MICROBIOLOGY, IMMUNOLOGY, MYCOLOGY,

VIROLOGY, BACTERIOLOGY AND PARASITOLOGY

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I. MICROBIOLOGY  Halophiles – live in high salt concentration environments

 Basophiles – live in high pressure environment
 study of microorganisms which are large and diverse group of
 Methanogens – live in high methane concentration
microscopic organisms that can occur as either single cell or in
environment
cluster arrangement including viruses which are microscopic
o PROKARYOTIC CELL STRUCTURE
but acellular
 Plasma Membrane – phospholipid bilayer
 Cytoplasm
I. CELLULAR STRUCTURES
 Inclusion Bodies – storage of energy; (ex. glycogen
 Eukaryotes – presence of true nucleus; nucleus enclosed by
granules; sulfur granules; polyhydroxybutyric acid
nuclear membrane
granules; magnetosomes; metachromatic granules)
o Fungi – multicellular
 Nucleoid – composed of genetic material
 Yeast – unicellular fungi; filamentas; saprophytic; process
 TRANSFER OF DNA
a cell wall (chitin)
o Conjugation – transfer of genetic material using
o Animals
plasmids
 Endoparasites – helminthes
o Transduction – bacteriophage – mediated transfer
 Ectoparasites – insects, arachnids
of genetic material
o Protozoans – considered as endoparasites; unicellular; free
o Transformation – direct transfer of genetic material
living
from donor to recipient cell
o Plants (e.g. algae) – multicellular; photosynthetic (cellulose);
 Specialized Structures
possess a cell wall
GRAM POSITIVE GRAM NEGATIVE
o EUKARYOTIC CELL STRUCTURE Peptidoglycan (7-8 layers) – Outer membrane
 Plasma Membrane – phospholipid bilayer crystal violet
 Cytoplasm – composed of fluid and organelles Plasma Membrane Peptidoglycan (1-2 layers)
 Organelles Teichoic Acid (cell wall; Periplasmic space
 Golgi Apparatus – packaging center; post-translational plasma membrane)
Plasma Membrane
modification; removes unnecessary peptides
 Endospores
 Mitochondria – “powerhouse of the cell”; oxidative
o Genus: Bacillus – aerobe; Clostridium – anaerobe
phosphorylation; 1% of DNA
o Dormant Stage: depleted with required nutrients
 Endoplasmic Reticulum
o Rough ER – ribosomal attachment sporulation
active cell
o Smooth ER – lipid attachment (vegetative) SPORES
 Ribosomes – site of protein synthesis; primary germination
ribosomal subunit (RSU); (80S  40S;  60S)
o heat resistant; desiccation resistant (Ca2+
 Nucleus – composed of genetic materials; biochemical
dipicolinate  heat resistant spore)
processes: DNA Replication (synthesis); Transcription
o Spore staining: malachite green; VR green
(synthesis of RNA – mRNA, tRNA, rRNA)
o Microscopy: Bacillus – non-swollen spore;
 Prokaryotes – pathogenic + non-pathogenic; absence of true
Clostridium - swollen spore
nucleus + organelles; with ribosomes, Golgi bodies,
 Plasmids – extrachromasomal genetic material (ex. R
endoplasmic reticulum; relatively small in size (diameter:
factor/ R plasmid – antimicrobial resistance)
<1µm)
 Teichoic Acid –primary surface antigen gram positive;
o Eubacteria – simple bacteria; pathogenic; cell wall – 1o
functions: (1) provides negative charged surface for
component: peptidoglycan (aka murein/mucopeptide)
gram positive; (2) surface antigen of gram positive
o Arachaebacteria – non-pathogenic; no cell wall; lives in
organisms  stimulates antibody production
extreme environmental conditions
 Outer Membrane – exclusively found in gram negative
 Thermophiles – (>85oC); lives in high temperature
organisms; composed of: lipopolysaccharides (LPS) &
environments
lipid A
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 Periplasmic Space – gram negative only; contains
hydrolytic enymes (ex. beta lactamases)
 Cell Wall – rigid structure that protects organism
against difference in osmotic pressure
o 1O component – peptidoglycan
o interlinking of peptidoglycan layer: N-
acetylmuramic acid (N-AM); N-acetylglucosamide
(N-AG)
PENICILLIN BINDING PROTEINS (PBP)
NAG
N-AM
 Glycocalyx – polysaccharide materials found outside
cell wall
o Capsule – firmly attached to cell, does exclude
particle
 Function: contribute to bacterial virulence 
escape phagocytosis
 General Rule:
α ALL cocci are non-encapsulated except:
streptococci
α ALL bacilli are non-encapsulated except:
Bacillus, Haemophilus, Klebsiella
o Slime Layer – loosely attached to cell, does not
exclude particle
 Function: contribute to bacterial attachment to
mucosal membrane
 Cell Appendages
o Flagella – (ex. Vibrionaceae)
 Function: locomotion/movement
 Highly Antigenic: H-antigen
 Primary Protein: flagellin
 Forms:
α Lophotrichous – tuft of flagella at 1 end
α Amphitrichous – single polar flagella at both
ends
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α Monotrichous – single polar flagella at 1 end
α Peritrichous – flagella all over the cell
o Pili – small rigid structure
 Function: special type of movement or
locomotion; twitching motion
 Forms:
α Ordinary Pili/Fimbriae
 Function: bacterial attachment
α Sex Pili
 Function: bacterial conjugation
o Axial Fillament – (ex. spirochetes  Leptospira
enterogans; Treponema palidum; Borrelia
burgdorferi; Borelia recurrentis)
 Function: spiral locomotion
II. OPTICAL METHODS/STAINING METHODS
 Optical Methods
o Light Microscope
 Bright Field Light Microscope – difference in contrast
black and white the specimen and surrounding medium;
killed and stained specimen
 Magnification: 1000x
 Ocular Lens: 10x
 Objective Lens: 100x
 Phase Contrast Light Microscope – provides
magnification of living cells which are unstained
 Dark Field Light Microscope – lighting system is just able
to reach sides of specimen; (ex. Treponema pallidum)
 Fluorescent Microscope – substances or specimen that
fluoresces – able to short wavelengths of light and emits
long wavelength of light; used in clinical diagnostic
microbiology; (ex. Auramin O – used for staining M.
tuberculosis)
 Differential Interference Contrast Microscope –
polarizer; provides 3D structure of spores, vacuoles and
granules
o Electron Microscope
 Transmission Electron Microscope – uses electron beam
coming from an electron gun focused by an electron
condenser into a thin specimen
 Scanning Electron Microscope – provides 3D structure of
microscopic surfaces of microorganism
© MANOR REVIEW CENTER NOTES (K.L)
 Staining Methods  Stages of Infectious Disease – imbalance of 3 agents of disease
o Gram Staining
FUNCTION GRAM + GRAM -

