7. Organic Acids
 Preservatives in pharmaceuticals and food industries
 Benzoic acid  fungistatic, while propionic acid is both bacteriostatic
& fungistatic.
8. Peroxygens
 Hydrogen Peroxide has broad spectrum activity against viruses,
bacteria, yeast and bacterial spores.
 Sporicidal activity requires higher concentrations (10-30%) of H 2O2
and longer contact time.
9. Phenols
 Antiseptic, disinfectant or preservative properties.
10. Quaternary Ammonium compounds

 Sporostatic
 Ex: Benzalkonium chloride, benzethonium chloride,
methylbenzethonium chloride
11. Vapor phase sterilants

 Heat sensitive medical devices and surgical supplies can be sterilized
by vapor phase system using ethylene oxide, hydrogen peroxide or
formaldehyede
Focus Questions
 Sporicidal

1. What is the difference between physical and chemical methods of
controlling microbial growth?
2. Why temperature is significant in controlling microbial growth?
Related Readings
To appreciate and further understand the above discussion, kindly read the
research article on “Perception and Regulatory Principles of Microbial
31
Growth Control” by Khonsari & Kollmann (2015) through
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439118/
Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT IV - - - - - - - - - - - - - - - - - - -
UNIT 5: Antimicrobial Drugs

1. Describe the History of Antimicrobials;
2. Distinguish the Clinical considerations in
using antimicrobial drugs and antimicrobial resistance; and
3. Determine the mechanism of action, spectrum of activity and
classification of antimicrobial drugs.
Introduction
Chemotherapeutic agents used to treat infectious diseases are

collectively referred to as antimicrobial agents which are commonly misuse
and abuse worldwide. Moreover, Cheng et al., (2016) mentioned in their
study that the outbreak of antimicrobial resistance, together with the lack
of newly developed antimicrobial drugs, represents an alarming signal for
both human and animal healthcare worldwide.
Selection of rational dosage regimens for traditional antimicrobial
drugs based on pharmacokinetic/pharmacodynamic principles as well as
development of novel antimicrobials targeting new bacterial targets or
resistance mechanisms are key approaches in tackling AMR.

Key Terms:
 CHEMOTHERAPEUTIC AGENT – is any drug used to treat any
condition or disease and collectively referred to as antimicrobial
agents.
32
 ANTIBIOTIC – is a substance produced by a microorganism that is
effective in killing or inhibiting the growth of other microorganisms.
 ANTIMICROBIAL RESISTANCE (AMR) – occurs when microbes such
bacteria, viruses, fungi and parasites no longer respond to the drugs
designed to kill them.
 NARROW SPECTRUM ANTIBIOTIC – Kill either Gram positive or
Gram negative microorganism.
 BROAD SPECTRUM ANTIBIOTIC – Kill both Gram positive and Gram
negative microorganism.
Lecture Notes
Did you know that Chemotherapeutic agents are collectively

referred to as antimicrobial agents? This is because we most
often hear the term “chemotherapy” used in conjunction with
cancer. Let`s find out the history and its development.
I. History of Antimicrobial Agents

 PAUL EHRLICH
 German chemist, began his search for chemicals that would
destroy bacteria, yet would not damage normal body cell.
 Discovered arsenic compound for syphilis which was
Arsphenamine (Salvarsan®)
 Father of Chemotheraphy
 ALEXANDER FLEMING
 Scottish Bacteriologist, accidentally discovered the first
antibiotic Penicillium notatum that inhibits Staphylococcus
species.
 Penicillin in 1928
 HOWARD WALTER FLOREY & ERNST BORIS CHAIN

 During World War II, Purified penicillin and demonstrated its
effectiveness in the treatment of various bacterial
infections.
 GERHARD DOMAGK
 Discovered that the red dye, Protonsil was effective against
Streptococcal infections in mice.
 Further research on Protonsil that was broken down in the
body into sulfanilamide ( Sulfa durg).
33
 SELMAN WAKSMAN
 He and his colleagues isolated Streptomycin (first
antituberculosis drug)
 Discovered chloramphenicol, tetracycline and erythromycin
in soil samples.
 The first to use the term “Antibiotic”
II. CHARACTERISTICS OF AN IDEAL ANTIMICROBIAL AGENT
The ideal antimicrobial should:
• Kill or inhibit the growth of microorganism
• Cause no damage to the host
• Cause no allergic reaction in the host
• Be stable when stored in solid or liquid form
• Remain in specific tissues in the body long enough to be effective
• Kill the pathogens before they mutate and become resistant to it.
How Antimicrobial Agents Work:
The five most common mechanisms of action of antimicrobial agents are as
follows:
1. Inhibition of Cell Wall synthesis
2. Damage to Cell membrane
3. Inhibition of Nucleic acid synthesis (either RNA and or DNA synthesis)
4. Inhibition of Protein Synthesis
5. Inhibition of Enzyme activity
III. PRINCIPLES OF ANTIMICROBIAL TREATMENT
 EMPIRIC TREATMENT – treatment of an infection before specific
culture information has been reported or obtained.
 DEFINITIVE TREATMENT – antimicrobial treatment based on
susceptibility testing
 PROPHYLACTIC THERAPY: treatment with antibiotics to prevent an
infection, as in intra-abdominal surgery
 POST-ANTIBIOTIC EFFECT- persistent suppression of bacterial growth
after limited exposure to an antimicrobial agent.
Bacteriostatic Agents
• Chloramphenicol, Clindamycin, Ethambutol, Macrolides
• Nitrofurantoin, Linezolid, Sulfonamides, Tetracyclines
• Trimethoprim
Bactericidal Agents
• Aminoglycosides, Beta-lactam antibiotics, Isoniazid, Metronidazole
• Pyrazinamide, Quinolones, Rifampicin, Vancomycin
INHIBITORS OF CELL WALL SYNTHESIS
34
• Beta-lactams, Cephalosporins, Monobactams, Carbapenems,
Vancomycin
INHIBITORS OF PROTEIN SYNTHESIS
• Aminoglycosides, Chloramphenicol, Tetracyclines, Macrolides,
Clindamycin, Linezolid
INHIBITORS OF NUCLEIC ACID SYNTHESIS
Sulfonamides
Trimethoprim
INHIBITORS OF DNA GYRASE
(involved in the replication, transcription, and repair of bacterial DNA)
Quinolones
IV. CELL WALL SYNTHESIS INHIBITORS:
1. PENICILLIN
 First introduced in the 1940s
 Bactericidal: inhibit cell wall synthesis
 Also called “beta-lactams”
 MOA: Inhibits cell wall synthesis
 Inhibits dipeptidoglycan synthesis
 Acylate D-transpeptidase
Figure 1: General structure of Penicillin

(Researchgate, 2020)
TYPES:
 NATURAL PENICILLINS
 PENICILLINASE-RESISTANT PENICILLINS
 AMINOPENICILLINS
 EXTENDED-SPECTRUM PENICILLINS
1. Natural Penicillin
Penicillin G (Benzylpenicillin)
 Susceptible to β-lactamases
 acid-labile (given IM, IV)
 pneumococcal pneumonia, rheumatic fever, syphilis, leptospirosis
Penicillin V (Phenoxymethylpenicillin)
35
 acid-stable (given PO)
 same spectrum as Penicillin G
2. PENICILLINASE-RESISTANT
 Methicillin, Oxacillin, Cloxacillin, Nafcillin
 Effective against Staphylococcus aureus
 Methicillin-resistant S. aureus (MRSA): Vancomycin
3. AMINOPENICILLINS
 Amoxicillin, Ampicillin
 extended spectrum against g (-) (Haemophilus influenzae, Escherichia
coli, Salmonella typhi)
4. ANTI-PSEUDOMONAL
- Carbenicillin, Piperacillin, Ticarcillin, Mezlocillin, Azlocillin
SIDE EFFECTS OF PENICILLINS:
1. hypersensitivity - rashes, anaphylaxis
2. diarrhea
3. nephritis (Methicillin)
4. hemorrhage (anti-pseudomonal)
5. electrolyte disturbance
DRUG INTERACTIONS:
+ Probenecid: inhibits renal excretion of Penicillin
+ static drugs: antagonism
 PENICILLIN-BETA-LACTAMASE INHIBITOR
 Bacteria produce enzymes capable of destroying penicillins.
 These enzymes are known as beta-lactamases.
 As a result, the medication is not effective.
 Chemicals have been developed to inhibit these enzymes such as
clavulanic acid, tazobactam and sulbactam
 These chemicals bind with beta-lactamase and prevent the
enzyme from breaking down the penicillin.
PENICILLIN-BETA-LACTAMASE INHIBITOR COMBINATION DRUGS:

 ampicillin + sulbactam = Unasyn®
 amoxicillin + clavulanic acid = Augmentin ®
 ticarcillin + clavulanic acid = Timentin ®
 piperacillin + tazobactam = Zosyn ®
Mechanism of Action (MOA) of Penicillins:
 Penicillins enter the bacteria via the cell wall.
 Inside the cell, they bind to penicillin-binding protein (PBP).
 Once bound, normal cell wall synthesis is disrupted.
 Result: bacteria cells die from cell lysis.
36
 Penicillins do not kill other cells in the body.
2. CEPHALOSPORIN
 Semisynthetic derivatives from a fungus
 Structurally and pharmacologically related to penicillins
 Bactericidal action and Broad spectrum
 Divided into groups according to their antimicrobial activity
 more resistant to β-lactamases
 ↑ g(-) activity
Figure 5: General Structure of Cephalosporin

(Online Biology Notes, 2020)
First Generation:
 Cefadroxil, Cephalexin, Cephradine, Cefazolin,
Cephalothin,
Cephapirin
 Effective against Proteus mirabilis, Escherichia coli, Klebsiella
 Good gram-positive coverage
 Poor gram-negative coverage
Second Generation:
 Cefaclor, Cefamandole, Cefmetazole, Cefoxitin, Cefuroxime
 Cefonicid, cefotetan, Cefprozil, ceforanide
 (+ Haemophilus influenzae, Enterobacter, Neisseria gonorrhea)
 Good gram-positive coverage
 Better gram-negative coverage than first generation
Third Generation:
 Cefixime, ceftizoxime, Cefpodoxime proxetil , ceftriaxone
 Cefoperazone, ceftazidime, cefotaxime, moxalactam
 (+ Haemophilus influenzae, Enterobacter, Neisseria gonorrhea)
 (+ Serratia, Salmonella, Shigella)
 Most potent group against gram-negative
 Less active against gram-positive
Fourth Generation:
37
 Cefepime, Cefpirone
 greater activity against g(+) Cocci, Enterobacter, Pseudomonas
than 3rd Generation
3. CARBAPENEMS
 - resist β-lactamases
 - broad spectrum for mutli-drug resistant bacteria
 - Imipenem, Meropenem
 - Imipenem + Cilastatin (inhibits dehydropeptidase in kidney →
prevents formation of toxic metabolite)
 - S/E: seizures
4. MONOBACTAMS
 Aztreonam
 - against g(-) aerobic bacteria: E. coli, Serratia, Proteus, Salmonella,
Hemophilus, Klebsiella, Pseudomonas
V. Protein Synthesis Inhibitors:
1. TETRACYCLINES
 Active against Gram-positive and Gram-negative bacteria,
spirochetes, mycoplasma, rickettsiae and chlamydiae
 MOA: Bind to 30S ribosomal subunit and prevent the binding of
aminoacyl tRNA to the mRNA-ribosome complex
 Forms stable chelates with many metals, including calcium,
magnesium and iron
 They are distributed into the milk of lactating mothers and will cross
the placental barrier into the fetus.
 S/E: Discoloration of baby`s teeth
Examples: Tetracycline, Rolitetracycline, Chlortetracycline, Oxytetracycline
Methacycline, Demeclocycline, Meclocycline, Doxycycline, Minocycline
Tigecycline
2. AMINOGLYCOSIDES
 Streptomycin – the first aminoglycoside antibiotic
used in chemotherapy
 All are absorbed very poorly following oral administration
 Ototoxic and nephrotoxic
 Synergistic with β-lactam antibiotics
 MOA: They bind to 30S ribosomal subunit to form a complex that
cannot initiate proper amino acid polymerization.
Examples:
 Streptomycin:
 Derived from Streptomyces griseus
38
 Greatest drawback is the rapid development of resistant
strains  Neurotoxic
 Neomycin
 Derived from Streptomyces fradiae
 Tx of GI infections, dermatological infections and acute
bacterial peritonitis
 Low incidence of toxic reactions
 Kanamycin
 Derived from Streptomyces kanamyceticus
 Amikacin
 Resists attack by most bacteria-inactivating enzymes and,
therefore, is effective against bacteria that are resistant to
other aminoglycosides
 Gentamicin
 Derived from Micromonospora purpurea
 Strong activity against P. aeruginosa and Gram-negative
enteric bacilli
 Other examples: Tobramycin, netilmicin and
Spectinomycin
(bacteriostatic)
3. MACROLIDES
 Spectrum of activity resembles that of penicillin plus Mycoplasma,
Chlamydia, Campylobacter and Legionella
 Also effective against Neisseria and Treponema pallidum
 MOA: Binds to a selective site on the 50S ribosomal subunit to
prevent the translocation step of bacterial protein synthesis.
Examples:
 Erythromycin
 From Streptomyces erythraeus
 For the treatment of various upper respiratory and soft-tissue
infections caused by Gram-positive bacteria; gonorrhea and
syphilis
 Stearate, estolate – oral
 Ethylsuccinate – oral, IM
 Glucoheptonate, lactobionate – IV
 Clarithromycin
 Fully retains erythromycin’s antibacterial properties with
increased acid stability, oral bioavailability and reduced GI side
effects.
 The presence of food does not significantly affect its
absorption.
 Azithromycin
39
 It is more active against Gram-negative bacteria and less active
against Gram-positive bacteria
 Food decreases absorption by as much as 50%
4. CHLORAMPHENICOL
 binds to 50s
 derived from Streptomyces venezuelae
 broad spectrum, life-threatening infections
 Used for meningitis, brain abcess, typhoid fever, anaerobes
 Side-effect: Gray baby syndrome (no glucuronidation)
VI. Inhibitors of Nucleic Acid Synthesis:
1. Quinolones:
 MOA: inhibit DNA gyrase or topoisomerase III
 Alter DNA of bacteria, causing death
 Lower respiratory tract infections, Bone and joint infections,
Infectious diarrhea, UTI, Skin infections, STDs
Examples: Ciprofloxacin (Cipro®), Enoxacin (Penetrex®),