CONVALESCENCE PERIOD
crystal violet primary stain blue violet blue violet

INCUBATION PERIOD

PRODROMAL PERIOD

DECLINE PERIOD
iodine mordant blue violet blue violet

ACME PERIOD
ethanol decolorizer blue violet colorless
saffranin counterstain blue vioet pink red
o Acid-Fast Staining – Ziehl-Neelsen Staining; hot method and
cold method
FUNCTION
carbol fuschin primary stain
heat mordant
TIME
ethanol decolorizer
methylene blue counterstain a. Incubation Period – pre-pathogenesis period; absence of
o Negative Staining – cell/specimen appears colorless; signs and symptoms; varies on characteristic of organism;
primary stain: nigrosin (ex. Rabies  the nearer the site of the bite to the brain, the
o Flagella Staining – stain: unstable colloidal suspension of shorter the incubation period)
tannic acid which forms a precipitate b. Prodromal Period – presence of prodromes or mild signs
o Capsule Staining – stain: (1) hot solution of crystal violet and symptoms (non-pathognomonic) of infection; (ex.
then rinsing with copper sulfate; (2) india ink – use for measles  3Cs: cough, corysa, conjunctivitis)
Cryptococcus neoformans (pigeon fluconazole) c. ACME Period – period of illness; presence of major signs and
o Nucleoid Staining – stain: Feulgen stain – sensitive for DNA symptoms (pathognomonic); (ex. measles  rashes, Koplik
o Spore Staining – stain: malachite green; carbol fucshin spots)
d. Decline Period – signs and symptoms subsides
III. GROWTH, CULTIVATION, AND REPRODUCTION e. Convalescence Period – body is restored to its healthy
 Primary Method of Reproduction – bacteria: binary fission condition
(asexual reproduction)  Epidemiologic Triangle
 Stages of Microbial Growth

LAG PHASE
LOG PHASE
STATIONARY PHASE
DEATH PHASE

TIME

o Lag Phase – phase of adjustment; synthesis of important

 Koch’s Postulates
macromolecules/nutrients; susceptible to effects of
o Causative Agent – suspected microorganism must be
antimicrobials
present in all stages of disease
o Log Phase – exponential growth rate; rapid increase in
o Environment/Pure Culture Media – suspected
number of microorganisms at a constant maximum rate;
microorganism must be grown in pure culture media
accumulation of toxic waste
o Healthy Host – suspected microorganism when inoculated
o Stationary Phase – phase of equilibrium; cell division = cell
or introduced to a healthy host, must cause same disease
death
o Disease Host – suspected microorganism when isolated
o Death Phase – cell death > cell division
from disease host, must be same organism
 Occurrence of Disease
o Endemic Disease – presence of clinical cases all year round;
January to December; (ex. schistosomiasis – Samar, Leyte;
malaria – Palawan, Mindoro; filariasis – Bicol)
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 o Epidemic Disease – outbreak; sudden increase in number of o Enterobacteriaceae
clinical case at a certain place and time period  Rapid Lactose Fermenters (EKE) – E. coli; Klebsiella;
o Sporadic Disease – scattered or isolated number of clinical Enterobacter
cases at a certain place or time period  Slow Lactose Fermenters (SCAPE Edward Haf) – Serratia;
o Pandemic Disease – affects more than one continent; Citrobacter; Arizona; Providencia; Erwinia; Edwardsiella;
highest level: level 6; (ex. 2009 – influenza AH1N1; 2014 – Hafnia
Ebola virus = level 4)  Non-Lactose Fermenters (SPPS) – Shigella; Proteus;
 Culture Media Pseudonomas; Salmonella
TYPE OF CULTURE CULTURE MEDIA o Hemolytic Reaction
MEDIA  α-Hemolytic Reaction – partial hemolysis  green (ex.
Simple Media – 1. Nutrient Agar Streptococcus pneumoniae; Viridans streptococci;
used for non- 2. Nutrient Broth
fastidious
Streptococcus mutans)
microorganisms  β-Hemolytic Reaction – complete hemolysis  colorless;
Enriched Media – 1. Milk Agar  high protein nutrition further subclassified into Lancefield Classification (A-G)
used for fastidious 2. Chocolate Agar  sheep’s blood (1%);  Group A – Streptococcus pyogenes
microorganisms; high hemoglobin nutrition
 Group B – Streptococcus agalactiae
contains special
nutrients, vitamins,  Gamma-Hemolytic Reaction – no visible reaction
minerals needed for
development IV. CONTROL OF MICROORGANISMS
Differential Media 1. Eosin Methylene Blue (EMB)  Chemotherapy – Paul Ehrlich  (1) atineoplastics; (2)
– subclassifies large & MacConkey Agar (MCA) – subclassify antimicrobials
group of group of enterobacteriaceae into lactose
microorganisms and non-lactose fermenters  Antibiotics – compounds sourced from microorganisms that
into categories; VR LF NLF can inhibit growth of other microorganisms
EMB metallic green colorless
presence of visible o Classifications
MCA pink colorless
reaction a. Based on their Source – (ex. bacteria, fungi)
2. Blood Agar Plate (BAP) – both enriched
and differential media; identification of ANTIBIOTIC SOURCE
streptococci based on hemolytic Bacitracin Bacillus subtilis
reactions Polymyxin Bacillus polymyxa
Penicillin Penicillum notatum
3. Mannitol Salt Agar (MSA) –
Griseofulvin Penicillum griseofulvum
subclassifies group of staphylococci
Gentamicin MIcromonospora purpurea
- s. aureus  golden yellow Streptomycin Streptomyces griseus
- s. epidermidis  porcelain white Vancomycin Streptomyces orientalis
- s. saprophyticus  no visible reaction Chloramphenicol Streptomyces venezuelae
Selective Media – 1. EMB & TCA – both differential and Clindamycin Streptomyces lincolnensis
allows growth of selective media Nystatin Streptomyces noursei
one group of 2. Saboraud Dextrose Agar (SDA) – Amphotericin B Streptomyces nodosus