Lomefloxacin (Maxaquin®), Norfloxacin (Noroxin®) Ofloxacin (Floxin®)
VII. Inhibitors of Folate Synthesis:
1. Sulfonamides:
 Bacteriostatic action
 MOA: Prevent synthesis of folic acid required for synthesis of purines
and nucleic acid
 Does not affect human cells or certain bacteria—they can use
preformed folic acid
 One of the first groups of antibiotics
Examples: sulfadiazine, sulfamethizole, sulfamethoxazole, sulfisoxazole
VIII. Anti-TB Drugs:
 Why TB is difficult to treat?
 waxy layer of mycolic acid (cell wall: mycolic acid +
peptidoglycan + arabinogalactan)
 intracellular, surrounded by caseous material
 slow growth & cost of treatment
 resistance in the wake of AIDS
First line of therapy:
 RIFAMPICIN
 ISONIAZID
 PYRAZINAMIDE
 ETHAMBUTOL
 STREPTOMYCIN
 more effective, less toxic, cheaper
40
 DOTS (directly observed therapy short course)
IX. ANTIMICROBIAL RESISTANCE
 Antimicrobial resistance (AMR) is a global health and development
threat. It requires urgent multi-sectoral action in order to achieve the
Sustainable Development Goals (SDGs).
 Antimicrobial Resistance (AMR) occurs when bacteria, viruses, fungi
and parasites change over time and no longer respond to medicines
making infections harder to treat and increasing the risk of disease
spread, severe illness and death.
 As a result of drug resistance, antibiotics and other antimicrobial
medicines become ineffective and infections become increasingly
difficult or impossible to treat.
 Bacteria can acquire resistance to antimicrobial agents as a result of
chromosomal mutation or the acquisition of new genes by
transduction, transformation, and most commonly, conjugation.
Focus Questions
1. What is the difference between narrow spectrum and broad spectrum
antibiotic?
2. What are the advantages and disadvantages of empiric therapy?
Related Readings

read the article “Antimicrobial Drugs in Fighting against Antimicrobial
Resistance” by Cheng, G., Dai, M., Ahmed, S., Hao, H., Wang, X., & Yuan, Z.
(2016) through https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824775/
Learning Assessment
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UNIT 6: Principles of Pathogenicity and

Epidemiology
1. Describe the host-parasite relationship and reservoirs; 2.
Determine the mode of transmission of various diseases; and
3. Describe the epidemiology of the major infectious disease.
41
Introduction
Gulis and Fujino (2015) mentioned that the health of populations

depends on many different factors. Epidemiology is a discipline that has a
crucial role in describing health status, identifying risk factors, and analyzing
relationships between health and different hazardous agents. Moreover,
epidemiology is one of the essential disciplines of public health, its major
aim is to contribute to fulfilment of the definition of public health as “a
science and art to promote health and prevent disease by organized effort
of society”.

Key Terms:
 EPIDEMIOLOGY – the study of relationships between the various
factors that determine the frequency and distribution off diseases.
 PATHOGEN – refers to disease-causing microorganism
 PATHOGENESIS – the steps or mechanisms involved in the
development of the disease.
 PATHOGENICITY – the ability to cause disease
 PATHOLOGY – the study of disease
 HOST – In a parasitic relationship, the organism on or in which a
parasite lives.
 RESERVOIR of INFECTION- any person, animal, plant, soil or
substance in which an infectious agent normally lives and multiplies.
Lecture Notes
Did you know that epidemiologist are scientists who specialize in

the study of diseases and injury patterns in populations and ways
to prevent or control diseases and injuries? Let`s find out the
significance of epidemiology in our society.
I. Epidemiology
42
 Epidemiology is the study of relationships between the various factors
that determine the frequency, distribution and determinants of
diseases in human populations, and ways to prevent, control, or
eradicate diseases in populations.
 Epidemiologist used some specific terms used to describe the
status of a particular infectious disease in a given population. The
following sections briefly describe these terms:
 INFECTIOUS DISEASE
 are diseases caused by pathogens
 COMMUNICABLE DISEASE
 are infectious diseases that can be transmitted from one
human to another.
 CONTAGIOUS DISEASE
 are communicable diseases that are easily transmitted from
one person to another.
 ZOONOTIC DISEASES
 also known as zoonoses, are infectious diseases that humans
acquire from animal sources.
 INCIDENCE OF A PARTICULAR DISEASE
 is defined as the number of new cases of that disease in a
defined population during a specific time period.
 MORBIDITY RATE
 The number of new cases of a particular disease that occurred
during a specified time period per a specified population.
 MORTALITY RATE
 The ratio of the number of people who died of a particular
disease that occurred during a specified time period per a
specified population. Also known a s death rate.
 PERIOD PREVALENCE
 the number of cases of the disease existing in a given
population during a specific time period.
 POINT PREVALENCE
 the number of cases of the disease in time
 SPORADIC DISEASE
 is a disease that occurs only occasionally within the population
of a particular geographic area.
 ENDEMIC DISEASE
 are diseases that are always present within the population of a
particular geographic area.
 EPIDEMIC DISEASE
43
 are diseases that occur in a greater than usual number of cases
in a particular region and usually occur within a relatively short
period of time.
 PANDEMIC DISEASE
 is a disease that is occurring in epidemic proportions in many
countries simultaneously-sometimes worldwide.
II. INTERACTIONS BETWEEN PATHOGENS, HOSTS AND ENVIRONMENTS

A traditional model of infectious disease causation, known as the
Epidemiologic Triad. It consists of an external agent, a host and an
environment in which host and agent are brought together, causing the
disease to occur in the host.
 AGENT
 refers to an infectious microorganism or pathogen: a virus,
bacterium, parasite, or other microbe.
 Generally, the agent must be present for disease to occur.
 HOST
 refers to the human who can get the disease.
 A host offers subsistence and lodging for a pathogen and may
or may not develop the disease.
 The level of immunity, genetic makeup, level of exposure, state
of health, and overall fitness of the host can determine the
effect a disease organism will have on it.
 ENVIRONMENT
 Refers to extrinsic factors that affect the agent and the
opportunity for exposure.
 Environmental factors include physical factors such as geology
and climate, biologic factors such as insects that transmit the
agent, and socioeconomic factors such as crowding, sanitation,
and the availability of health services.
III. CHAIN OF INFECTION

There are six components in the infectious disease process also known as
Chain of infection:
Figure 1: Chain of infection

(Magonlinelibrary, 2020)
44
1. There must first be a pathogen (Virus, bacteria, parasites)
2. There must be a source of pathogen or reservoir (is any person, animal,
arthropod, plant, soil or substance in which an infectious agent normally
lives and multiplies.)
3. There must be a portal of exit (way for the pathogen to escape the
reservoir).
4. There must be mode of transmission (way of the pathogen to travel from
one person to another).
5. There must be a portal of entry (Way of pathogen to gain entry into
another person).
6. There must be a susceptible host
IV. Strategies for breaking the Chain of Infection
A. Broad Goals for breaking the Chain of Infection:
 Eliminate or contain the reservoirs of pathogens or curtail the
persistence of a pathogen at the source.
 Prevent contact with infectious substances from exit pathways.
 Eliminate means of transmission
 Block exposure to entry pathways
 Reduce or eliminate the susceptibility of potential hosts.
B. Specific methods of breaking the chain of infection:

 Proper hygiene
 Maintain good nutrition, adequate rest and reduce stress
 Obtaining immunizations against common pathogens
 Proper Patient Isolation Procedure
 Proper disposing of sharps and infectious wastes
 Observe proper PPE when necessary
V. RESERVOIRS OF INFECTION
Note: Reservoirs of infection may be living hosts or inanimate objects A.
Living Reservoir- include humans, household pets, farm animals, wild
animals, certain insects, and certain arachids.
1. Human Carrier
 The most important reservoirs of human infectious diseases
are other humans or carriers.
 Carrier is a person who is colonized with a particular pathogen
Types of Carrier
 Passive carrier – carry the pathogen without ever having the disease.
45
 Incubatory carrier – is a person who is capable of transmitting a
pathogen during the incubation period of a particular infectious
disease.
 Convalescent carriers – harbor and can transmit a particular
pathogen while recovering from an infectious disease.
 Active carriers – have completely recovered from the disease, but
continue to harbor the pathogen indefinitely and is able to pass the
infection to others.
Disease Pathogen Animal Mode Of Transmission
Reservoir(s)
VIRAL DISEASES
Avian Influenza birds Direct or indirect contact with

Influenza virus infected birds
Lassa fever Lassa virus Wild Rodents Inhalation of contaminated
dust or aerosols
Marburg Marburg Monkeys Contact with blood or tissues
disease virus from infected monkeys
Rabies Rabies virus Rabid Dogs, Animal bite
cats, bats,
skunks, foxes
Yellow fever Yellow fever Monkeys Aedes aegypti mosquito bite
virus
BACTERIAL
Anthrax Bacillus Cattle, sheep, Inhalation, ingestion, entry

anthracis goats through cuts, contact with
mucous membranes
Bovine TB Mycobacter Cattle Ingestion
ium bovis
Brucellosis Brucella Cattle, swine, Inhalation, ingestion of
spp. goats contaminated milk, entry
through cuts, contact with
mucous membranes
Campylobac Campylobac Wild Ingestion of contaminated food

ter infection ter spp. mammals, and water
cattle, sheep,
pets
Cat-Scratch Bartonella Domestic Cats Cat scratch,, bite or lick
disease henselae
Ehrlichiosis Ehrlichia Deer, mice Tick bite
spp.
Endemic Rickettsia Rodents Flea bite
typhus typhi
46
Leptospirosi Leptospira Cattle, rodents, Contact with contaminated
s spp. dogs animal urine
Lyme Borrelia Deer, rodents Tick bite
disease burgdorferi
Plague Yersinia Rodents Flea bite
pestis
Relapsing Borrelia spp Rodents Tick bite
fever
Rickettsial Rickettsia Rodents Mite bite
pox akari
Rocky Rickettsia Rodents, dog Tick bite
Mountain rickettsii
spotted
fever
Salmonellos Salmonella Poultry, Ingestion of contaminated food
is spp. livestock,
reptiles
Scrub typhus Orientia Rodents Mite bite
tsutsugamu
shi
Tularemia Francisella Wild animals Entry through cuts, inhalation,
tularensis tick or deer fly bite
Q fever Coxiella Cattle, sheep, Tick bite, air, mild contact with
burnetti goats infected animals
FUNGAL DISEASES
Tinea Various Various Contact with infected animals
(ringworm) dermatophy animals
infections tes including dogs
PROTOZOAL DISEASES
African Subspecies Cattle, Wild Tsetse Fly bite
Trypanosom of game animals
iasis Trypanosom
a brucei
American Trypanosom Wild & Trypomastigotes in the feces
Trypanosom a cruzi domestic of reduviid bug are rubbed
iasis animals into bite wound or the eye
(Chagas
disease)
Babesiosis Babesia Deer, mice, Tick bite
microti voles
Leishmanias Leishmania Rodents, dog Sandfly bite
is donovani
Toxoplasmo Toxoplasma Cats, pig, Ingestion of oocyst in cat
sis gondii sheep feces, or cysts in raw or
47
undercooked meat
HELMINTH DISEASES
Dog Dipylidium Dogs, cats Ingestion of flea containing the
Tapeworm caninum larval stage
infection
Rat Hymenoleps rodents Ingestion of beetle containing
Tapeworm is diminuta the larval stage
Echinococco Echinococcu Dogs Ingestion of eggs
sis (hydatid s granulosis
disease)
Table 1: Examples of Zoonotic Disease
(Engelkirk, P. & Engelkirk, J.D., 2015) VI.
PATHOGENESIS OF INFECTIOUS DISEASE:
A. Four Periods or Phases in the Course of an Infectious Disease:
1. The Incubation Period
 The time that elapses between arrival of the pathogen and the onset
of symptoms
 The length of the incubation period is influenced by many factors
such as:
 Overall health & Nutritional status of the host
 Immune status of the host
 Virulence of the pathogen
 Number of pathogens that enter the body
2. The Prodromal Period
 The time during which the patient feels “out of sorts” but does not
yet experiences the actual symptoms of the disease.
3. The Period of Illness

 The time during which the patient experiences the typical symptoms
associated with that particular disease (e.g., sore throat, headache,
sinus congestion)
 Communicable diseases are most easily transmitted during this third
period.
4. The Convalescent period
 The time during which the patient recovers.
 For certain infectious diseases, especially viral respiratory diseases,
the convalescent period can be quite long.
B. LOCALIZED VS. SYTEMIC INFECTIONS

 An infection may be localized or it may spread, becoming a systemic
or generalized infection.
48
 Once an infectious process is initiated, the disease may remain
localized or it may spread; examples of localized infections are
pimples, boils and abscesses.
 When the infection spreads throughout the body it is said to have
become a systemic or generalized infection; an example is miliary
tuberculosis caused by Mycobacterium tuberculosis.
C. Acute, Subacute, and Chronic Diseases

 A disease may be acute, subacute, or chronic, depending on the
length of its incubation period and duration.
 An ACUTE DISEASE is one that has a rapid onset, and is usually
followed by a relatively rapid recovery; examples are measles,
mumps, and influenza.
 A CHRONIC DISEASE has a slow onset and lasts a long time; examples
are tuberculosis, leprosy, and syphilis.
 A SUBACUTE DISEASE is one that comes on more suddenly than a
chronic disease, but less suddenly than an acute disease; an example
would be bacterial endocarditis.
D. Symptoms of a Disease Versus Signs of a Disease

 A symptom of a disease is defined as some evidence of a disease that
is experienced by the patient; something that is subjective; for
example, aches or pains, ringing in the ears, blurred vision, nausea,
dizziness, etc.
 There are symptomatic and asymptomatic diseases. In a
symptomatic disease, the patient is experiencing symptoms. In an
asymptomatic disease, the patient is not experiencing any
symptoms.
 A sign of a disease is defined as some type of objective evidence of a
disease; for example, elevated blood pressure, abnormal heart
sounds, abnormal pulse rate, abnormal laboratory results, etc.
E. Steps in the Pathogenesis of Infectious Diseases:

A common sequence of steps in the pathogenesis of infectious diseases is:
1. Entry of the pathogen into the body.
2. Attachment of the pathogen to some tissue(s) within the body
3. Multiplication of the pathogen.
4. Invasion or spread of the pathogen.
5. Evasion of host defenses. 6. Damage to host tissue(s).
Focus Questions

1. What are specific diseases that are currently pandemic and epidemic?
49
2. Why epidemiology is significant to public health?
Related Readings

read the article “Predicting Microbial Growth in a Mixed Culture From
Growth Curve Data” by Ram et al., (2019) through
https://www.pnas.org/content/116/29/14698.
Learning Assessment
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UNIT 7: Introduction to Basic Immunology

1. Describe the fundamentals of
immunology;
2. Determine the general and specific defense mechanisms; and
3. Differentiate innate and adaptive immunity.
Introduction
Marshall et al., (2018) mentioned that beyond structural and

chemical barriers to pathogens, the immune system has two fundamental
lines of defense: innate immunity and adaptive immunity. There is a great
deal of synergy between the adaptive immune system and its innate
counterpart, and defects in either system can provoke illness or disease,
such as inappropriate inflammation, autoimmune diseases,
immunodeficiency disorders and hypersensitivity reactions.