microorganism and selective only for fungal growth; Erythromycin Streptomyces erythreus
inhibits other provides an acidic pH (pH = 5.6) Cycloserine Streptomyces orchidaceus
groups 3. Colistin-Nalidixic Acid (CNA) – selective b. Based on Spectrum of Activity
only for gram positive organisms  Narrow Spectrum – (ex. Aztreonam)
4. Theyer-Martin – selective for gram-
 Broad Spectrum – (ex. Carbopenems; Tetracylines)
negative diplococcic, Neisseriae;
modified chocolate agar c. Based on Antimicrobial Activity
5. Lowenstein-Jenssen Media – very  Bacteriostatic Agents – inhibits growth and
selective only for Mycobacterium reproduction of microorganisms; general rule  ALL
tuberculosis; very expensive  protein synthesis inhibitors and antimetabolites are
extrapulmonary TB
bacteriostatic except aminoglycosides
6. Thiosulfate Citrate Bile Sucrose (TCBS)
– selective only for Vibrionaceae  Bactericidal Agents – kills pathogens; general rule 
7. Leoffler’s Serum Media & Tellurite ALL cell wall synthesis inhibitors are bactericidal
Media – selective only for d. Based on Mechanism of Action
Corynebacterium diphtheriae MECHANISM OF ACTION ANTIBIOTICS
8. Skirrow’s Agar & Campy BAP – Inhibitor of Cell Wall Synthesis  Beta Lactams – Penicillins;
selective only for Campylobacter jejuni Cephalosporins; Carbapenems;
9. Bordet-Gengou Agar – selective only Monobactams
for Bordetella pertussis  Glycopeptides – Vancomycin;
Anaerobic Media 1. Candle Jar Method Teicoplanin; Telavancin
2. Thioglycollate Agar  Cycloserine
 Polypeptide
3. GasPak®
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 Inhibitor of Protein Synthesis  30s Inhibitors – Tetracyclines; 2.) Cephalosporins
Aminoglycosides RANGE OF EFFECTIVENESS NOMENCLATURE
 50s Inhibitors – Macrolides; G+ G-
Chloramphenicol; 1st +++ + ALL starts with CEPH except
Lincosamides; Oxazolidinones; Cefazolin, Cefadroxil
Streptogramins
2nd ++ ++ ALL starts with CEPH; nothing
Inhibitor of Nucleic Acid  Rifamycins ends in –ONE or –IME except
Synthesis  Quinolones/Fluoroquinolones Cefuroxime, Lovacarbef
Antitubercular Agents  First Line Agents (RIPE) – 3rd + +++ ALL starts with CEF; ALL ends
Rifampicin; Isoniazid; with –ONE or –IME except
Pyrazinamide; Ethambutol Cefdinir, Ceftibulen,
 Second Line Agent – Cefditoren, Moxalactam
Aminoglycosides; 4th +++ ++ Cefepime, Cefipirome
Fluoroquinolones; 5th Ceftaroline fosamil
Ethonamides; p-aminosalycilic
acid
COMMONLY USED CEPHALOSPORINS:
Antimetabolites  Sulfonamides  Cefazolin – only 1st generation ceph in parenteral form;
 Pyrimethamine/Trimethoprim clinical use  surgical prophylaxis
Miscellaneous Agents  Nitroimidazole
 Cefuroxime – extensively used for treatment of
 Mupirocin
 Polymyxin community-acquired pneumonia
 Urinary Antiseptics –  Cephamycins – 2nd generation cephs with activity for
Nitrofurantoin; Methenamine
anaerobic infection (Cefoxitin, Cefotetan, Cefmetazole)
A. Inhibitors of Cell Wall Synthesis
 Ceftaroline Fosamil – only ceph active against MRSA and
 Beta Lactam
MRSE
o MOA: inhibits cell wall synthesis by binding to penicillin-
 Ceftriaxone & Cefotaxime – used for treatment of
binding proteins (PBP)
meningitis (except: Listeria monocytogens)
o Clinical Use:
 Cefexime – used for treatment of gonococcal or non-
 effective for gram positive and gram negative
gonoccocal urethritis and cervicitis
 ineffective for:
 Cefoperazone & Ceftazidime – has activity for
(1) wall-less microorganisms (ex. mycoplasma)
Pseudomonas infection
(2) microorganisms with atypical cell wall component (ex.
3.) Carbapenems – widest spectrum among beta-lactam
mycobacterium)
antibiotics
(3) intracellular parasites (ex. legionella; brucella;
 Imipenem + Cilastatin  dihydropeptidase enzyme
chlamydia; rickettsia)
inhibitor
(4) resistant microorganisms (ex. MRSA; MRSE)
 Meropenem
o Adverse Effects: allergic reaction; anaphylactic reaction;
cross-sensitivity reaction  PENs & CEPHs; Jarisch-  Ertapenem
Herxheimer Reaction – idiosyncratic reaction 4.) Monobactam – (ex. Aztreonam) – only effective for aerobic
1.) Penicillins and gram negative organisms
a. Natural Penicillins  Glycopeptides
 Pen G – benzyl penicillin; poor oral bioavailability; o Vancomycin
parenteral (IV/IM)  MOA: inhibits cell wall synthesis by binding to terminal
peptide D-ala-D-ala terminus of nascent peptide chain
 Pen V – phenoxymethyl penicillin; good oral
 Clinical Use: formerly DOC for Pseudomembranous colitis;
bioavailability; oral
DOC for treatment infection caused by MRSA and MRSE
b. Isoxazolyl Penicillins – antistaphylococcal penicillins;
 Adverse Effect: Red Man Syndrome – form of phlebitis or
resistant to action of beta lactamases; prototype:
allergic reaction; management: prophylaxis  N-
methicillin – withdrawn due to nephrotoxicity; (ex.
diphenhydramine (via slow IV infusion)
cloxacillin; oxacillin; dicloxacillin; nafcillin)
o Teicoplanin – same MOA, same spectrum; IV and IM
c. Extended Spectrum Penicillins – increases gram
o Telavancin
negative coverage; increases gram negative membrane
 Chemical Structure: semisynthetic lipoglycopeptide
penetration
derived from Vancomycin
 Aminopenicillins – (ex. amoxicillin; ampicillin;
 MOA: same with Vancomycin; alters membrane potential
bacampicillin)
and membrane permeability
 Carboxypenicillins – has activity for Pseudomonas
o Dalbavacin
infection – (ex. carbenicillin; ticarcillin)
 Chemical Structure: semisynthetic lipoglycopeptide
 Ureidopenicillins – (ex. piperacillin; azlocillin;
derived from Teicoplanin
mezlocillin)