Key Terms:
 IMMUNITY – the status of being immune or resistant to an
infectious disease.
50
 IMMUNOGOBULINS – also known as antibodies, are
glycoprotein molecules produced by plasma cells (white blood
cells).
 ANTIBODIES – are proteins produced by the immune system in
response to antigens.
Lecture Notes
Did you know that epidemiologist are scientists who specialize in

the study of diseases and injury patterns in populations and ways
to prevent or control diseases and injuries? Let`s find out the
significance of epidemiology in our society.
I. INTRODUCTION
 Immunology is the scientific study of the immune system and
immune responses.
 The primary functions of the immune system are to:
 Differentiate between “self’ and “non-self”
 Destroy that which is “non- self”
 Cells involved in immune responses originate in bone marrow; 3
lines of lymphocytes are derived from lymphoid stem cells of bone
marrow: B lymphocytes (or B cells), T lymphocytes (or T cells) and
natural killer cells (NK cells)
 Immune responses involve complex interactions among many
different types of body cells and cellular secretions.
II. Major Arms of the Immune System:

1. HUMORAL IMMUNITY
 involves the production of antibodies in response to antigens.
 After their production, these humoral (circulating) antibodies remain
in blood plasma, lymph, and other body secretions where they
protect against the specific pathogens.
 person is immune to a particular pathogen because of the presence
of specific protective antibodies that are effective against that
pathogen.
 is mediated by antibodies, it is also known as Antibody-Mediated
Immunity (AMI).
2. CELL-MEDIATED IMMUNITY
 involves various cell types, with antibodies playing only a minor role,
if any.
51
 an immune response that does not involve antibodies but rather
involves the activation of macrophages and NK-cells, the production
of antigen-specific cytotoxic T-lymphocytes, and the release of
various cytokines in response to an antigen .
II. IMMUNITY
 When one is resistant to a certain disease, he/she is said to be
immune.
 The condition of being immune is usually referred to as Immunity.
 Immunity that results from the active production or receipt of

protective antibodies during one’s lifetime is called Acquired
Immunity.
 If the antibodies are actually produced within the person’s body, the
immunity is called Active Acquired Immunity; which is long lasting.
 In Passive Acquired Immunity, the person receives antibodies that

were produced by another person or by more than one person, or, in
some cases, by an animal; such protection is usually only temporary.
TYPES OF ACQUIRED IMMUNITY
ACTIVE ACQUIRED IMMUNITY
Natural Active Acquired Immunity that is acquired in response
Immunity to the entry of a live pathogen into
the body (i.e., in response to an
actual infection)
Artificial Active Acquired Immunity that is acquired in response
Immunity to vaccines
PASSIVE ACQUIRED IMMUNITY
Natural Passive Acquired Immunity that is acquired by a
Immunity fetus when it receives maternal
antibodies in utero or by an infant
when it receives maternal
antibodies contained in colostrum
Artificial Passive Acquired Immunity that is acquired when a
Immunity person receives antibodies
contained in antisera or gamma
globulin
Table 1: Types of acquired Immunity
(Engelkirk, P., & Engelkirk, J.D., 2015)
 People who have had a specific infection usually have developed
some resistance to reinfection by the causative pathogen because of
the presence of antibodies and stimulated lymphocytes. This is called
Natural Active Acquired Immunity.
52
 Antibodies that protect us from infection or reinfection are called
Protective Antibodies.
 Artificial Active Acquired Immunity is the type of immunity results
when a person receives a vaccine.
III. VACCINES
 A vaccine is defined as material that can artificially induce
immunity to an infectious disease, usually after injection or, in
some cases, ingestion of the material.
 An ideal vaccine is one that:
1. Contains enough antigenic determinants to stimulate the
immune system to produce protective antibodies.
2. Contains antigenic determinants from all the strains of the
pathogen that cause that disease (e.g., the three strains of
virus that cause polio); such vaccines are referred to as
multivalent or polyvalent vaccines
3. Has few (preferably, no) side effects
4. Does not cause disease in the vaccinated person
 According to the CDC, American children should receive the following
vaccines between birth and entry into school
(http://www.cdc.gov/vaccines):
 Hepatitis B (Hep B) vaccine
 Rotavirus vaccine
 Diphtheria toxoid–tetanus toxoid–acellular pertussis
(DTaP) vaccine
 Haemophilus influenzae type b (Hib) conjugate vaccine
 Inactivated poliovirus vaccine
 MMR vaccine
 Varicella (chickenpox) vaccine
 The protective antibodies and/or memory cells produced in response
to the vaccine then remain in the recipient’s body to “do battle with”
a particular pathogen, should that pathogen enter the recipient’s
body at some time in the future.
TYPES OF DESCRIPTION EXAMPLES
VACCINE
53
The process of weakening Attenuated Viral Vaccines:
LIVE pathogens is called attenuation. adenovirus, chicken pox
Most live vaccines are avirulent (varicella), measles
A (nonpathogenic) mutant (rubeola), mumps, German
strains of pathogens that have measles (rubella), polio
T
been derived from the virulent (oral Sabin vaccine),
T rotavirus, smallpox, yellow
(pathogenic) organisms; this is
E fever Attenuated Bacterial
accomplished by growing them for
N many generations under various Vaccines: BCG (for
U conditions or by exposing them to protection against TB),
A cholera, tularemia, typhoid
mutagenic chemicals or radiation.
T fever
Attenuated vaccines should not be
E (oral
administered to
vaccine)
D immunosuppressed individuals,
because even weakened
VACCINE pathogens could cause disease in
these persons.
Vaccines made from pathogens Inactivated Viruses:
that hepatitis A, influenza,
have been killed by heat or Japanese encephalitis,
INACTIVATED chemicals—called inactivated encephalitis vaccines,
vaccines—can be produced faster polio (subcutaneous Salk
VACCINES
and more easily, but they are less vaccine), rabies
Inactivated Bacterial
effective than live vaccines. This is
Vaccines: anthrax, cholera,
because the antigens on the dead
pertussis, plague, typhoid
cells are usually less effective and fever (subcutaneous
produce a shorter period of vaccine),
immunity. Q fever
SUBUNIT A subunit vaccine (or acellular
VACCINES vaccine) is one that uses antigenic Anthrax, hepatitis B, Lyme
(antibody-stimulating) portions of disease, whooping cough
a
pathogen, rather than using the
whole pathogen.
It is made by conjugating bacterial Hib (for protection against
capsular antigens (which by H. influenzae type
themselves are not very antigenic) b),meningococcal meningitis
CONJU- to molecules that stimulate the (Neisseria meningitidis
GATE immune system to produce serogroup C), pneumococcal
VACCINES antibodies against the less pneumonia
antigenic capsular antigens.
A toxoid is an exotoxin that has Diphtheria, tetanus.
been inactivated (made nontoxic) Commercial antisera
by heat or chemicals. Toxoids can containing antitoxins are
be injected safely to stimulate the used to treat diseases such
TOXOID production of antibodies that are as tetanus and botulism.
capable of neutralizing the Such antisera are also used
54
VACCINES exotoxins of pathogens, such as in certain types of
those that cause tetanus, laboratory tests, known as
botulism, and diphtheria. IDPs.
Antibodies that neutralize toxins
are called antitoxins, and a serum
containing such antitoxins is
referred to as an antiserum.
Table 2: Types of Vaccines
 In Natural Passive Acquired Immunity, small antibodies (such as
immunoglobulin G [IgG], present in the mother’s blood cross the
placenta to reach the fetus while it is in the uterus (in utero).
 The colostrum, the thin, milky fluid secreted by mammary glands a
few days before and after delivery contains maternal antibodies to
protect the infant during the first months of life.
 Artificial Passive Acquired Immunity is accomplished by transferring
antibodies from an immune person to a susceptible person.
 After a patient has been exposed to a disease, the length of the
incubation period usually does not allow sufficient time for
postexposure vaccination to be an effective preventive measure.
IV. Cells of the Immune System:
 Bone marrow: The site in the body where most of the cells of the
immune system are produced as immature or stem cells.
 Stem cells: These cells have the potential to differentiate and mature
into the different cells of the immune system.
 Thymus: An organ located in the chest which instructs immature
lymphocytes to become mature T-lymphocytes.
 B-Cells: These lymphocytes arise in the bone marrow and
differentiate into plasma cells which in turn produce
immunoglobulins (antibodies).
 Cytotoxic T-cells: These lymphocytes mature in the thymus and are
responsible for killing infected cells.
 Helper T-cells: These specialized lymphocytes “help” other T-cells
and B-cells to perform their functions.
 Plasma Cells: These cells develop from B-cells and are the cells that
make immunoglobulin for the serum and the secretions.
 Immunoglobulins: These highly specialized protein molecules, also
known as antibodies, fit foreign antigens, such as polio, like a lock
and key. Their variety is so extensive that they can be produced to
match all possible microorganisms in our environment.
 Neutrophils (Polymorphonuclear PMN Cell): A type of cell found in
the blood stream that rapidly ingests microorganisms and kills them.
 Monocytes: A type of phagocytic cell found in the blood stream
which develops into a macrophage when it migrates to tissues.
55
 Red Blood Cells: The cells in the blood stream which carry oxygen
from the lungs to the tissues.
 Platelets: Small cells in the blood stream which are important in
blood clotting.
 Dendritic Cells: Important cells in presenting antigen to immune
system cells:
The major cell types that participate in immune responses are:
1. T lymphocytes (T cells)
 cells directly attack cells infected with viruses, and they also
act as regulators of the immune system.
 There are two major categories of T cells: helper T cells and
cytotoxic T cells.
Helper T cells are also known as T-helper cells, TH cells, and CD4+
cells.
 The term CD4+ cells refers to the fact that these cells possess
on their surface an antigen designated as CD4.
 The primary function of helper T cells is secretion of cytokines.
Cytotoxic T-Cells are also known as T cytotoxic cells, TC cells,
and CD8+ cells.
 The term CD8+ cells refers to the fact that these cells possess
on their surface an antigen designated as CD8.
 The primary function of cytotoxic T cells is to destroy virally
infected host cells, foreign cells, and tumor cells.
2. B lymphocytes (B cells)
 are specialized cells of the immune system whose major
function is to produce antibodies (also called immunoglobulins
or gamma-globulins).
 develop in the bone marrow from hematopoietic stem cells.
 When B-cells encounter foreign material (antigens), they
respond by maturing into another cell type called plasma cells.
3. NK cells
 They easily kill cells infected with viruses.
 They are said to be “natural killer” cells as they do not require the
same thymic education that T-cells require.
 derived from the bone marrow and are present in relatively low
numbers in the bloodstream and in tissues.
 They are important in defending against viruses and possibly
preventing cancer as well.
4. Macrophages
 A macrophage is a type of phagocyte, which is a cell responsible for
detecting, engulfing and destroying pathogens and apoptotic cells.
 Macrophages are produced through the differentiation of monocytes,
which turn into macrophages when they leave the blood.
56
 Macrophages also play a role in alerting the immune system to the
presence of invaders.
V. CLASS OF IMMUNOGLOBULINS
TYPES OF FUNCTIONS
IMMUNOGL
OBULINS
IgA The predominant immunoglobulin class in saliva, tears,
seminal fluid, colostrum, breast milk, and mucous secretions
of the nose, lungs, and gastrointestinal tract.
Protects external openings and mucous membranes from the

attachment, colonization, and invasion of pathogens. IgA
IgD Found in large quantities on the surface of B cells. Its function

is unknown, but it is possible that the IgD molecules on the B
cell’s surface serve as antigen receptors and determine which
specific antigen that particular B cell is able to respond to.
IgE IgE is produced in response to allergens. Found on

the surfaces of basophils and mast cells. Plays a major role in
allergic responses.
IgG The only class of immunoglobulin that can cross the placenta.
Maternal IgG antibodies that cross the placenta help protect
the newborn during its first months of life.
IgM IgM antibodies are the first antibodies formed in the
primary response to antigens (including pathogens.
Because of its large size, IgM does not cross the placenta.
Provides protection in the earliest stages of infection.
Table 3: Classes of Immunoglobulins
Focus Questions

1. What are the similarities and differences of acquired immunity and
passive immunity?
2. What is the importance of Vaccine?
Related Readings

read the article “An introduction to immunology and immunopathology” by
Marshall, J.S., Warrington, R., Watson, W. et al. (2018) through
https://doi.org/10.1186/s13223-018-0278-1
Learning Assessment 57
given via Schoology at the end of the week after our virtual consultation
- - - - - - - - - - - - - - - - - - - END OF UNIT VII - - - - - - - - - - - - - - - - - -
UNIT 8: Microbial Diseases of the Skin and

Eyes
1. Determine the etiological agents affecting the skin and eyes;
2. Determine the drug of choice for specific disease of the skin and
eyes; and
3. Describe the clinical manifestations of specific diseases of the skin
and eyes.
Introduction
Yousef, Alhajj and Sharma (2020) mentioned that skin is the largest
organ in the body and covers the body's entire external surface. The skin's
structure is made up of an intricate network which serves as the body’s
initial barrier against pathogens, UV light, and chemicals, and mechanical
injury. However, it also develop mild to moderately severe infections when
not treated properly including our eyes.
This unit will focus on the etiology of the skin and eyes infections. It
includes the drug of choice for every specific diseases based on the National
Antibiotic Guidelines set by Department of Health-Philippines.