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 Cycloserine
o MOA: inhibits cell wall synthesis by inhibiting activity of: (1)
alanine racemase, (2) D-ala-D-alanyl ligase
o Clinical Use: 2nd line of agent for Mycobacterium
tuberculosis resistant to the first line agents
 Polypeptide (ex. Bacitracin) – poor oral bioavailability 
topical
o Chemical Structure: mixed cyclic polypeptide
B. INHIBITORS OF PROTEIN SYNTHESIS
 Inhibitors of 30s Ribosomal Subunit
1.) Tetracyclines – (ex. Tetracyclines; Doxycycline;
Minocycline; Demedocyline)
o widest/broadest spectrum among antibiotics (gram
positive, gram negative, wall less organisms, intracellular
parasites; spirochetes, plasmodium)
o Chemical Structure: naphthacene ring
o MOA: inhibition of binding of aminoocyl tRNA to mRNA
 prevents peptide elongation
o Adverse Effects: (contraindicated in patients < 8 yrs old)
 Permanent yellow staining of teeth
 Hypoplasia of teeth
 Use of expired tetracyclines  Fanconi-like
Syndrome
 Ototoxicity  Minocycline
 Phototoxicity  Demeclocycline
2.) Aminoglycosides
o Source: Micromonaspora (-micins); Streptomyces (-
mycins)
o MOA: inhibit protein synthesis: (1) prevention of
formation of initiation complex, (2) misreading of mRNA
complex, (3) formation of nonfunctional polysomes
o Pharmacodynamic Properties: concentration dependent
killing; postantibiotic effect; synergistic effect
o Adverse Effects:
 Ototoxicity – Kanamycin; Amikacin; Neomycin
 Vestibulotoxicity – Streptomycin; Gentamicin
 Nephrotoxicity – Neomycin; Gentamicin; Tobramycin
 Inhibitors of 50s Ribosomal Subunit
1.) Macrolides
o Chemical Structure: large lactone ring
o MOA: blocks peptide exit tunnel  dissociation of
peptidyl tRNA from ribosome
o Erythromycin
 Clinical Use: alternative for patients allergic to B-
lactam antibiotics
 Adverse Effect: abdominal discomfort; stimulates
motillin receptors (increases peristalsis); jaundice –
associated with use of erythromycin estolate salt
o Clarithromycin – least associated with adverse effects
 Chemical Structure: methylated erythromycin
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 Clinical Use: treatment for infection caused by
staphylococci and streptococci; treatment for peptic
ulcer disease caused by H. plyori
o Azitrhromycin
 Pharmacokinetics: (1) excellent distribution to body
tissues; (2) longer t ½
 Dosing: once a day for 3-5 days
 Adverse Effect: arrhythmia
2.) Chloramphenicol
o MOA: inhibition of peptidyl transferase; (RLE: peptide
elongation)
o Adverse Events: nitro group
 aplastic anemia – low RBC, WBC, platelets
 Grey Baby Syndrome – lacking for enzyme for
glucoronidation
o Toxic Dose: > 50mg/kg/day
o Clinical Use: alternative for treatment of typhoid fever
(enteric fever)
3.) Lincosamides – MOA: same as macrolides
o Lincomycin
 Chemical Structure: sulfur containing antibiotic
o Clindamycin – DOC for anaerobic infections above
diaphragm; alternative treatment for toxoplasmosis (+
pyrimethamine); treatment of skin and soft tissue
infection caused by staphylococci and streptococci
4.) Oxazolidinones – (ex. Linezolid – treatment of VRSA, VRSE)
o MOA: inhibits 23s subunit of the 50s subunit
5.) Streptogramins
o Ratio: 70 (A) : 30 (B)
 Streptogramin A – Dalfopristin
 Streptogramin B – Quinupristin
o Clinical Use: treatment of VRSA, VRSE
C. INHIBITORS OF NUCLEIC ACID SYNTHESIS
 Rifamycin – (ex. Rifampicin; Rifabutin)
o MOA: Inhibition of RNA polymerase (RLE: transcription)
o Clinical Use: treatment of pulmonary and extrapulmonary
tuberculosis; treatment of cutaneous tuberculosis (leprosy)
o Adverse Effect: Red-orange discoloration of body fluids (ex.
sweat, urine, saliva)
 Quinolones/ Fluoroquinolones
o MOA: inhibitor of:
 Topoisomerase II (DNA Gyrase) – relaxation of
supercoiled DNA
 Topoisomerase IV – separates DNA strand
o Addition of fluorine:
 Increase gram negative coverage
 Improved penetration to gram negative membrane
© MANOR REVIEW CENTER NOTES (K.L)
 First  Nalidixic acid and Cinaxacin E. ANTIMETABOLITES
Generation  Moderate gram (-) activity SULFONAMIDES
 Limited use for uncomplicated UTI PABA
Second  Ciprofloxacin, Ofloxacin, Norfloxacin, Eroxacin, X
X dihydropteroate synthetase
Generation Lomefloxacin PYRIMETHAMINE/TRIMETHOPRIM

 Improved gram (-) activity Dihydrofolate

 Has activity for gram (+) and atypical microorganisms dihydrofolate reductase X X
Third  Levofloxacin, Sparfloxacin, Gemifloxacin, Gatifloxacin,
Tetrahydrofolate
Generation Moxifloxacin
 Retained gram (-) activity
 Improved activity for gram (+) and atypical Purine Bases
microorganisms
Fourth  Trovafloxacin
Generation  Retained activity for gram (-), gram (+), and atypical Nucleic Acid Synthesis
microorganisms
 Sulfonamides
 Has activity for anaerobic microorganisms
o Chemical Structure: PABA-like
o COMMONLY USED FLUOROQUINOLONES
o MOA: inhibition of dihydropteroate synthetase
 Ciprofloxacin – used as treatment and prophylaxis for
o Adverse Effects:
anthrax
 Respiratory Fluoroquinolones – used for treatment of lower  Steven-Johnson Sydrome
Counterindicated: G6PD Deficient
respiratory tract infections and upper respiratory tract
G6PD↓ NADPH↓ oxidized glutathione –(glutathione
infection; (Levofloxacin; Gatifloxacin; Gemifloxacin;
reductase)-> reduced glutathione (master antioxidant)
Moxifloxacin)
 Jaundice
 Ciprofloxacin and Levofloxacin – treatment of
uncomplicated UTI  Pyrimethamine/Trimethoprim
o MOA: inhibition of enzyme dihydrofolate reductase
 Adverse Effects: bone/cartilage toxicity; (ex. tendinitis;
o Adverse Effects: megaloblastic anemia  management:
phototoxicity)
leucovorin
D. ANTITUBERCULAR AGENTS  Combinations:
o Sulfamethoxazole + Trimethoprim (Co-Trimoxazole) – DOC
 First Line Agents – (HRZE or RIPE)
for Pneumocystis jiroveci pneumonia
o Isoniazid
o Sulfadiazine + Pyrimethamine (Daraprim®) – DOC for
 Chemical Structure: isonicotinic hydrazine
toxoplasmosis
 MOA: inhibits mycolic acid synthesis
o Sulfadoxime + Pyrimethamine (Fansidar®) – treatment of
 Pharmacokinetics: acetylation
malaria
 Enzyme: N-acetyltransferase; fast acetylators  rapid
development of resistance
F. MISCALLANEOUS AGENTS
 Management: ethambutol
 Adverse Effects: peripheral neuritis  management: Vit  Nitroimidazoles – (ex. Metronidazole; Tinidazole)
B6 (Pyridoxine) o Clinical Use: DOC for trichomoniasis, amobiasis, giardiasis
o Rifampicin (TAG); DOC for anaerobic infection below diaphragm; DOC
o Pyrazinamide – short term therapy; Adverse Effect: for Pseudomembranous colitis
hepatotoxicity o Adverse Effect: metallic aftertaste + etOH  disulferam-like
o Ethambutol effect
 MOA: inhibits arabinosyl transferase  ↓arabinoglucan  Mupirocin – pseudomonic acid; topical
 Adverse Effects: red-green visual disturbance (optic o MOA: inhibits staphylococcal isoleucyl tRNA synthetase
neuritis) o Clinical Use: treatment of skin infection caused by
staphylococcus (Impetigo)
 Second Line Agents
o Aminoglycosides – Streptomycin IM  Polymyxin – (ex. Polymixin B; Polymixin E – Colistin); topical
o Fluoroquinolones – Levofloxacin or Moxifloxacin o MOA: acts like cationic detergents  disruption of cell
o Ethionamides membrane
o Cycloserine
o p-Aminosalicylic Acid G. URINARY ANTISEPTICS
 Nitrofurantoin – active at an acidic pH; for uncomplicated UTI
 Methanamine – prodrug  formaldehyde (urinary
antiseptic); active at an acidic pH; for uncomplicated UTI

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 H. DRUG-DRUG RELATIONSHIPS  Natural Killer Cells (NK cells) – Antibody Dependent
 Addition (1+1 = 2) – bacteriocidal + bacteriocidal; except: Cellular Cytotoxicity (ADCC); indirectly attacks viruses and
penicillins + aminoglycosides tumor/cancer cells
 Synergistic (1+1 = 3) – bacteriostatic + bacteriostatic
 Antagonism (1+1 = 0) – bacteriocidal + bacteriostatic III. NON-SPECIFIC IMMUNITY – Innate Immunity
 Potentiation (1+0 = 2) – penicillins + β lactamase inhibitors;  Inflammation
(ex. amoxicillin + clavulanic acid; ampicillin + sulbactam; o 5 Cardinal Steps:
piperacillin + tazobactam; imipenem + cilastatin)  Rubor – redness
 Calor – heat
II. IMMUNOLOGY  Tumor – swelling/edema
 Dolor - pain
 physiological process in which body (self) recognizes itself
 Functio Laesa – loss of function
from foreign (non-self)
 Chemotaxis – movement of neutrophils to site of infection
 Types of Immunity:
o Margination
NON-SPECIFIC (INNATE) SPECIFIC (ADAPTIVE)
 does not require antigen  requires antigen recognition o Diapedesis
recognition  antigen specific  Phagocytosis
 not antigen specific  lagtime before response
 Complement System
 response is immediate  result to antibody production
 does not result to antibody  results to immunologic memory o Primary Goal – to create membrane attack complex (C5b, C6,
production C7, C8, C9)
 does not result to immunologic o MAC:
memory
 Classical Pathway
I. CELLS INVOLVED IN IMMUNITY  Alternative Pathway
 Mannose-Binding Lectin
 Granulocytes (BEN)
o Basophils – for histamine release; present during acute
allergic reaction; found in peripheral circulation
 Mast Cells – for histamine release; found near
organs/tissues Bacteria MAC
o Eosinophils – present during type I HS reaction and
N
helminthic infestation
o Neutrophils – for phagocytosis; present in bacterial
IV. SPECIFIC IMMUNITY – Adaptive Immunity
infection and acute inflammation
 Branches:
 Agranulocytes
o Humoral Immunity – B-cells
o Monocytes + Macrophages
o Cellular-Mediated Immunity – T-cells
 Monocytes – young macrophages; no phagocytic
 Lymphoid Organs
effect
o Primary Lymphoid Organs – site of maturity; (ex. bone
o Macrophages – for phagocytosis and antigen presentation;
marrow; thymus)
(>2 weeks) – present during chronic inflammation
o Secondary Lymphoid Organs – site of activation; (ex. tonsils;
 Lymphocytes – mature/activated in lymphoid organs lymph nodes; spleen; Peyer’s Patches)
o B Lymphocytes/B Cells – for antigen presentation; matures
 Immunoglobulins
into 2 types of cells: (1) Plasma Cells – antibody production;
(2) – Memory Cells – immunologic memory
 Example: Vaccination:
 Measles – 1 strain; 9 months
 Dengue Virus – 1, 2 (memory cells), 3, 4
o T Lymphocytes/T Cells
 Helper T Cells – aka CD4 + cells; attacked by HIV;
stimulates B cells and cytotoxic T cells
 Cytotoxic T Cells – aka CD8 + cells; for directly attacks;
viruses and tumor/cancer cells o Immunoglobulin A – aka secretory immunoglobulin; found
B CELLS HELPER T CELLS CYTOTOXIC T CELL in body secretions/fluids (saliva; sweat; tears; colostrum)
o Immunoglobulin E – responsible for type I hypersensitivity
PLASMA CELLS MEMORY CELLS CT CT CT
CT (allergy)