Key Terms:
 Infectious Disease – diseases that are caused by pathogens, following
colonization of some body site by the pathogen.
 Etiology of disease – The science of the causes or origins of disease
 Etiological agent – It refers to a viable microorganism, or its toxin,
that causes or may cause disease in humans or animals.
Lecture Notes
58
Did you know that there are microorganisms that can cause infection to the
skin and eyes? As a future pharmacist, it is essential to familiarize the
treatment to various infectious diseases of the skin and eyes.
I. MICROBIAL DISEASES OF THE SKIN

 Skin is a type of nonspecific host defense mechanism, serving as a
physical barrier.
 It is part of the body’s first line of defense.
 The indigenous microbiota of the skin, a low pH, and the presence of
chemical substances such as lysozyme and sebum also serve to
prevent colonization of the skin by pathogens.
 Different types of bacteria dominate the dry, moist, and sebum-rich
regions of the skin.
II. BACTERIAL INFECTIONS OF THE SKIN

A. Skin abscess, Boils, Furuncles
 Furuncle is a localized pyogenic (pus-producing) infection of the skin,
usually resulting from folliculitis; also known as a boil.
Figure 1: Furuncle
(MSD Manual, 2020)
Etiology: S. aureus: Methicillin sensitive (MSSA), Methicillin resistant
(MRSA) Community-associated MRSA is of increasing concern for effective
management.
Treatment: Incision and drainage is the mainstay of therapy.
1ST LINE THERAPY (DOT: 5-10 days): Cloxacillin or Cephalexin (Oral)
Oxacillin or Cefazolin (Parenteral)
nd
2 LINE THERAPY (DOT 7-10 days):
Clindamycin, Cotrimoxazole, Doxycycline, or Linezolid (Oral)
Clindamycin, Vancomycin or Linezolid (Parenteral)
B. Folliculitis
 Inflammation of a hair follicle, the sac that contains a hair shaft.
Folliculitis is infection of the hair follicle with purulent exudate in the
epidermis.
Hot tub folliculitis is almost always caused by P. aeruginosa, is usually
selflimited and no treatment is indicated.
59
Systemic therapy in cases of large and multiple lesions should be treated
with Penicillinase resistant antibiotics.
Figure 2: Folliculitis
(MEDICUS APP, 2020)
Etiology: S. aureus (most common), P. aeruginosa (from exposure to
inadequately chlorinated swimming pools, whirlpools and hot tubs),
Aeromonas hydrophila (following water exposure).
Treatment:
1st Line: Topical antibiotic therapy for mild cases of folliculitis such as
mupirocin ointment if staphylococcal etiology.
Oral Agents: cloxacillin & cephalexin DOT:
5-10 days
C. Impetigo
 Acute, highly contagious infection of the superficial layers of the
epidermis and common among children.
 Classified as either non-bullous (impetigo contagiosa) or bullous.
Figure 3: Non-Bullous & Bullous Impetigo

(MedicineNet, 2020) Treatment:
Etiology Preferred Regimen
Streptococcus sp. (Group A causes Mupirocin ointment 2% tid OR
honey crust impetigo) (Group B, C, G Fusidic acid 2% cream bid
are less common) DOT: 7-12days
Methicillin-susceptible Cloxacillin OR Cephalexin Mild to
Staphylococcus aureus bullous DOT: 7days
impetigo:
Suspected or confirmed Clindamycin or Cotrimoxazole or
methicillinresistant Staphylococcus Doxycycline
60
aureus bullous impetigo: DOT: 7days
D. Mastitis
 is an inflammation of breast tissue that sometimes involves an
infection.
 Poor breastfeeding technique and incomplete emptying are
contributing factors.
Figure 4: Mastitis
(Baby Center, 2020)
Etiology: S. aureus; Bacteroides sp. (less often); Peptostreptococcus;
Selected coagulase-negative staphylococci; Corynebacterium sp.-rare; can
cause distinctive granulomatous inflammation.
Treatment:
If MRSA is not present If MRSA is present or possible
OUTPATIENT
Cloxacillin 500mg PO qid OR Clindamycin 300mg PO qid OR

Cephalexin 500mg PO qid Cotrimoxazole 160/800mg 1-2 tabs PO
bid
INPATIENT
Oxacillin 2g IV q4h Vancomycin 30mg/kg/d IV in 2- 3 div

doses
E. Cellulitis
 is a common, potentially serious bacterial skin infection. The
affected skin appears swollen and red and is typically painful and
warm to the touch.
 infection involving the deeper dermis and subcutaneous fats.
Figure 5: Cellulitis
(WebMD, 2020)
Etiology:
61
For Purulent Cellulitis: Most cases of cellulitis are attributed to S. aureus.
For Non-purulent Cellulitis: Usually caused by beta-hemolytic Streptococci
(e.g. Group A, B, C, G streptococci) and
methicillin-susceptible Staphylococcus aureus (MSSA).
Treatment:
For Purulent Cellulitis
1st Line (Empiric Therapy to cover for S. aureus)
Oral: Cloxacillin Parenteral: Oxacillin & Cefazolin
2nd line (For suspected/confirmed MRSA):
Oral: Clindamycin, Cotrimoxazole Parenteral: Clindamycin, Linezolid,
or Doxycycline Vancomycin
For Non-purulent Cellulitis
1st line (empiric therapy to cover both Strep and Staph)
Oral: Cephalexin, Amoxicillin- Parenteral: Cefazolin or Ampicillin
Clavulanic acid + Sulbactam
2nd line (For suspected/confirmed MRSA):

Oral: Clindamycin or Cotrimoxazole, Clindamycin or Vancomycin or
Plus Doxycycline, amoxicillin Linezolid
F. Necrotizing Fasciitis/Gas Gangrene
 is a rare bacterial infection that spreads quickly in the body and can
cause death.
 It can destroy skin, fat, and the tissue covering the muscles within a
very short time. The disease sometimes is called flesh-eating
bacteria.
Figure 6: Necrotizing Fasciitis

(Millenium Family Practice, 2020)
Etiology: S. aureus (CA-MRSA), Group A streptococci, Clostridium sp.: C,
perfringens (most common), C. septicum, C. tertium
Treatment:
1st Line: Vancomycin, Piperacillin + Sulbactam
2nd Line: Cefotaxime, Clindamycin, Pen G, Clindamycin + Penicillin (For
group A streptococcal necrotizing fasciitis and clostridial myonecrosis)
III. VIRAL INFECTIONS OF THE SKIN
A. Chicken pox and Shingles
62
 Chickenpox (also known as varicella) is an acute, generalized viral
infection, with fever and a skin rash. Vesicles also form in mucous
membranes.
 It is usually a mild, self-limiting disease, but can be severely damaging
to a fetus.
 May developed Reye`s syndrome when aspirin is given to children
younger than 16 years of age who has chicken pox.
Figure 7: Chicken pox

(Healthline Media, 2020)
 Shingles (also known as herpes zoster) is a reactivation of the
varicella virus, often the result of immunosuppression.
 Shingles involves inflammation of sensory ganglia of cutaneous
sensory nerves, producing fluid-filled blisters, pain, and paresthesia.
Figure 8: Shingles
(Insider, 2020)
Etiology:
Herpes zoster virus (Varicella zoster virus)
Treatment:
Immunocompetent host, chickenpox:
Child age 2-12 y.o., mild to moderate disease: no treatment
For patients at increased risk of moderate or severe varicella; chronic
cutaneous or pulmonary diseases:
Aciclovir or Valaciclovir (DOT: 5 days)
B. Measles
 is an acute, highly communicable viral disease with fever,
conjunctivitis, cough, photosensitivity (light sensitivity), Koplik spots
in the mouth, and red blotchy skin rash
63
Figure 9: Measles
(CHOC, 2020)
 Koplik spots are small red spots, in the center of which can be seen a
minute bluish white speck when observed under a strong light.
Figure 10: Koplik spots

(American Family Physician, 2020)
Etiology: caused by measles virus (also known as rubeola virus). It is an
RNA virus in the family Paramyxoviridae
Treatment: Use Airborne Precautions for hospitalized patients until 4
days after the onset of rash. The incubation period for measles is
between 10 and 14 days. Measles can be prevented with
measlescontaining vaccine, which is primarily administered as the
combination measles-mumps-rubella (MMR) vaccine.
IV. FUNGAL INFECTIONS OF THE SKIN
A. Cutaneous Candidiasis
 The skin is infected with candida fungi. This type of infection is
fairly common. It can involve almost any skin on the body, but
most often it occurs in warm, moist, creased areas such as the
armpits and groin.
Etiology: Candida albicans Other Candida spp.
64
Figure 11: Cutaneous Candidiasis
(Science Dir
ect, 2020)
Treatment:
1st Line: Topical therapy for 3-5d
Clotrimazole 1% cream; Miconazole 2% cream; Ketoconazole 2% cream
applied bid.
2nd Line: If topical treatment does not work:
Fluconazole 100-200mg PO q week until normal nail anatomy restored
Alternatives: Itraconazole 200mg PO bid x 1 week x 3 consecutive
months or Terbinafine 250 mg PO od x 3 months
B. Tinea corporis/cruris
 Tinea corporis is a rash caused by a fungal infection. It's usually a red,
itchy, circular rash with clearer skin in the middle.
 Tinea corporis is a superficial dermatophyte infection characterized
by either inflammatory or noninflammatory lesions on the glabrous
skin.
Figure 12: Tinea corporis

(International Journal of Infectious Diseases, 2020)
 Tinea cruris is a fungal infection that causes a red and itchy rash in
warm and moist areas of the body. The rash often affects the groin
and inner thighs and may be shaped like a ring. Also known as “Jock
itch”
65
Figure 12: Tinea cruris
(PCDS, 2020)
Etiology: Certain spp. of dermatophytes of the following genera:
Epidermophyton, Microsporum and Trichophyton
Treatment:
1st line: Terbinafine 1% cream bid x 3-4 weeks (recommended) or
Ketoconazole 2% cream qd or bid x 2-4 weeks OR
Clotrimazole 1% cream, powder, solution bid x 2-4 weeks
2nd line: Topical therapy ineffective or intolerant to topical medications,

or with extensive and/or disabling, multifocal or inflammatory disease,
deeper infection with hair follicle involvement: Terbinafine or
Itraconazole or Fluconazole (oral)
C. Tinea pedis
also known as Athlete`s Foot
is a fungal infection that usually begins between the toes. It
commonly occurs in people whose feet have become very sweaty while
confined within tightfitting shoes.
Figure 13: Tinea pedis

(MSD manual, 2020)
Etiology: Trichophyton rubrum, Trichophyton interdigitale, Trichophyton
mentagrophytes.
Treatment:
1st line: Terbinafine 1% cream qd x 2-4 weeks (recommended) or
Ketoconazole 2% cream bid x 3-6 weeks or Clotrimazole 1% bid x 2-4
weeks
2nd line: Terbinafine or Fluconazole (oral)
66
D. Tinea versicolor (Pityriasis versicolor)
 is a common fungal infection of the skin. The fungus interferes
with the normal pigmentation of the skin, resulting in small,
discolored patches.
 Fine, scaly rash with patches of discolored skin with sharp
borders commonly found on back, underarms, upper arms, chest,
and neck.
Figure 14: Tinea Versicolor

(MSD manual, 2020)
Etiology: Malassezia furfur
Treatment:
1st Line: Ketoconazole 2% shampoo daily for 3 days;
Selenium sulfide 2.5% shampoo
Extensive disease: Fluconazole (oral) 2nd
Line: Itraconazole (oral)
E. Tinea capitis (ringworm)
 is a fungal infection of the scalp, involving both the skin and hair. It is
also known as scalp ringworm.
 Itchy, red, raised, scaly patches often sharply defined.
Figure 15: Tinea capitis

(Lineage Medical Inc., 2020) Etiology:
Trichophyton tonsurans, Microsporum canis
Treatment:
1st Line: Terbinafine (Oral)
2nd Line: Itraconazole, Fluconazole, or Griseofulvin (Oral)
V. EYE INFECTIONS
 Although the eye and skin have distinct anatomy, they are both in
direct contact with the external environment.
 An important component of the eye is the nasolacrimal drainage
system, which serves as a conduit for the fluid of the eye, called
tears.
67
 The conjunctiva is a frequent site of infection of the eye; like other
mucous membranes, it is also a common portal of entry for
pathogens.
VI. Bacterial Eye Infections:

A. Blepharitis
 is an inflammation of the eyelids in which they become red,
irritated and itchy with dandruff-like scales that form on the
eyelashes.
Figure 16: Blepharitis

(MSD Manual, 2020)
Etiology: unclear, but may include S. aureus and S. epidermidis as well as
associated seborrhea, rosacea, dry eye.
Treatment: Topical antibiotics may provide symptomatic relief. If
associated Acne rosacea: Doxycycline. Treatment involves patient
education about disease chronicity and need for long term commitment
to lid hygiene with regular application of warm compresses, gentle lid
massage and lid washing.
B. Hordeolum (Stye)
 is an acute, localized swelling of the eyelid that may be external
or internal and usually is a pyogenic (typically staphylococcal)
infection or abscess.
 red, painful bump on the surface of the eyelid. The bump may
resemble a pimple and be tender to the touch.
Figure 17:Hordeolum (Stye)

(MSD Manual)
Etiology:
External hordeolum: External infection of the superficial sebaceous
gland (eyelash follicle) and caused by S. aureus.
68
Internal hordeolum: Infection of the meibomian glands, and is also
called meibomianitis. It is usually caused by S. aureus, including
methicillinsensitive and –resistant species.
Treatment:
External hordeolum: (Preferred Regimen: No antibiotic), Warm moist
compress (40-45 degree Celsius) continuously using cotton, gauze or
face towel over the affected area for 10 to 15 minutes; may repeat as
often as necessary.
Internal hordeolum: Pediatric:
Cloxacillin (oral) Adults:
For MSSA: Cloxacillin (Oral) PLUS hot packs
For MRSA, community-associated: Cotrimoxazole (Oral)
For MRSA, hospital-acquired: Linezolid (Oral)
C. Bacterial Conjunctivitis
 is a condition characterized by inflammation of the conjunctiva, often
accompanied by a discharge of sticky fluid (described as acute
purulent conjunctivitis)
Figure 18: Bacterial Conjunctivitis

(MSD Manual,
2020)
Etiology & Treatment:

For Bacterial (non-gonococcal) conjunctivitis
Etiology: Preferred Regimen:
S. aureus, S. pneumoniae, Eye drops: Levofloxacin or
S. viridans, Tobramycin or Erythromycin or
Fusidic acid
H. influenzae, Moraxella sp. Eye drops: Tobramycin or
Levofloxacin
For Gonococcal Conjunctivitis
N. gonorrhoeae Ceftriaxone Plus Azithromycin Plus
Topical Levofloxacin or Tobramycin or
Erythromycin ointment
VII. Viral Eye Infections:
A. Herpes Keratitis
69
 is a viral infection of the eye caused by the herpes simplex virus
(HSV). There are two major types of the virus: Type I is the most
common and primarily infects the face, causing the familiar "cold
sore" or "fever blister." Type II is the sexually transmitted form of
herpes, infecting the genitals.
Figure 19: Herpes Keratitis

Etiology: Herpes simplex 1 and 2
Treatment: Ganciclovir 0.15% or Aciclovir 3% ophthalmic ointment
B. Viral Conjunctivitis
 is a highly contagious acute conjunctival infection usually caused by
adenovirus.
 Irritation, photophobia, and watery discharge may manifest and also
known as “Pink eye”.
Etiology: Adenovirus
Treatment: No antibiotic
Consider short course topical antibiotic-steroid drops one to two drops
every 3 to 4 hours for 7 to 14 days in cases with severe inflammation,
membranes or epithelial defects.
Figure 20: Viral Conjunctivitis

(Medscape, 2020)
VIII. Fungal Eye Infections:

A. Fungal keratitis
 is an infection of the cornea (the clear dome covering the colored part of
the eye) that is caused by a fungus.
70
Figure 21: Fungal keratitis
(University of IOWA,
2016)
Etiology:
Aspergillus, Fusarium, Candida
Treatment:
Obtain specimen for fungal wet mount and cultures. Empiric therapy is not
recommended for fungal keratitis. It is important to try to identify organism
Focus Questions
from corneal scrapings. Never give topical steroid and never patch the eye.
Daily debridement is advised to enhance penetration of anti-fungal agents.
Topical cycloplegic (atropine sulfate 1%) one drop 3 times a day until free
of pain.

1. What are the ways to prevent skin and eye infections?
2. What are the factors that leads to development of mild to severe skin
and eye infections?
Related Readings
Related readings will be posted via schoology to supplement the foundation

of the topics discussed in Unit 8 module.
Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT VIII - - - - - - - - - - - - - - - - - -
UNIT 9: Microbial Diseases of the Respiratory System
71
1. Determine the etiological agents affecting the respiratory
system;
2. Determine the drug of choice for specific disease of the
respiratory system; and
3. Describe the clinical manifestations of specific diseases of the
respiratory system.
Introduction
Indigenous microbiota of the Upper respiratory Tract (URT) may

cause opportunistic infections of the respiratory system. Infectious diseases
of the URT are more common than infectious diseases of the Lower
respiratory tract (LRT). They may predispose the patient to more serious
infections. LRT infections are the most common cause of death from
infectious diseases.
This unit will focus on the etiology of respiratory tract infections. It
includes the drug of choice for every specific diseases of both URTI & LRTI
based on the National Antibiotic Guidelines set by Department of
HealthPhilippines.

Key Terms:
 URTI – is an infection of your upper respiratory tract. This
includes your throat, nose, pharynx, larynx, sinuses, and
trachea (windpipe).
 LRTI – infection affecting the lower part of the breathing
system (the breathing tubes and lungs).
 Etiology of Disease – The science of the causes or origins of
disease
72
I.
Lecture Notes
In relation to the previous unit, you familiarize the various skin

and eye infections. In this unit, we will discover the different
infectious diseases that affects our respiratory system.
UPPER RESPIRATORY TRACT INFECTIONS (URTI)

A. Pharyngitis or Tonsillitis
 are infections in the throat that cause inflammation. If the tonsils are
primarily affected, it is called tonsillitis. If the throat is primarily
affected, it is called pharyngitis. If you have both, it’s called
pharyngotonsillitis.
 Tonsillopharyngitis is acute infection of the pharynx, palatine tonsils,
or both. Symptoms may include sore throat, dysphagia, cervical
lymphadenopathy, and fever.
Figure 1: Tonsillitis/Pharyngitis
(Healthline Media,2020)
Etiology: Group A, C, G; Streptococci; Fusobacterium Treatment:

1st Line Therapy
Pediatrics Adults
Phenoxymethylpenicillin (Pen V) Phenoxymethylpenicillin (Pen V)
or Amoxicillin trihydrate (Oral) Benzathine Penicillin G
2nd Line Therapy
Amoxicillin trihydrate, Amoxicillin trihydrate,
Erythromycin ethylsuccinate, Erythromycin ethylsuccinate,
Clarithromycin, Azithromycin Clarithromycin, Azithromycin
Alternative to the macrolides Alternative to the macrolides
for severe penicillin allergy: for severe penicillin allergy:
Clindamycin Clindamycin
B. ACUTE EPIGLOTTITIS
73
 rapidly progressive infection causing inflammation of the epiglottis
(the flap that covers the trachea) and tissues around the epiglottis
that may lead to abrupt blockage of the upper airway and death.
 Requires urgent hospitalization. May present with life-threatening
upper airway obstruction, especially in pediatrics.
Figure 2: Acute Epiglottitis

(Pulse Notes, 2020) Etiology:
H. influenzae Type b; S. pneumonia
Treatment:
Pediatric:
1st line: Ceftriaxone (parenteral)
2nd line: Ampicillin-Sulbactam (Parenteral)
Adult:
1st line: Ceftriaxone (Parenteral)
2nd line: Levofloxacin (Parenteral) plus
Clindamycin (Parenteral)
C. RHINOSINUSITIS
defined as inflammation of the sinuses and nasal cavity.
Can be divided among four subtypes: acute, recurrent acute,
subacute and chronic, based on patient history and a limited physical
examination.
Figure 3: Rhinosinusitis
(Clinic Barcelona, 2020)
Etiology: pneumonia; H. influenzae; M. catarrhalis; S. aureus; Anaerobic
bacteria; Some other streptococcal species
Treatment:
1st Line of Therapy: Co-amoxiclav 2nd
Line of therapy:
74
Pedia: Co-amoxiclav or Cefuroxime, For patients with severe penicillin
allergy (pediatric):
Type 1: Clarithromycin , Type 2: Cefuroxime
Adult: Doxycycline
For patients with severe penicillin allergy (adult): Type
1: Doxycycline, Type 2: Cefuroxime
II. Lower Respiratory Tract Infections (LRTI)
A. Bronchitis
 is a condition in which the airways in the lungs, called bronchial
tubes, become inflamed and cause coughing, often with mucus.
 This mucus and the swelling of the tubes make it harder for your
lungs to move oxygen in and carbon dioxide out of your body.
Figure 4: Bronchitis
(Study.com, 2020) Etiology:
Infants or children < 2y: Adenovirus (most common)
Children 2-5y: Respiratory syncytial virus; Parainfluenza 3 virus; Human
metapneumovirus
Adolescent and adults: Usually viral M. pneumoniae in 5%; Chlamydophyla
pneumoniae in 5%
Treatment:
Pedia: < 5yrs.: Antibiotics are indicated only with associated sinusitis or
heavy growth on throat culture for S. pneumoniae, Group A Streptococci,
H. influenzae; or there is no improvement in 1 week. Otherwise, treatment
is symptomatic.
Adult: Antibiotics are usually not indicated. Antitussive
+/- inhaled bronchodilators.
B. Influenza (Flu)
 Flu is a contagious respiratory illness caused by influenza viruses
that infect the nose, throat, and sometimes the lungs. It can cause
mild to severe illness, and at times can lead to death.
75
Figure 5: Flu virus
(News Medical, 2020)
Etiology: Influenza A and B

Treatment: Olsetamivir
C. Community Acquired Pneumonia (CAP)
 is one of the most common infectious diseases and is an important
cause of mortality and morbidity worldwide.
is defined as pneumonia that is acquired outside the hospital.
Pediatric CAP (PCAP) classification:
PCAP A/B (non-severe): No or mild dehydration; no malnutrition; no pallor;
awake; no signs of respiratory failure; respiratory rate of ≥50-≥60/min
(312mos.), ≥40-≤50/min (1-5yrs.), ≥30-≤35/min (>5 yrs.)
PCAP C (severe): Moderate dehydration; moderate malnutrition; with
pallor; irritable (+ intercostal/subcostal retractions, head bobbing,
cyanosis); respiratory rate of >60-≤70/min (3-12 mos.), >50/min (1-5 y),
>35/min (>5y); NO grunting; NO apnea
CAP D (very severe): Severe dehydration; severe malnutrition; with pallor;
lethargic/ stuporous/in coma (+ supraclavicular/intercostal/subcostal
retractions, head bobbing, cyanosis, grunting, apnea; respiratory rate
>70/min (3-12 mos.), >50/min (1-5 y), >35/min (>5y).
Etiology:
For Pediatric: S. pneumoniae in 30%-50%, H. influenzae type b in 10%-30%,
S. aureus, K. pneumoniae, Non-typeable H. influenzae
For Children (>5 years) and adolescents: S. pneumoniae, M. pneumoniae,
C. pneumoniae
For Adults: S. pneumoniae, H. influenzae, C. pneumoniae, M. catarrhalis
Enteric Gram (-) bacilli (among those with co- morbid illness) Treatment:
For Pediatric:
PCAP A or B:
If with complete Hib vaccination: Amoxicillin
If with no Hib vaccination or incomplete or unknown vaccination history:
Co-amoxiclav or cefuroxime, if allergic to Amoxicillin, consider macrolide:
Azithromycin or Clarithromycin
76
PCAP C:
If with complete Hib vaccination:
Penicillin G or Ampicillin (IV)
If with no Hib vaccination or incomplete or unknown vaccination history:
Ampicillin-sulbactam (IV) or Cefuroxime (IV) or Ceftriaxone (IV)
PCAP D:
Refer to Specialist. Admit to critical care unit, refer to specialist for
antibiotic guidance.
For Children (>5 years) and adolescents: Macrolides oral suspension such
as Erythromycin, Clarithromycin or Azithromycin
For Adults:
Without co-morbid illness: Amoxicillin or Azithromycin or Clarithromycin
With stable co-morbid illness: Co-amoxiclav or Cefuroxime axetil bid +/-
Azithromycin or Clarithromycin
D. EMPYEMA
 is defined as a collection of pus in the pleural cavity, gram-positive,
or culture from the pleural fluid. Empyema is usually associated with
pneumonia but may also develop after thoracic surgery or thoracic
trauma.
 pus gathers in the area between the lungs and the inner surface of
the chest wall called Pleural space.
Figure 6: Empyema
(Radiopedia, 2020)
Etiology:
Acute Empyema: S. aureus; S. pneumoniae; S. pyogenes; H. influenza
Chronic Empyema: Mostly anaerobic organisms Mycobacterium
tuberculosis
Treatment:
For Acute Empyema:
Pedia: Clindamycin + Ceftriaxone (IV)
Adult: Vancomycin + Ampicillin-Sulbactam or Vancomycin + Ceftriaxone +
Metronidazole
For Chronic Empyema:
Refer to specialist and rule out for possible tuberculosis
77
E. Hospital Acquired Pneumonia (HAP) and Ventilator-associated
pneumonia (VAP)
 Hospital Acquired Pneumonia or also known as Nosocomial
Pneumonia is an infection of the lungs that occurs during a hospital
stay.
 includes pneumonia that was not incubating at the time of hospital
admission and develops at least 48 hours after hospital admission in
patients who are not receiving mechanical ventilation.
 Ventilator-associated pneumonia (VAP) is pneumonia that develops
48 hours or longer after mechanical ventilation is given by means of
an endotracheal tube or tracheostomy.
 results from the invasion of the lower respiratory tract and lung
parenchyma by microorganisms.
ETIOLOGY & TREATMENT:
PEDIATRIC POPULATION
ETIOLOGY TREATMENT
S. aureus; S. pneumonia Vancomycin or Linezolid
P. aeruginosa, A. baumanii, K. Ceftazidime +
pneumoniae; Klebsiella spp., E. coli, Aminoglycoside: Amikacin or
Enterobacter spp.; Proteus spp.; Serratia Gentamicin
marcesens
For Multi-drug resistant (MDR) Piperacillin-Tazobactam or
pathogens: Meropenem or Cefepime
P. aeruginosa, K. pneumonia,
Acinetobacter spp., Stenotrophomonas
maltophilia, Burkholderiacepacia,
Methicillin-resistant S. aureus
FOR ADULTS
Not at high risk of mortality and no Piperacillin-Tazobactam or

factors increasing the likelihood of MRSA Cefepime or Meropenem
(IV)
Not at high risk of mortality but with Piperacillin-Tazobactam or
factors increasing the likelihood of MRSA Cefepime or Meropenem or
Aztreonam PLUS Vancomycin
or Linezolid
High risk of mortality and with risk factor Piperacillin-Tazobactam or
for MDR Cefepime or Meropenem or
Aztreonam PLUS Levofloxacin
or Amikacin PLUS
Vancomycin or Linezolid
Focus Questions
78
1. Why is it essential to rule out the specific pathogens before giving
treatment to the patient?
2. What are the factors that contributes to the development of respiratory
infections?
Related Readings
Related readings will be posted via Schoology to supplement the
foundation of the topics discussed in Unit 9 module.
Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT IX - - - - - - - - - - - - - - - - - - -
UNIT 10: Microbial Diseases of the

Digestive System
1. Determine the etiological agents affecting the digestive system;
2. Determine the drug of choice for specific disease of the digestive
system; and
digestive system.
Introduction
The GI tract consists of a long tube with many expanded areas

designed for digestion of food, absorption of nutrients, and elimination of
undigested materials. Transient and resident microbes continuously enter
and leave the GI tract. Most of the microorganisms ingested with food are
destroyed in the stomach and duodenum by the low pH of gastric contents
and are inhibited from growing in the lower intestines by the resident
microbiota (microbial antagonism).
This unit will focus on the etiology of infections in our digestive
system. It includes the drug of choice for every specific diseases digestive
system based on the National Antibiotic Guidelines set by Department of
HealthPhilippines.
79
Key Terms:
 COLITIS – the Inflammation of the colon (the large intestine).
 DIARRHEA – An abnormally frequent discharge of semisolid or
fluid fecal matter. Some laboratory workers define diarrheal
specimens as “stool specimens that conform to the shape of
the container.”
 DYSENTERY- Frequent watery stools, accompanied by
abdominal pain, fever, and dehydration. The stool specimens
may contain blood or mucus.
Lecture Notes
Did you know that there are pathogens that can caused infections
to the gastrointestinal tract? Let`s find out the clinical
manifestations and treatment of various Infections.
GIT
I. GIT Bacteria Infections

A. Bacterial Gastritis and Gastric Ulcers
 Infection with Helicobacter pylori can cause chronic bacterial gastritis
and duodenal ulcers.
 Gastritis is suspected when a person has upper abdominal pain with
nausea or heartburn.
 Urea breath test can be used as diagnostic technique for gastric ulcer.
 People with duodenal ulcers may experience gnawing, burning,
aching, mild-to-moderate pain just below the breastbone, an empty
feeling, and hunger.
Figure 1: Gastric Ulcer