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 o Immunoglobulin M – largest immunoglobulin  Mycoses
(macroglobulin); first to respond during infection o Hypersensitivity Reaction
o Immunoglobulin G – most dominant immunoglobulin; o Mycotoxicosis – ingestion of preformed fungal toxin; (ex.
crosses placental barrier Aflatoxin – stale peanuts acted upon Aspergillus, carcinogen
o Immunoglobulin D – has no known function; found in B cell  hepatocellular carcinoma; Ergotoxin – wheat acted upon
receptor by Claviceps purpurea)
 Hypersensitivity Reaction o Mycetisma – ingestion of a poisonous fungi; (ex. Amanita
o Antibody Mediated Hypersensitivity Reaction – Type I, II, III phalloides)
 Type I Hypersensitivity Reaction – aka Intermediate o Fungal Infections
Hypersensitivity Reaction; (ex. allergy; atropy;  Superficial Mycoses
anaphylaxis); mediated by IgE MYCOSES CAUSATIVE AGENT CLINICAL
MANIFESTATIONS
 Type II Hypersensitivity Reaction – aka Cytotoxic
Black Piedra – Piedraia hortae Black nodules found on
Hypersensitivity Reaction; (ex. blood transfusion reaction aka Tinea nodosa hairshaft
– ABO incompatibility, Rh incompatibility; erythroblastosis White Piedra Trichosporon beigelii Beige nodules found on
hairshaft
fetalis; grave’s disease)
Pityriasis – aka Malasssezia furfur Hypo/hyperpigmented
 Type III Hypersensitivity Reaction – aka Antigen-Antibody Tinea vesicolor serpentine skin lesions
Complex Formation; mediated by IgG; (ex. rheumatic Tinea Nigra Exophiala werneckii Brown to black lesions
heart disease; acute glomerulonephritis; arthus reaction; found on palms and
soles
vasculitis; serum sickness; SLE)
 Cutaneous Mycoses
o Cellular Mediated Hypersensitivity
 Causative Agent: Dermatophytes
 Type IV Hypersensitivity Reaction – aka Delayed
o Epidermophyton – affects skin and nails
Hypersensitivity Reaction; (ex. tuberculin skin test/PDD;
o Microsporon – affects skin and hair
contact dermatitis)
o Trichophyton – affects skin, nails, and hair
 Clinical Manifestation: Tinea/Ringworms
III. MYCOLOGY TINEA PART OF BODY DERMATOPHYTES
 Forms Tinea Pedis feet T. rubrum;
E. mentagrophytes;
o Molds – multicellular; filamentous; lives at room E. Acossum
temperature (20-25oC) Tinea Cruris – jock groin area T. rubrum;
o Yeasts – unicellular; non-filamentous; lives at body itch E. mentagrophytes;
E. Acossum
temperature (37oC) Tinea Unguium – nail/hands T. rubrum;
 Characteristics – multicellular and filamentous (except yeasts); onchomycosis E. mentagrophytes;
E. Acossum
saphrophytic; parasitic/pathogenic; plant-like
Tinea Corporis trunk/body T. rubrum;
 Morphology E. flocossum
o Hyphae – filamentous; microtubular structures found in Tinea Barbae beard area E. mentagophytes
molds Tinea Capitis scalp area E. mentagophytes;
M. canis
o Septum – cross-walled structures; found inside a hyphae  Subcutaneous Mycoses – introduced into SQ/hypodermis
o Conidia & Spores – primary method of asexual reproduction area via a skin incision/trauma
 Phyla MYCOSES CAUSATIVE AGENT CLINICAL
PHYLA SEXUAL ASEXUAL MANIFESTATIONS
REPRODUCTION REPRODUCTION Chromoblastomycosis Phialophora verrucosa; warty-
Fonsaccrea pedrosoi; like/verracous skin
Phylum zygospores sprorangium/spores
Fonsacaea compacta; lesions found along
Glomerulomycota, Rhinocladiella aquaspersa; draining of
Order Mucorales – Chladophialophora carrionii lymphatics
formerly known as Mycetoma – aka Pseudallescheria boydii; suppuration;
Phylum Madura Foot; Modurella mycetomatis; abcess formation;
Zygomycota associated with Modurella grisea; granuloma
Phylum ascospores conidia barefoot individuals Exophiala jeanselmei; formation
Acremonium falciforme
Ascomycota –
Sporotrichosis – aka nodules found
largest phylum;
Occupational Disease along draining of
aka “sac” fungi of Gardeners; lymphatics
Phylum basidiospores conidia/spores MOT: rose thorns; tree
Basidiomycota – barks; and soil
aka “club” fungi Phaeohyphomycosis Phialophora richardsiae; solitary
Wangiella dermatitidis; encapsulated cyst
Bipolaris spicifira; found on skin
I. MEDICAL MYCOLOGY Exophiala jeanselmei;
Alternaria (sp. of molds);
 study of fungal diseases (mycoses) and associated treatment curvuloria; Exorhilum
rostratum
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 Systemic/Endemic Mycoses III. ANTIFUNGAL
 Causative Agent: Thermally Dimorphic Fungi  Superficial Mycoses – oral; topical
 Mode of Transmission: respiratory (initial site of lungs) o Griseofulvin – fungistatic
 Mode of Treatment:  no known MOA; PROPOSED MOA: protects early formed
o Mild to Moderate – Itoconazole (DOC) skin against dermatophytic infection
o Moderate to Severe – Amphotericin B (DOC)  Pharmacokinetics: ↑absorption: high lipid/fatty meal
MYCOSES CAUSATIVE CLINICAL TISSUE FORM/  Clinical Use: treatment of skin infection caused by
AGENT MANIFESTATION MICROSCOPIC
FORM dermatophytes
Coccidiomycosis Coccidioides Valley spherules o Terbenafine – fungicidal
– First Outbreak: immitis; Fever/Desert containing
San Joaquin Coccidioides Rheumatism endospores  MOA: inhibition of squalene epoxidase  ↑↑↑
Valley, California posadasii squalene epoxide
Histoplasmosis Histoplasma mimics signs and oral yeasts
– Spelunker’s capsulatum symptoms of PTB inside o Nystatin – topical; poorly absorbed
Disease; (cough hemolysis) macrophages  Chemical Structure: polyene antifungal
MOT: inhalation
of spores from  MOA: inhibition of ergosterol synthesis
bat droppings  Clinical Use: effective for skin infection caused by yeasts
South American Paracoccidioides painful mouth and large, multiple
Blastomycosis brasiliensis pharyngeal ulcers budding yeast o Azoles
North American Blastomyces pulmonary/lung thick walled  MOA: inhibition of fungal CYP450
Blastomycosis dermatitidis infiltrates lesions yeast with
or ulcerations broad based  Chemical Structures:
found
genitalia, bones
on single bud
 Imidazoles – less selective in inhibiting human CYP450;
and CNS-brain (ex. Ketoconazole; Topical Azoles – Clotrimazole,
 Opportunistic Mycoses Ticonazole, Miconazole)
MYCOSES CAUSATIVE
AGENT
CLINICAL
MANIFESTATION
TREATMENT
 Triazoles – more selective in inhibiting fungal CYP450;
Candidiasis Candida cutaneous/mucosal – Nystatin (ex. Fluconazole; Voriconazole; Itraconazole;
albicans – oral thrush, diaper (DOC);
formation of rash, vaginosis, Ketoconazole
Posaconazole)
germ tube; intertriginous  Adverse Effects: antiadrogenic effects (Males:
C. glabrata; infections,
C. tropicalis; onychomycosis;
gynecomastia; Females: galactorrhea); enzyme inhibition
C. krusei; systemic – associated o Topical Agents
C. lusetanei with prosthetic
devices;
Standard  Salicylic Acid – APAP solution
Treatment –
chronic
Amphotericin  Salicylic Acid + Benzoic Acid – Whitfield’s ointment
mucocutaneous –
associated with
B+  Selenium Sulfide – Selsun Blue Shampoo
Flucytosine;
immunocompromised
Alternative -  Potassium Iodide Solution – DOC for sporotrichosis
state and
endocrinopathies (ex.
Fluconazole  Less Serious Mycoses
diabetes mellitus) o Ketoconazole – 1st azole available for clinical use
Cryptococcosis Cryptococcus cryptococcus Meningitis –
–MOT: spores neoformans meningitis Fluconazole o Fluconazole – (1) excellent penetration into BBB; (2) good
inhaled from (DOC); water solubility; least associated with adverse effects
pigeon Systemic:
droppings; Amphotericin o Itraconazole – 2nd line treatment for systemic/endemic
Capsule B + mycoses
Staining: india Flucytosine
ink  Life Threatening Mycoses
Pneumocystis Pneumocystis pneumonia Cotrimoxazole
Jiroveci jiroveci – (DOC)
o Amphotericin B – grandfather of antifungals; + flucytosine =
Pneumonia Humans synergistic effect
(former
protozoan)
 MOA: binds to ergosterol in fungal membrane and create
Aspergillosis Aspergillus bronchopulmonary Variconazole holes (cytoplasmic leakage)
fumigatus; aspergillus; invasive (DOC)
Aspergillus aspergillosis;
 Clinical Use: initially use to decease fungal burden
flavus aspergilloma – fungal  Adverse Effects: nephrotoxicity – acute renal failure with
ball
Mycomycosis Zygomucor rhinocerebellar Posaconazole wasting K+ and Mg2+
infection (DOC) o Flucytosine
 Chemical Structure: pyrimidine analogue
 Prodrug  5-fluorouracil (antifungal)
 MOA: (1) taken up cytosine permease; (2) converted to 6-
fluorouracil; (3) 5-fluorouracil is converted to:
fluorodoxyuridine monophosphate (FDUMP),
fluorouridine triphosphate (FUTP)