(Good Times, 2020)
80
Etiology: H. pylori is a curved, microaerophilic, capnophilic, Gram-negative
bacillus that is found on the mucus- secreting epithelial cells of the stomach
Treatment:
Omeprazole PLUS Clarithromycin PLUS Amoxicillin or Metronidazole
B. Cholera
 Cholera is an acute, bacterial diarrheal disease with profuse watery
stools, occasional vomiting, and rapid dehydration.
 Transmission occurs via the fecal–oral route, contact with feces or
vomitus of infected people, ingestion of fecally contaminated water
or foods (especially raw or undercooked shellfish and other seafood)
Etiology: The etiologic agents of cholera are certain biotypes of Vibrio

cholerae
Figure 2: Vibrio cholerae

(Shutterstock, 2020)
Treatment:
Intravenous and oral hydration are both associated with greatly decreased
mortality and remain the mainstay of treatment for cholera. Antibiotics are
given as soon as the patient can tolerate oral medication. Doxycycline is
recommended as first-line treatment for adults (including pregnant
women) and children. If resistance to doxycycline is documented,
azithromycin and ciprofloxacin are alternative options.
C. Typhoid Fever
 a systemic bacterial disease with fever, severe headache, malaise,
anorexia, a rash on the trunk in about 25% of patients, nonproductive
cough, and constipation.
Etiology: Salmonella typhi (also known as the typhoid bacillus), a
Gramnegative bacillus that releases endotoxin and produces exotoxins.
Figure 3: Salmonella typhi

(Outbreak News Today, 2020)
81
Treatment: Ciprofloxacin (Oral or IV)
Alternatives: chloramphenicol, amoxicillin or cotrimoxazole
II. GIT Parasitic Infections
A. Amebiasis
 Amebiasis or amebic dysentery is a protozoal, gastrointestinal
infection that may be asymptomatic, mild, or severe and is often
accompanied by dysentery, fever, chills, bloody or mucoid diarrhea or
constipation, and colitis.
 The amebas may invade mucous membranes of the colon, forming
abscesses and amebomas, which are granulomas that are sometimes
mistaken for carcinoma.
Etiology: Entamoeba histolytica
Figure 3:Entamoeba histolytica

(CDC, 2020)
Treatment: Metronidazole (Oral or IV)
Intravenous and oral hydration as supportive treatment
B. Giardiasis
 is a protozoal infection of the duodenum (the uppermost portion of
the small intestine) and may be asymptomatic, mild, or severe.
 Patients experience diarrhea, steatorrhea (loose, pale, malodorous,
fatty stools), abdominal cramps, bloating, abdominal gas, fatigue, and
possibly weight loss.
Etiology: Giardia lamblia (also called Giardia intestinalis), a flagellated

protozoan
Figure 4:Giardia lamblia

(Southwest Journal, 2019)
C. Balantidiasis
82
 is a protozoal gastrointestinal infection of the colon causing diarrhea
or dysentery, colic, nausea, and vomiting.
Etiology: Balantidium coli, a ciliated protozoan
Figure 5:Balantidium coli

(CDC,2020)

III. GIT Viral Infections
Table 1: Classification of Viral Hepatitis

(Burton's Microbiology for the Health Sciences, 2015)
Focus Questions
83
1. What are GIT diseases that are currently prevalent in our country?
2. What are the factors that contributes to the development of various GIT
infections?
Related Readings
Learning Activities
- - - - - - - - - - - - - - - - - - - END OF UNIT X - - - - - - - - - - - - - - - - - - -
UNIT 11: Microbial Diseases of the

Cardiovascular and Lymphatic System
1. Determine the etiological agents affecting the cardiovascular
and lymphatic system;
2. Determine the drug of choice for specific disease of the
cardiovascular and lymphatic system; and
cardiovascular and lymphatic system.
Introduction
The circulatory system consists of the cardiovascular system and the

lymphatic system. The cardiovascular (cardio for heart, and vascular for the
various types of blood vessels) system includes the heart, arteries,
capillaries, veins, and blood. Blood is composed of plasma (the liquid
portion) plus the various cellular elements. Bergh et al., (2017) mentioned
that severe infections in adulthood are associated with subsequent short-
term cardiovascular disease. Whether hospital admission for sepsis or
pneumonia is associated with persistent increased risk (over a year after
infection) is less well established.
On the contrary, lymphatic system consists of lymphatic vessels,
lymphoid tissue (including lymph nodes, tonsils, thymus, and spleen), and
lymph (the liquid that circulates through the lymphatic system). Lymph
occasionally picks up microorganisms from the intestine, lungs, and other
areas, but these transient organisms are usually quickly engulfed by
phagocytic cells in the liver and lymph nodes. This unit will focus on the
84
etiology of the cardiovascular and lymphatic system infections. It includes
the drug of choice for every specific diseases based on the National
Antibiotic Guidelines set by Department of Health-Philippines.

Key Terms:
▪ Infectious Disease – diseases that are caused by pathogens, following
colonization of some body site by the pathogen.
▪ Etiology of disease – The science of the causes or origins of disease
▪ Etiological agent – It refers to a viable microorganism, or its toxin, that
causes or may cause disease in humans or animals.
▪ Endocarditis – Inflammation of the endocardium— the endothelial
membrane that lines the cavities of the heart.
▪ Myocarditis – Inflammation of the myocardium—the muscular walls of
the heart.
▪ Pericarditis – Inflammation of the pericardium—the membranous sac
around the heart.
▪ Lymphadenitis – Inflamed and swollen lymph nodes.
▪ Lymphangitis – Inflamed lymphatic vessels.
Lecture Notes
Did you know that there are microorganisms that can cause infection to the
heart and various parts of our lymphatic system? As a future pharmacist, it
is essential to familiarize the treatment to various infectious
diseases of the cardiovascular & lymphatic system
I. CARDIOVASCULAR INFECTIONS:
▪ Cardiovascular (cardio for heart, and vascular for the various types of
blood vessels) system includes the heart, arteries, capillaries, veins,
and blood.
▪ Blood is composed of plasma (the liquid portion) plus the various
cellular elements.
▪ The presence of bacteria in a person’s bloodstream is known as
bacteremia.
85
Figure 1: Bacteremia
(Health Jade, 2019)
▪ Septicemia is a disease in which the patient experiences chills, fever,

and prostration (extreme exhaustion) and has bacteria and/or their
toxins in their bloodstream.
Figure 2: Sepsis
(The Hospital for Sick Children, 2020)
▪ Risk Factors for cardiovascular Infections:

✔ Damage Heart valves
✔ Congenital heart Defects
✔ Implanted heart Device
✔ History of endocarditis
✔ History of illegal IV drug use
✔ Poor Dental Health
✔ Long Term-Catheter use
✔ Geriatric Population
▪ Endocarditis is a life-threatening inflammation of the inner lining of
your heart's chambers and valves (endocardium).
86
Figure 3: Endocarditis
(Jungle Roots Children's Dentistry & Orthodontics, 2020)
▪ Endocarditis is usually caused by an infection. Bacteria, fungi or other

germs from another part of your body, such as your mouth, spread
through your bloodstream and attach to damaged areas in your
heart.
Figure 4: Endocarditis Cross Section

(The Society for Cardiovascular Angiography and Interventions, 2020)
II. Infective Endocarditis (IE) Diagnostic Criteria

⮚ In general, diagnostic criteria for IE is also known as Modified
Duke`s criteria.
A. Pathological criteria (any one):
1. Histology or culture
of a cardiac
vegetation, an
embolized
87
vegetation, or
intracardiac abscess
from the heart
revealing
microorganisms.
2. Active endocarditis
B. Clinical Criteria:
MAJOR CRITERIA MINOR CRITERIA
1. Positive blood culture 1. Predisposing factor:
with typical IE microorganism, known cardiac lesion,
defined as one of the recreational drug injection
following: 2. Fever >38°C
Typical microorganisms consistent 3. Embolism evidence:
with IE from 2 separate blood arterial emboli, pulmonary
cultures and presence of viridians infarcts, Janeway
group Streptococci, or S. bovis lesions, conjunctival/intracranial
including S. aureus, or hemorrhages
communityacquired enterococci Or 4. Immunological
Coxiella burnetii detected by at least problems: glomerulonephritis,
one positive blood culture or IgG Osler’s nodes, Roth spots,
antibody titer for Q fever phase 1 rheumatoid factor
antigen. 5. Microbiologic evidence:
Positive blood culture (that
2. Evidence of endocardial doesn't meet a major
involvement with positive criterion) or serologic
echocardiogram. evidence of infection with
organism consistent with IE
but not satisfying major
criterion
Table 1: Clinical Criteria for Infective Endocarditis
(DOH- National Antibiotic Guidelines, 2017) III.
Microbial Diseases of the Heart:
1. Native Valve Infective Endocarditis
⮚ One of the most important life-threatening infectious diseases,
and its timely diagnosis, antibiotic treatment, and
management of complications is critical to optimal outcomes.
⮚ Typical symptoms are variable and depend on the valve
involved, the age and co-morbid diseases status of the patient,
the etiologic organism, the extent and location of metastatic
complications, and the duration of the infection.
88
Figure 5: Native Valve Infective Endocarditis
(Massachusetts Medical Society, 2020) Etiology
& Treatment:
A. FOR EMPIRIC THERAPY:
Etiology: Streptococcus viridans (30-40%), Other streptococci (15-25%),
Enterococci (5-18%), Staphylococci (20-35%), Haemophilus sp.,
Aggregatibacter sp., Cardiobacterium hominis, Eikenella corrodens, and
Kingella species (HACEK) (5%), Culture negative 10% Treatment:
COMMUNITY ACQUIRED HEALTHCARE-ASSOCIATED
PEDIATRICS
Ampicillin-sulbactam IV PLUS Vancomycin IV PLUS Gentamicin IV
Gentamicin IV PLUS Cefepime IV or Ceftazidime IV
ADULTS
Ampicillin IV PLUS Gentamicin IV or Vancomycin IV PLUS Gentamicin IV
Vancomycin PLUS Ceftriaxone IV or PLUS Cefepime IV or Ceftazidime IV
Gentamicin IV
❖ At least 3 sets of blood cultures must be obtained.
❖ Transthoracic echocardiogram (TTE) must be done in all suspected
cases.
❖ Transesophageal echo (TEE) must be done when TTE is negative if
there is ongoing suspicion of IE or concern about intracardiac
complications.
B. PATHOGEN-SPECIFIC TREATMENT:
PEDIATRIC ADULT
Aqueous crystalline Penicillin G Na Pen G or Ceftriaxone IV PLUS
IV or Ceftriaxone IV Gentamicin IV
If unable to tolerate Penicillin or
89
Ceftriaxone: Vancomycin
B.1. Etiology: S. viridans or S.
bovis (S. gallolyticus) with
Penicillin G MIC
❖ PEDIATRIC: Suspect occult bowel pathology (e.g., tumor) when the

etiologic agent is S. bovis.
❖ ADULT: A 2-week combination regimen is reasonable with
uncomplicated IE, rapid treatment response and without renal
disease. Treatment with vancomycin must achieve trough
concentration of 10-15 mcg/mL. Obtain the trough level before the
4th dose.
B.2. Etiology: Enterococci, penicillin-resistant, aminoglycoside-sensitive
Treatment: Vancomycin PLUS Gentamicin (IV) (Both Pedia & Adult)

❖ Potential increased nephrotoxicity and ototoxicity with this
combination. Dose must be adjusted to achieve vancomycin target
trough concentration of 15-20 mcg/mL.
B.3. Etiology: Methicillin-susceptible Staphylococcus aureus (MSSA) or

Methicillin-resistant S. aureus (MRSA)
Treatment:
Methicillin-susceptible Staphylococcus aureus (MSSA)
PEDIATRICS ADULT
Oxacillin IV WITH or WITHOUT Oxacillin or Cefazolin (IV)
Gentamicin IV
Methicillin-resistant S. aureus (MRSA)
Vancomycin IV Vancomycin IV
B.4. Etiology: Haemophilus sp, Aggregatibacter sp, Cardiobacterium

hominis, Eikenella corrodens, and Kingella species (HACEK)
Treatment:
Ceftriaxone or Ampicillin-Sulbactam IV (Both Pediatric & Adult)
2. PROSTHETIC VALVE INFECTIVE ENDOCARDITIS
⮚ refers to infection of one or more prosthetic heart valves. The timing
of the infection after surgical valve replacement reflects different
pathogenic mechanisms that, in turn, influence the clinical
presentation.
A. EMPIRIC THERAPY:
Etiology:
90
Early (<2 months post-surgery): S. epidermidis and S. aureus mostly Late
(>2 months post-surgery): S. epidermidis, S. viridans, enterococci, S.
aureus
Figure 6: Prosthetic Valve Infective Endocarditis

(American Society for Microbiology, 2020)
Treatment: (Both Pedia & Adult)
Vancomycin(IV) PLUS Gentamicin (IV) PLUS Rifampicin (P.O.)
Early surgical consultation is recommended. Surgical indications:
• Signs and symptoms of congestive heart failure due to valve
Dehiscence.
• Intracardiac fistula and prosthetic valve dysfunction
• Persistent bacteremia despite 5-7 days of treatment
• Heart block, annular or aortic abscess
• Recurrent emboli
• Caused by fungal or highly resistant organisms
B. PATHOGEN SPECIFIC THERAPY
Etiology: Methicillin-susceptible S. aureus (MSSA)
Treatment: For Pediatrics and Adults; Oxacillin (IV) PLUS Rifampicin
(P.O.)
PLUS Gentamicin (IV)
Etiology: Methicillin-resistant S. aureus (MRSA)
Treatment: For Pediatrics and Adults; Vancomycin (IV) PLUS Rifampicin
(P.O.) PLUS Gentamicin
3. BACTERIAL PURULENT PERICARDITIS
⮚ is defined as a localized infection of the pericardial space
characterized by gross pus in the pericardium or microscopic
purulence (>20 leukocytes per oil immersion field).
⮚ This distinction is important since purulent material in the

pericardium is not synonymous with infectious pericarditis, and
not all infections produce purulent effusions.
91
⮚ Purulent pericarditis was a frequent complication of pneumococcal
pneumonia.
⮚ In modern times, most cases of purulent pericarditis are
associated with nosocomial bloodstream infections (such as in the
setting of dialysis), thoracic surgery, or immunosuppression (eg,
HIV, chemotherapy).
Figure 7: Bacterial Purulent Pericarditis

(Springer Nature Switzerland, 2020)
A. Etiology: S. aureus, Group A Streptococcus, S.

pneumoniae, Enterobacteriaceae Treatment:
PEDIATRICS ADULTS
Vancomycin (IV) PLUS Ceftriaxone Vancomycin (IV) PLUS Ceftriaxone
(IV) (IV), Levofloxacin (IV) or
Aminoglycosides such as
(Gentamicin or Amikacin)
❖ Initial antibiotic regimen should consist of 2 or more drugs, when
etiologic agent cannot be detected rapidly. Drainage usually
necessary.
B. Etiology: Methicillin-resistant S. aureus is isolated and/or with history
and clinical features for MRSA infection; S. pneumoniae resistant to
extended-spectrum cephalosporins, or nosocomial infections.