PAGE 10 OF 18 © MANOR REVIEW CENTER NOTES (K.L)

  Clinical Use: treatment for systemic yeast infection; +  Prion Diseases
amphotericin B  Bovine Spongiform Encephalopathy – Mad Cow’s
o Echinocandins Disease
 MOA: inhibition of β-1,3-D-glucan synthesis
 Examples: caspofungin; anidulafungin; micafungin
o Voriconazole
o Posaconazole – broadest spectrum among azoles;  Scrapie – prion disease in sheeps
zygomucor, aspergillus, candida (ZAC)  Kuru – association with human cannibalism; tribe in
Papua New Guinea
IV. VIROLOGY  Creutzfeld-Jakob Disease – associated with use of
 Characteristics – obligate intracellular parasites; acellular human growth hormone from corpse
(nucleic acids + proteins); does not replicate (replication
happens inside cell) II. GENERAL PROPERTIES OF DNA & RNA VIRUSES
DNA VIRUSES EXCEPTION:
 Morphology  Double Stranded  Parvoviridae (ss)
o Nucleic Acid Core – either DNA or RNA  Icosahedral  Poxviridae
o Viral Capsid – protein part; for protection and basis for viral  Nucleus  Poxviridae (cytoplasm)
(replication)
symmetry
NAKED DNA ENVELOPED DNA
o Viral Envelope – enveloped virus – more vulnerable to  Adenoviridae  Hepadnaviridae
effects of surfactants; naked virus  Parvoviridae  Poxviridae
 Papilloviridae  Herpesviridae
 Viral Symmetry
 Polyomaviridae
o Cubic/Icosahedral – spherical RNA VIRUSES EXCEPTION:
 General Rule: (1) all DNA viruses except POXVIRIDAE; (2)  Single Stranded  Reoviridae (ds)
all RNA (+) sense viruses except FLAVIVIRIDAE,  Enveloped  Picornaviridae; Reoviridae; Caliciviridae (PRC)
 Cytoplasm  Retroviridae; Orthomyxoviridae; Influenza
CORONAVIRIDAE, RETROVIRIDAE  Spherical – (nucleus)
o Helical Helical  Rabies Virus (helical-bullet shape)
 General Rule: all RNA (-) sense viruses except
AENAVIRIDAE III. DNA VIRUSES
o Complex – neither cube nor helical; Poxviridae, Flaviviridae,  Adenoviridae
Aenaviridae, Coronaviridae, Retroviridae (PoFACoR) o Sites of Infection: conjunctiva; pharynx; small intestine;
 Viral Genome urinary bladder
o Double Stranded (DS) o Clinical Manifestation: pink conjunctivitis (sore eyes);
 General Rule: all DNA viruses except PARVOVIRIDAE pharyngitis (sore throat); gastroenteritis; hemorrhagic cystis
o Single Stranded (SS)  Parvoviridae – simplest DNA virus (single stranded);
 General Rule: all RNA viruses except REOVIRIDAE Parvovirus B19 (humans); red blood cell (tropism)
o Segmented Viruses – Bunyaviridae, Arenaviridae, o Clinical Manifestation:
Reoviridae, Orthomyxoviridae (BARO)  Erythema Infectiosum – aka “5th disease”; slapped cheek
 Viral Life Cycle appearance (children); severe arthralgia (adults)
o Lysogenic Stage – no signs and symptoms (avirulent stage);  Glove and Socking Syndrome – rashes found on hands
synthesis and packaging of virions (mature viral particles) and lower extremeties
o Lytic Stage – presence of signs and symptoms; release of  Transient Aplastic Anemia
virions  Pure Red Cell Aplasia
 Steps in Viral Infection – ASPERSP  Hydrops Fetalis
1. Attachment of virus to host cell  Papillomaviridae – human papilloma virus
2. Penetration of virus into host cell HPV STRAINS DISEASES
1 Plantar Warts
3. Expression of viral genome
2 Common Skin Warts
4. Replication of virus 3 Cutaneous Warts
5. Synthesis of virions 7 Butcher’s Hand Warts
6. Packaging and release of virions 6, 11 Anogengenital Warts, Laryngeal Carcinoma
16, 18 Cervical Carcinoma
 Unconventional Virus
o Prevention:
o Viroid – single stranded; smallest pathogen that can infect
 Papanicolau Smear (Pap Smear) – early detection; start at
plants
age 21 years old
o Prions – only composed of proteins; heat resistant;
desiccation resistant
PAGE 11 OF 18 © MANOR REVIEW CENTER NOTES (K.L)
  Vaccination  Hepadnaviridae – Hepatitis B
 Gardasil (Quadrivalent) – HPV 6, 11, 16, 18
 Cervarix (Bivalent) – HPV 16, 18
 Polymaviridae – BK virus; JC virus; Ki and Wu virus; Merkett
cell virus; SVAD virus
 Poxviridae – brick shape virus
o Orthopox
 Monkey Pox – 1o member; clinical manifestation: cervical
and inguinal lymphadenopathy IV. RNA VIRUSES
 Small Pox – variola; eradicated (last case was 1978 –  RNA (+) SENSE – immediately translated into proteins;
Somalia); clinical manifestation: skin lesions (starts at (PiCoTCaFlaRe2)
head/facial area; skin lesions are of same stages) o Picornaviridae – smallest RNA virus
 Vaccinia – 1o component of small pox vaccine; model  Enterovirus
virus in terms of structure and replication a. Polio Virus
 Cow Pox – ancestor of vaccinia; rodents (host); clinical  Clinical Manifestation: paralytic poliomyelitis
manifestation: hemorrhagic/red-based skin lesions  Prevention: vaccination
o Parapox  Sabin – live attenuated virus; oral (OPV)
 ORF Virus – found in sheeps; clinical manifestation:  Salk – killed virus; IM (IPV)
benign pustular dermatitis; aka occupational disease b. Rhino Virus – most common cause of common colds
among sheep handlers c. Coxsakie Virus
o Mollusca Pox  Coxsackie A – herpangian (vesicular pharyngitis);
 Mollusca Contagiosum Virus – clinical manifestation: hand-foot-mouth disease; hemorrhagic
small, pink warty-like skin lesions found at back, buttocks, conjunctivitis
and genitalia  Coxsackie B – pleurodynia; pericardis; myocarditis
o Yatapox – Yaba Pox; Tana Pox  Aphtho Virus – foot and mouth disease
 Herpesviridae – latency period – asymptomatic; cytopathic  Kobu Virus
effects – formation of “giant” cells  Cardio Virus
FAMILY STRAIN COMMON NAME CLINICAL MANIFESTATIONS  Hepato Virus – Hepatitis A
Alpha 1 Herpes Simplex Virus 1 – gingivastomatitis; cold sores;
Herpes non-sexually fever blisters; hepatic o Coronaviridae – solar/petal shape; clinical manifestations:
transmitted encephalitis SARS; MERS; gastroenteritis; common colds
2 Herpes Simplex Virus 2 – genital herpes; neonatal
sexually tranmitted sepsis; hepatic meningitis o Togaviridae – arbovirus (arthropod borne)
3 Varicella-Zoster Virus skin lesions (starts at trunk);  Alpha Virus – Chinkungunya Virus – crippling arthritis
Varicella (chicken pox); skin lesions are of different
stages (most are vesicular)  Rubi Virus – Rubella (german measles) – clinical
Zoster (shingles)  skin lesions are dermatomal manifestations: 3-day maculopapular rash; congenital
reactivation of varicella (dermatomes); more painful
defects: cataract formation (blindness), deafness, valvular
Beta 5 Cytomegalovirus (CMV) 90-95%  asymptomatic
Herpes – most common 5-10%  symptomatic:
defects; forchheimer spots – petechiae seen at soft palate
congenital infection* stillbirth; intrauterine; o Calciviridae
growth retardation;
blindness; deafness; mental  Callci Virus/Norwalk Virus – Norwalk Ohio Elementary
retardation School (first outbreak); clinical manifestations: viral
6 Human Herpes Virus 6 roseola – aka infanten
7 Human Herpes Virus 7 subitum; 6th disease gastroenteritis
Gamma 4 Epstein-Barr Virus (EBV) infectious mononucleosis o Flaviviridae – arbovirus
Herpes (IM) – aka kissing disease,
monospot test (diagnosis);  Dengue Virus
burkitt’s lymphoma;  Vector: aedes aegypti; aedes albopictus
hodgkin’s and nonhodgkin’s
lymphoma; gastric carcinoma  Clinical Manifestations: dengue hemorrhagic fever
8 Human Herpes Virus 8 kaposi sarcoma  3 Clinical Phases:
*Organisms that can cross placenta: toxoplasma gondii; rubella; cytomegalovirus;
herpes/HIV/Hepa B; syphilis (TrOCHeS – Toxoplasmosis, Other agents, Rubella, (1) Febrile Phase – occurs below D2 – D7 of illness
Cytomegalovirus, Herpes Simplex) (2) Critical Phase – occurs at D5 – D6 of illness; signs and
symptoms include: plasma leakage; bleeding;
severe organ involvement; can last for 24 – 48
hours
(3) Convalescence Period – recovery phase

PAGE 12 OF 18 © MANOR REVIEW CENTER NOTES (K.L)