Vancomycin IV
❖ Empirical and determined partly by the nature of concomitant
infection. Once a pathogen is isolated and the antimicrobial
susceptibilities are known, the most specific antimicrobial agent is
continued IV for 3-4 weeks.
C. Etiology: S. pneumoniae (including penicillin-resistant strains), N.
meningitidis, H. influenzae type B (for children who may be inadequately
immunized)
92
Cefuroxime or Ceftriaxone
❖ An aminoglycoside should be added when:
1. Purulent pericarditis occurs after surgery
2. in association with UTI
3. in the immunocompromised
4. ACUTE RHEUMATIC FEVER
⮚ is a nonsuppurative sequela that occurs two to four weeks following
group A Streptococcus (GAS) pharyngitis and may consist of arthritis,
carditis, chorea, erythema marginatum, and subcutaneous nodules.
⮚ Damage to cardiac valves may be chronic and progressive, resulting
in cardiac decompensation.
Figure 8: Acute Rheumatic Fever

(Slideshare.net, 2020)
Etiology: Group A Streptococcus spp.
Primary Prevention:
1st Line Therapy
Pediatrics Adults
Phenoxymethylpenicillin (Pen V) Phenoxymethylpenicillin (Pen V)
or Amoxicillin trihydrate (Oral) Benzathine Penicillin G
2nd Line Therapy
Amoxicillin trihydrate, Amoxicillin trihydrate,
Erythromycin ethylsuccinate, Erythromycin ethylsuccinate,
Clarithromycin, Azithromycin Clarithromycin, Azithromycin
Alternative to the macrolides for Alternative to the macrolides for
severe penicillin allergy: severe penicillin allergy:
Clindamycin Clindamycin
❖ Therapy for acute rheumatic fever is symptomatic to control the

inflammation, decrease the fever, and keep cardiac failure in check.
Secondary Prevention (Prevention of Recurrent Attacks):
Benzathine Pen G (IV) or Pen V (P.O.)
For individuals allergic to penicillin: Erythromycin or Azithromycin
93
❖ Referral to a pediatric cardiologist is important. Prevention of
recurrent episodes of Group A Streptococcus (GAS) pharyngitis is the
most effective method to prevent severe Rheumatic Heart Disease
(RHD).
❖ An individual with a previous attack of rheumatic fever in whom GAS
pharyngitis develops is at high risk for a recurrent attack of rheumatic
fever.
IV. Lymphatic System Infections:
⮚ The lymphatic system consists of lymphatic vessels, lymphoid tissue
(including lymph nodes, tonsils, thymus, and spleen), and lymph (the
liquid that circulates through the lymphatic system).
⮚ Lymph occasionally picks up microorganisms from the intestine, lungs,
and other areas, but these transient organisms are usually quickly
engulfed by phagocytic cells in the liver and lymph nodes.
⮚ The lymphatic system contains many lymphocytes
V. Microbial Diseases of Lymphatic System
1. MUMPS
⮚ Mumps is an acute viral infection characterized by fever and swelling
and tenderness of the salivary glands.
⮚ Complications can include orchitis (inflammation of the testes),
oophoritis (inflammation of the ovaries), meningitis, encephalitis,
deafness, pancreatitis, arthritis, mastitis, nephritis, thyroiditis, and
pericarditis.
⮚ Transmission occurs via droplet spread and direct contact with the
saliva of an infected person.
Figure 9: MUMPS
(Medic Test, 2020)
Etiology: Mumps is caused by mumps virus, an RNA virus in the
genus Rubulavirus, family Paramyxoviridae.
Treatment:
⮚ Mumps vaccine is the best way to decrease your risk of getting
mumps.
94
⮚ It is usually given as part of a combination vaccine that protects
against three diseases: measles, mumps, and rubella (MMR).
⮚ This vaccine is only licensed for use in children who are 12 months
through 12 years of age. Children should get two doses of MMR
vaccine:
⮚ the first dose at 12 through 15 months of age, and ⮚
the second dose at 4 through 6 years of age.
⮚ Patients diagnosed with mumps should be isolated for 5 days from
the onset of symptoms to minimize the risk of infecting others.
2. Infectious mononucleosis
⮚ Infectious mononucleosis (also called “mono” or the “kissing disease”)
is an acute viral disease.
⮚ It may be asymptomatic or may be characterized by fever, sore throat,
lymphadenopathy (especially posterior cervical lymph nodes),
splenomegaly (enlarged spleen), and fatigue.
⮚ Infectious mononucleosis is usually a self-limited disease of 1 to
several weeks’ duration and rarely fatal
⮚ Transmission occurs from person to person by direct contact with
saliva.
⮚ Kissing facilitates spread among adolescents. EBV can be transmitted
via blood transfusion.
Figure 10: Infectious mononucleosis

(MSD Manual, 2020)
Etiology:
⮚ The etiologic agent of infectious mononucleosis is Epstein–Barr virus
(EBV), which is also known as human herpesvirus 4.
⮚ It is a DNA virus in the family Herpesviridae.
⮚ EBV infects and transforms B cells, although it also infects other types
of cells.
⮚ EBV is known to be oncogenic (cancer causing), causing or being
associated with lymphomas (e.g., Hodgkin disease and Burkitt
95
lymphoma), carcinomas (e.g., nasopharyngeal carcinoma and gastric
carcinoma), and sarcomas, among other cancers.
Treatment:
⮚ Treatment mainly involves getting enough rest, healthy diet and
drinking plenty of fluids.
⮚ Pain relievers: Nonsteroidal anti-inflammatory drugs (NSAIDs) ease
fever, inflammation, headaches and muscle aches.
Focus Questions
Guide Questions for Unit 11 discussions:
1. What are the ways to prevent cardiovascular and lymphatic system
infections?
2. What are the factors that leads to development of mild to severe
cardiovascular and lymphatic system infections?
Related Readings

Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT XI- - - - - - - - - - - - - - - - - - -
UNIT 12: Microbial Diseases of the Nervous System

1. Determine the etiological agents affecting the nervous system;
2. Determine the drug of choice for specific disease of the nervous
system; and
nervous system.
Introduction
The nervous system is composed of the CNS and the Peripheral

nervous system. The CNS consists of the brain, the spinal cord, and the
96
three membranes meninges that cover the brain and spinal cord. The
peripheral nervous system consists of nerves that branch from the brain
and spinal cord. Moreover, Faucher & Ploy (2018) mentioned that Bacterial
diseases of the nervous system comprise a broad range of diseases with
their related pathogens. Many bacterial infections can spread to the
nervous system, most of them by the hematogenous route.
This unit will focus on the etiology of nervous system infections. It
includes the drug of choice for every specific diseases nervous system
infections based on the National Antibiotic Guidelines set by Department of
Health-Philippines.

Key Terms:
▪ Meninges – the three membranes (the dura mater, arachnoid, and pia
mater) that line the skull and vertebral canal and enclose the brain and
spinal cord.
▪ Encephalitis – infection affecting the lower part of the breathing system
(the breathing tubes and lungs).
▪ Encephalomyelitis – Inflammation of the brain and spinal cord
▪ Meningitis – Inflammation of the membranes (meninges) that surround
the brain and spinal cord and can because by the ingestion of poisons,
the ingestion or injection of drugs, a reaction to a vaccine, or a
pathogen.
▪ Meningoencephalitis – Inflammation of the brain and meninges.
Lecture Notes
In relation to the previous unit, you familiarize the various

cardiovascular & lymphatic system infections. In this unit, we will
discover the different infectious diseases that affects our nervous
system.
▪ Myelitis – Inflammation of the spinal cord

I. Nervous System Infection:
97
⮚ The CNS is well protected and remarkably resistant to infection; ⮚
It is encased in bone, bathed and cushioned in cerebrospinal fluid
(CSF), and nourished by capillaries.
⮚ These capillaries make up the blood–brain barrier, supplying
nutrients but not allowing larger particles, such as
macromolecules (e.g., antibodies and most antibiotics), cells of
the immune system, and microorganisms, to pass from the blood
into the brain.
⮚ There are no indigenous microbiota of the nervous system.
⮚ Microbes gain access to the CNS through trauma (fracture medical
procedure), via the blood and lymph to the CSF, or along the
peripheral nerves.
II. Viral Nervous System Infections:
1. Encephalitis
⮚ an inflammation of the brain usually caused by viral infections. The
classic presentation is encephalopathy with diffuse or focal
neurologic symptoms, including the following: behavioral and
personality changes, with decreased level of consciousness, neck
pain, stiffness, photophobia, generalized or focal seizures.
⮚ Infection in neonates may include the following: herpetic skin lesions
over the presenting surface from birth or with breaks in the skin,
oropharyngeal involvement, keratoconjunctivitis, seizure, irritability,
bulging fontanels. Severe signs include jaundice, hepatomegaly and
shock.
Figure 1: Encephalitis (MyHealth

Malaysia, 2020)
▪ If Encephalitis is associated with measles, influenza, enteroviruses,
arboviruses
▪ Treatment:
✔ Supportive treatment
98
✔ Children should be immunized with measles vaccine
at 9 months, and measles, mumps, rubella (MMR),
and varicella vaccines at 12 months.
✔ A booster of MMR is given at 4-6 years old.
▪ If Encephalitis is caused by Herpes simplex
▪ Treatment: Aciclovir
2. Viral Meningitis
⮚ Viral meningitis is also known as aseptic meningitis and nonbacterial
or a bacterial meningitis.
⮚ It is a relatively common disease but, fortunately, is rarely serious.
⮚ Acute illness rarely exceeds 10 days duration.
⮚ Viral meningitis is characterized by sudden onset of febrile illness with
the signs and symptoms of meningeal involvement.
⮚ CSF findings include the presence of mononuclear white blood cells,
increased protein levels, normal glucose levels, and the absence of
bacteria, rash may develop.
⮚ When caused by an enterovirus, GI and respiratory symptoms may
occur.
Figure 2: Viral Meningitis

(Meningitis Research Foundation, 2020)
Etiology:
The most common causes of viral meningitis in the United States are
enteroviruses. Other causes include coxsackie viruses, arboviruses,
measles virus, mumps virus, herpes simplex viruses and VZVs,
lymphocytic choriomeningitis virus, and adenoviruses.
Treatment:
⮚ Viral meningitis usually resolves spontaneously over weeks or,
occasionally and treatment is mainly supportive.
⮚ Acyclovir (for suspected herpes simplex or herpes zoster) and
antiretroviral drugs (for HIV infection).
3. Rabies
⮚ is a usually fatal, acute viral encephalomyelitis of mammals, with
mental depression, restlessness, headache, fever, malaise,
paralysis, salivation, spasms of throat muscles induced by a slight
breeze or drinking water, convulsions, and death caused by
respiratory failure.
99
⮚ The paralysis usually starts in the lower legs and moves upward
through the body.
⮚ Rabies is endemic in every country of the world except Antarctica
and in every state except Hawaii.
⮚ Transmission is usually via the bite of a rabid animal, which
introduces virus-laden saliva.
Figure 3: Rabies (Jose

Ramon Alonso, 2016)
Etiology:
Rabies is caused by rabies virus, a bullet-shaped, enveloped RNA virus in
the family Rhabdoviridae.
Treatment:
Preexposure rabies prophylaxis: Human diploid cell rabies vaccine (HDCV),
A total of three 1-mL doses are given IM, one each on days 0, 7, and
between day 21 and 28.
Postexposure rabies prophylaxis:

⮚ The wound is cleansed immediately and thoroughly with soap and
water or benzalkonium chloride.
⮚ Deep puncture wounds are flushed with soapy water using moderate
pressure.
⮚ Wounds are usually left open.
⮚ Rabies immune globulin 20 IU/kg is infiltrated around the wound for
passive immunization; if injection volume is too much for distal areas
(eg, fingers, nose), some rabies immune globulin may be given IM.
⮚ HDCV is given in a series of four 1-mL IM injections (deltoid area is
preferred), beginning on the day of exposure (day 0), in a limb other
than the one used for rabies immune globulin.
III. Fungal Nervous System Infections
1. FUNGAL MENINGITIS
100
⮚ Candida may enter the central nervous system by hematogenous
spread, at the time of craniotomy, or through a ventricular shunt.
Manifestations of Candida meningitis may be similar to those of
acute bacterial meningitis. Culture of the CSF is the gold standard for
diagnosis.
⮚ Infection with the encapsulated yeast Cryptococcus neoformans can
result in harmless colonization of the airways, meningitis or
disseminated disease, especially in persons with defective
cellmediated immunity.
⮚ Cryptococcal meningitis is usually fatal without appropriate therapy,
and death may occur from 2 weeks to several years after symptom
onset. The most common symptoms include headache and altered
mental status, personality changes, confusion, lethargy, obtundation,
and coma.
Figure 4: Fungal meningitis

(CDC, 2020) Etiology
& Treatment:
For Candida meningitis: Amphotericin B deoxycholate (IV), however, BUN,

creatinine and K+ should be monitored at least weekly. Removal of shunts is
recommended.
For Cryptococcal Meningitis (NON-AIDS)

Induction Phase: Amphotericin B deoxycholate (IV)
Consolidation Phase: Fluconazole (P.O.)
❖ The ideal regimen includes flucytosine in the induction phase, but this
drug is not available in the Philippines. If CSF pressure >25 cm H20,
repeat the lumbar tap to drain fluid and control pressure.
For Cryptococcal Meningitis associated with HIV/AIDS
Induction Phase: Amphotericin B deoxycholate (IV) PLUS Fluconazole (IV)
Consolidation Phase: Fluconazole (IV or P.O.)
Suppression (chronic maintenance therapy): Fluconazole (IV or P.O.)
IV. Bacterial Nervous System Infections
1. ACUTE BACTERIAL MENINGITIS
101
⮚ is an inflammatory disease of the leptomeninges, the tissues
surrounding the brain and spinal cord as proven by a positive
bacterial CSF culture, PCR, gram stain or antigen test; or suspected by
clinical characteristics and/or CSF markers of inflammation.
⮚ In children, common signs and symptoms include fever, irritability,
poor feeding, bulging fontanel and seizures.
⮚ In adults, the classic triad of acute bacterial meningitis consists of
fever, nuchal rigidity, and a change in mental status.
⮚ Once suspected and awaiting laboratory results, empiric therapy
should be started right away to prevent complications and mortality.
Figure 5: Bacterial Meningitis

(Alamy Stock Photo, 2020)
▪ < 2 MONTHS OLD
Etiology: Escherichia coli, Streptococcus pneumoniae, Klebsiella,
Enterobacter, Group B Streptococcus (rare)
Treatment: Ampicillin or Cefotaxime IV/IM
▪ > 2 MONTHS - 5 YRS

Etiology: S. pneumoniae, H. influenzae, N. meningitidis (less common)
Treatment: Ceftriaxone (IV) OR Chloramphenicol (IV)
⮚ Add vancomycin if penicillin- or
cephalosporinresistant H. influenzae is suspected.
⮚ Cefuroxime should not be used for the treatment of
bacterial meningitis because of delayed sterilization
and a greater incidence of hearing loss.
⮚ Dexamethasone is of proven value for children with
H. influenzae b meningitis in children less than 5 yrs.
▪ >5 YRS - 18 YRS
Etiology: S. pneumoniae, N. meningitides
Treatment: Ceftriaxone (IV) OR Chloramphenicol (IV)
⮚ Patients with confirmed meningococcal meningitis
and not treated with Ceftriaxone should receive
either: Rifampicin (P.O.) or Ciprofloxacin (P.O.)
102
▪ >50 YRS
Etiology: S. pneumoniae, N. meningitidis, L. monocytogenes, aerobic
Gram-negative bacilli Treatment:
⮚ Ampicillin (IV) PLUS Ceftriaxone (IV)
⮚ For severe penicillin allergy: Vancomycin (IV) PLUS
⮚ Aztreonam (IV) or Ciprofloxacin (IV)
2. TETANUS (Lockjaw)
⮚ Tetanus is an acute neuromuscular disease induced by a bacterial
exotoxin called tetanospasmin, with painful muscular contractions,
primarily of the masseter (the muscle that closes the jaw) and neck
muscles, spasms,and rigid paralysis.
⮚ Spores of C. tetani are introduced into a puncture wound, burn, or
needlestick by contamination with soil, dust, or feces. Under
anaerobic conditions in the wound.
⮚ Spores germinate into vegetative C. tetani cells, which produce the
exotoxin in vivo.
Figure 6: Tetanus
(BYJU`S, 2020)
Etiology: Clostridium tetani, a motile, Gram-positive, anaerobic,
sporeforming bacillus hat produces a potent neurotoxin called
tetanospasmin. Treatment: Tetanus toxoid or human tetanus immune
globulin (HTIG)
Focus Questions

1. Why is it essential to rule out the specific pathogens before giving
treatment to the patient?
2. What are the factors that contributes to the development of nervous
system infections?
103
Related Readings
Learning Assessment
- - - - - - - - - - - - - - - - - - - END OF UNIT XII - - - - - - - - - - - - - - - - - - -
UNIT 13: Microbial Diseases of the Urinary and

Reproductive System
1. Determine the etiological agents affecting the urinary and
reproductive system;
2. Determine the drug of choice for specific disease of the urinary
and reproductive system; and
urinary and reproductive system.
Introduction
The Genitourinary or urogenital system consist of the urinary tract

and the genital tract. The urinary tract is usually protected from pathogens
by the frequent flushing action of urination. The acidity of normal urine also
discourages growth of many microorganisms. Indigenous microbiota are
found at and near the outer opening (meatus) of the urethra of both men
and women.
This unit will focus on the etiology of infections in our genitourinary
system. It includes the drug of choice for every specific diseases
genitourinary system based on the National Antibiotic Guidelines set by
Department of Health-Philippines.

104
Key Terms:
▪ Cystitis – Inflammation of the urinary bladder; the most
common type of UTI.
▪ Nephritis – inflammation of the kidneys
▪ Prostatitis – Inflammation of the prostate gland.
▪ Bartholinitis – Inflammation of the Bartholin ducts in women.
Lecture Notes
Did you know that there are pathogens that can caused infections
to the genitourinary tract? Let`s find out the clinical
manifestations and treatment of various GUT Infections.
I. URINARY TRACT INFECTIONS

⮚ Urinary tract infections (UTIs) can be divided into upper UTIs and
lower UTIs.
⮚ Upper UTIs include infections of the kidneys (nephritis or
pyelonephritis) and ureters (ureteritis).
⮚ Lower UTIs include infections of the urinary bladder (cystitis), the
urethra (urethritis), and, in men, the prostate (prostatitis).
⮚ UTIs may be caused by any of various microorganisms, introduced by
poor personal hygiene, sexual intercourse, the insertion of catheters,
and other means.
II. URINARY TRACT INFECTIONS IN CHILDREN
A. Acute Uncomplicated UTI
A.1. Etiology: E. coli, Klebsiella, Enterobacter, Enterococcus, Group B
Streptococcus
Treatment: Infants <2 months: Cefotaxime PLUS Amikacin
❖ If there are signs of sepsis, treat as neonatal sepsis. Adjust
therapy based on culture. Early onset is usually due to
maternal transmission. Use ceftriaxone if cefotaxime is not
available and the neonate is not jaundiced.
A.2. Etiology: E. coli, Klebsiella, Enterobacter, Citrobacter
Treatment: >2 months to 18 years: Amoxicillin-Clavulanic acid (P.O.) or
Cefuroxime (P.O.) Adolescent:
Oral: Cefuroxime or Nitrofurantoin (only for cystitis)
Parenteral: Ampicillin-Sulbactam IM or IV infusion or Cefuroxime
❖ Oral therapy is equally effective to IV therapy. IV therapy is
preferred for seriously ill children and for those who cannot
take oral therapy.
105
❖ Early antibiotic therapy is necessary to prevent renal
damage.
❖ Switch to oral therapy once patient has been afebrile for
24h and able to take oral medications.
❖ Cephalosporins are not useful if Enterococcus is suspected.
B. UTI, recurrent catheter related or with co-morbids

Etiology: Enterobacteriaceae, P. aeruginosa, Enterococcus
Treatment: Ceftriaxone PLUS Amikacin
⮚ Use cefotaxime instead of ceftriaxone in jaundiced patients. If
Pseudomonas is suspected, use ceftazidime instead of cefotaxime.
C. Prophylaxis for Recurrent UTI Treatment: Nitrofurantoin
III. URINARY TRACT INFECTIONS IN ADULTS
A. Uncomplicated UTI
Etiology: E. coli (75-90%), S. saprophyticus (5-15%) Treatment:
1st Line: Nitrofurantoin or Fosfomycin
2nd Line: Cefuroxime or Cefixime or Co-Amoxiclav
B. Recurrent UTI in Women
Treatment: Nitrofurantoin
⮚ Lactobacilli is not recommended. Cranberry juice and products can be
used. For post-menopausal women, intra-vaginal estriol nightly x2
weeks then twice-weekly for at least 8 months.
C. UTI in Pregnancy
Etiology: E. coli (70%), Other Enterobacteriaceae, Group B Streptococcus
Treatment: Cefalexin, Cefuroxime, Cefixime, Nitrofurantoin, Fosfomycin,
Amoxicillin-clavulanate
⮚ Avoid amoxicillin-clavulanate in those at risk of pre-term labor
because of potential for neonatal necrotizing enterocolitis.
⮚ Use nitrofurantoin from the 2nd trimester to 32 weeks only, if
possible, because of potential for birth defects and hemolytic
anemia. Avoid cotrimoxazole especially during the first and third
trimesters because of risk of teratogenicity and kernicterus.
Fluoroquinolones are contraindicated.
IV. REPRODUCTIVE SYSTEM INFECTIONS:
A. Gonorrhea
⮚ may present as asymptomatic mucosal infection, ophthalmia
neonatorum, urethritis, proctitis, pharyngitis, epididymitis, cervicitis,
Bartholin gland infection, pelvic inflammatory disease, endometritis,
salpingitis, peritonitis, and disseminated gonococcal infections.
⮚ Patients with disseminated gonococcal infection have myalgia
(muscular pain), arthralgia (joint pain), polyarthritis (inflammation of
106
joints), and a characteristic dermatitis—skin lesions located primarily
on the extremities.
⮚ Urethral discharge and painful urination are common in infected men,
usually starting 2–7 days after infection. Infected women may be
asymptomatic for weeks or months, during which time severe
damage to the reproductive system may occur.
⮚ Transmission occurs via direct mucous membrane-to-mucous
membrane contact, usually sexual contact; adult-to-child (may
indicate sexual abuse); and mother-to-neonate during birth.
Etiology: Neisseria gonorrhoeae Treatment:
1st Line: Ceftriaxone IV/IM (Pedia), Ceftriaxone IM PLUS Azithromycin
(Adult) 2nd Line: Oral Cefixime PLUS Azithromycin (Both Pedia & Adult)
B. Syphilis
⮚ Syphilis is a treponemal disease that occurs in four stages:
⮚ (a) primary syphilis—a painless lesion known as a chancre which
develops at the site where Treponema pallidum entered the genital
mucosa or skin through a break in the surface;
⮚ (b) secondary syphilis—a skin rash (especially on the palms and
soles) about 4–6 weeks later, with fever and mucous membrane
lesions,
⮚ followed by (c) a long latent period (as long as 5–20 years); and then
⮚ (d) tertiary syphilis—with damage to the CNS, cardiovascular system,
visceral organs, bones, sense organs, and other sites.
⮚ Damage to the CNS or heart is usually not reversible.
⮚ Transmission occurs via direct contact with lesions, body secretions,
mucous membranes, blood, semen, saliva, and vaginal discharges of
infected people, usually during sexual contact; blood transfusions; or
transplacentally from mother to fetus.
Etiology: Treponema pallidum Treatment:
Pediatric: Benzathine penicillin G IM
Adult:
1st line: Benzathine penicillin G IM
2nd line: Doxycycline PO or Tetracycline PO or Ceftriaxone IV/IM or
Azithromycin 2g PO
Focus Questions

1. What are GUT diseases that are currently prevalent in our country?
107
2. What are the factors that contributes to the development of various GUT
infections?
Related Readings
Learning Assessment
References
Burton's Microbiology for the Health Sciences Paul Engelkirk, Paul G.

Engelkirk, Janet L. Duben-Engelkirk Lippincott Williams & Wilkins,
2015 Hugo and Russell's Pharmaceutical Microbiology, 8th Edition Stephen
P. Denyer (Editor), Norman A. Hodges (Editor), Sean P. Gorman (Editor),
Brendan F. Gilmore (Editor), Copyright August 2011
Jawetz, Melnick, &Adelberg’s Medical Microbiology, 27 Ed. Karen C. Carroll,
Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A.
Mietzner, Barbara Detrick, Thomas G. Mitchell, James H. McKerrow,
Judy A. Sakanari, Copyright © 2016
National Antibiotic Guidelines (2017) by Department of Health-Philippines
Retrieved last September 07, 2020 from
https://www.ncbi.nlm.nih.gov/books/NBK7919/#:~:text=Metabolism
%20refers%20to%20all%20the,in%20bacteria%20to%20generate%20
energy. by Peter Jurtshuk, Jr.
Retrieved last October 08, 2020 from
https://primaryimmune.org/immunesystem-and-primary-
immunodeficiency By Immune Deficiency Foundation (2020)
108

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LET’S BEGIN!

UNIT 1: Introduction to Microbiology

It is more or less a gospel truth that in science the ultimate credit,

To attend the following intended learning outcomes for the first

Figure 1: Anton Van Leeuwenhoek & his 1st observation on microbes

Figure 3: Needham`s Experiment

Figure 5: Schröder & Dusch Experiment

Figure 7: Fermentation process

Figure 8: Bacillus anthracis shape

Figure 9: Corynebacterium diphtheria

Figure 11: Leukocytes

Figure 12: Phagocytosis

Figure 13: Antibodies

Figure 14: Salvarsan

Guide questions for Unit 1 discussions:

UNIT 2: Prokaryotes and Eukaryotes

Microorganisms or microbes are microscopic organisms that exist as

To attend the following intended learning outcomes, the lesson of

Can you determine ifcertain

Table 1: DISTINGUISHING FEATURES OF PROKARYOTES & EUKARYOTES

Figure 2: Eukaryotic Cell structure

PROKARYOTIC CELL STRUCTURE

Figure 4: Prokaryotic Cell

Figure 5: Peptidoglycan Structure of Gram (+) & Gram (-) bacteria

Figure 10: Archaea

Figure 11: Virus

Figure 12: Prions

Guide questions for Unit 2 discussions:

In order to appreciate and further understand the above discussion, kindly

UNIT 3: Microbial Growth and Metabolism

Microbial metabolism is the means by which a microbe obtains the

To attend the following intended learning outcomes the lesson of the

Did you know that microorganisms also need nutrients to sustain

THE POPULATION GROWTH CURVE:

3. The stationary growth phase

4. The decline or death phase

Figure 1: Logarithmic growth of bacteria

B. Mesophiles: “Middle loving”. Most bacteria.

C. Thermophiles: “Heat loving”.

Organisms can be classified as:

C. Alkaliphiles: “Alkali loving”.

Guide questions for Unit 3 discussions:

In order to appreciate and further understand the above discussion, kindly

- - - - - - - - - - - - - - - - - - - END OF UNIT III - - - - - - - - - - - - - - - - - - -

UNIT 4: Microbial Control

In certain environments, it is necessary to control the growth of

This unit will focus on the concepts of microbial control which

To attend the following intended learning outcomes for the first

I. INHIBITING THE GROWTH OF MICROBES

II. MICROBICIDAL AGENTS

III. MICROBISTATIC AGENTS

IV. ASEPTIC AND ASEPSIS TECHNIQUE

V. USING PHYSICAL METHODS TO INHIBIT MICROBIAL GROWTH

VI. USING CHEMICAL METHODS TO INHIBIT MICROBIAL GROWTH

6. Heavy Metal Derivatives

10. Quaternary Ammonium compounds

11. Vapor phase sterilants

Guide questions for Unit 4 discussions:

UNIT 5: Antimicrobial Drugs

Chemotherapeutic agents used to treat infectious diseases are

To attend the following intended learning outcomes the lesson of the

Did you know that Chemotherapeutic agents are collectively

I. History of Antimicrobial Agents