  Classification:  Clinical Manifestations: morbilliform rashes all over
o Probable Dengue – recent travel/residency in a body; Koplik spots; opposite lower molar
place with dengue epidemic; fever + 2 of the  Complications: otitis media – most common;
following: nausea/vomiting, rashes, muscle pneumonia – most fatal; sub sclerosing
aches/joint pains, mucosal bleeding, positive panencephalitis (SSPE) – chronic complication
tourniquet test – > 20 petechiae/sq. inch, CBCPC –  Prevention: MMR vaccine – given at 9 months
leukopenia  Pneumovirus – Respiratory Syncytial Virus (RSV) – clinical
o Dengue with Warning Signs – abdominal pain; manifestations: acute bronchiolitis (< 1 year old)
persistent vomiting; mucosal bleeding; clinical sign  Filoviridae – thread-like virus
of plasma leakage (low BP); lethargy/restlessness; o Ebola Virus
liver enlagement (> 2 cm); laboratory confirmation  MOT: direct contact to body fluids (ex. blood)
(↓platelets; ↑hematocrit)  5 Strains:
o Severe Dengue – severe hemorrhage/bleeding; a. Zaire & Sudan – most virulent; 2014 West Africa
severe plasma leakage; severe organ involvement Outbreak
(liver + kidneys) b. Tail Forest
 Yellow Fever Virus c. Bundibugyo
 Japanese Encephalitis Virus – most common cause of viral d. Reston – found in Philippines and China; sourced from
encephalitis in Asia; vector: culex mosquito Philippine Macaque Monkey; does not cause disease in
 St. Louis Encephalitis Virus humans; disease in swines/pigs
 Zika Virus  Clinical Manifestations: severe bleeding in all outlets of
 West Nile Fever Virus body
 Hepacivirus – Hepatitis C o Marburg Virus – came from African Green Monkey
o Retroviridae – presence of reverse transcriptase (RNA   Arenaviridae
DNA); promote effect of oncogenes o Lassa Virus – house rat
 Human T Lymphocyte Virus (HTLV) – clinical o Tacaribe Complex – South American Hemorrhagic Fever
manifestations: leukemia  Junin Virus – Argentine Hemorrhagic Fever
 Human Immunodeficiency Virus (HIV) – tropism: helper T  Machupo Virus – Bolivian Hemorrhagic Fever
cells; strains: (1) HIV 1 – Philippines; (2) HIV 2 – Africa  Guanarito Virus – Venezuelan Hemorrhagic Fever
o Reoviridae – double stranded  Sambia Virus – Brazilian Hemorrhagic Fever
 Coltivirus – vector: dermacentor andersoni (tick); clinical  Lymphocytic Choriomeningits (LCM) – house mouse
manifestations: Colorado tick fever/mountain fever  Bunyaviridae – arbovirus
 Rotavirus – most common cause of diarrheal illness in o Encephalitis – arbovirus; phlebo virus; la crosse virus
infants o Hemorrhagic Fever – Harta Virus; Dobrava Virus; Sin
 Orbivirus Nombre Virus; Puumala Virus
 RNA (-) SENSE – (ParFABOR)  Orthomyxoviridae – influenza virus
o Paramyxoviridae o Influenza A – most antigenically unstable  genetic
 Respiro Virus rearrangement; cause of major epidemics; antigens:
a. Para Influenza Virus – aka laryngotracheobronchiolitis Haemaggglutinin (H); Neuraminidase (N)
(LTB); signs and symptoms: barking cough o Influenza B – may cause epidemics
 Viral Group: 1, 2, 3 o Influenza C – most antigenically stable; does not cause
 Mild URTI: 4 epidemics
 Rubula Virus  Rhabdoviridae
a. Mumps Virus o Rabies Virus – helical-bullet shape
 Host: humans  Incubation Period: 1 – 3 months (usual)
 MOT: respiratory droplets  Clinical Manifestations: rabies encephalitis – 100% fatal
 Clinical Manifestations: infectious parotitis  General Rule:
 Complication: orchitis – inflammation of prostate a. Observation Period: 10 days
glands b. All suspected rabid animals should be sacrificed for
 Mobili Virus autopsy
a. Measles – Rubeola c. Check for negri bodies for confirmation in autopsy
 Host: humans  Levels of Exposure
 MOT: respiratory droplets a. Casual Contact – wash area with soap and water; do not
 Prodromes: 3 C’s – cough, coryza, conjunctivitis give vaccine; do not give rabies immune globulin (RIG)
PAGE 13 OF 18 © MANOR REVIEW CENTER NOTES (K.L)
 b. Minor Scratches/Abrasions – wash area with soap and
water; give vaccine; do not admin RIG
c. Transdermal Wound – wash area with soap and water;
administer vaccine and RIG
V. ANTIVIRALS
 Treatment for Respiratory Viral Infection
o Neuraminidase Inhibitors – (ex. Oseltamivir; Zanamivir); for
influenza A, B
o Inhibitors of Viral Uncoating – (ex. Amantadine;
Rimantadine); for influenza A
o Ribavirin – DOC for treatment of respiratory syncytial virus
infection (RSV) in children; combine with interferon alpha
for treatment for Hepatitis C
 Treatment for Hepatic Viral Infection – Interferon Alpha;
Lamivudine – hepatitis B, HIV; Adefovir; Entecavir; Telbivudine
 Treatment for Herpetic Viral Infection – Acyclovir; Cidofovir;
Ganciclovir – herpes resistant to Acyclovir; Foscarnet;
Fumivirsen; Penaclovir; Famciclovir; Trifluridine
 Treatment for Retroviral Infections
o Mode of Treatment
 2 NRTI’s + 1 NNRTI’s
 Lamivudine + Tenofovir + Efavirenz
 Lamivudine + Zidovudine + Efavirenz
o Nucleoside Reverse Transcriptase Inhibitors (NRTI’s) – end
in –ine; (DAZZLE ST)
 Didanosine; Abacavir; Zidovudine; Zalcitabine;
Lamivudine; Emtricitabine; Stavudine; Tenofovir
o Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI’s)
– (NEED)
 Nevirapine; Efavirenz; Etravirine; Delaviridine
o Protease Inhibitors – end in –vir; (Trip sa SRI LANFA)
 Tripranavir; Saquinavir; Ritonavir; Indinavir; Lopenavir;
Ampenavir; Nelfinavir; Fosamprenavir; Alazanivir
o Entry Inhibitors – Enfaviritide; Maraviroc
o Integrase Inhibitors – Raltegravir
V. BACTERIOLOGY
I. GRAM POSITIVE
 Staphylococci
o Staphylococcus aureus – acute infevtive endocarditis;
catalase (+); coagulase (+); most abundant: anterior nares;
 Clinical
 Manifestations: abcess formation – stye, furuncle,
carbuncle; food poisoning – toxic producer
(enterotoxin), projective vomiting; toxic shock syndrome
– sepsis, toxic shock syndrome  TTST-1 (toxin
responsible), associated with child-bearing age women
that uses tampons; acute infective endocarditis;
osteomyelitis
 Treatment: penicillins
o Staphylococcus epidermis - most common microorganism
on skin; most contaminant of laboratory samples;
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associated with infections of implants, prosthetic devices;
catalase (+); coagulase (-)
o Staphylococcus saprophyticus – most common cause of
UTI in sexually active women
 Streptococci
o Streptococcus pneumonia – lancet shaped; capsulated 
Quellung reaction
 Clinical Manifestations: bacterial pneumonia  adults
 Treatments: penicillins (amoxicillin); cephalosporins
(cefuroxime)
o Streptococcus mutans – α-hemolysis; clinical
manifestations: dental carries
sucrose -(fermentation)-> lactic acid -> destroys
enamel -> dental cones
o Viridans – α-hemolytic; causing subacute infective
endocarditis; treatment: pen G (DOC)
o Streptococcus pyogenes – only group A, β-hemolytic
 Clinical Manifestations: most common cause of
bacterial pharyngitis, sore throat/strep throat
 Complications: peritonsilar abcess formation;
functional otitis media; scarlet fever (2nd disease);
rheumatic heart disease; acute glomerulonephritis
 Treatments: penicillins (amoxicillin)
o Streptococcus agalactiae – group B, β-hemolytic; clinical
manifestations: neonatal sepsis meningitis; normal flora
in vagina
 Non-Spore Forming Aerobic Bacilli
o Corynebacterium diptheriae – Chinese letter appearance
in microscope  metachromatic granules (Babes-Ernest
Bodies); clinical manifestations: diphtheria – formation of
necrotic membrane, found in tonsil area, bull-neck
appearance; Dacron Swab; DOC  macrolides
(Erythromycin, Azithromycin); prevention: Diptheria
vaccine, Pentavax  (1) D; (2) P (3) T; (4) Hep B; (5) Hib
(Haemophilus Influenzae Type B)
o Listeria monocytogenes – clinical manifestations:
meningitis, granulomatosis infantiseptica; treatment:
penicillin (ampicillin)
 Spore Forming Bacteria
o Bacillus (Aerobes)
 Bacillus cereus
 Clinical Manifestations: food poisoning
 Types:
o Emetic Type – associated with contaminated fried
rice
o Diarrheal Type – associated with saucy/meaty
food
 Bacillus anthracis – discovered by Robert Cobb; anthrax
 Forms:
o Cutaneous Anthrax – most common form;
necrotic tissue, black eschar
o Pulmonary Anthrax – Woolsorter’s Disease;
zoonotic disease; most fatal form of anthrax;
© MANOR REVIEW CENTER NOTES (K.L)
 widening of mediastinum (compartment of o PPD Skin Test/Tuberculin Skin Test – used to
thoracic cavity), death due to inability to breathe determine TB exposure; reading: after 48-72 hours
o Gastrointestinal Anthrax – rarest form;  positive result = > 15 mm
treatment: antibiotic (ciprofloxacin)  Culture: Lowenstein-Jenssen Media – used to determine
o Clostridium (Anaerobes) extrapulmonary TB
 Clostridium botulinum – botolinum toxin (botox)  Prevention: TB-DOTS
 MOT: inhibition of 1o excitatory transfer neuron o 5 Pillars: (1) tool for diagnosis; (2) adequate drug supply;
(acetylcholine) (3) treatment partner; (4) LGU support; (5) proper
 Clinical Manifestations: flaccid paralysis; floppy reading and monitoring
baby syndrome – associated with ingestion of o Follow Up: 2nd, 5th, 6th month of treatment
contaminated honey o Failure of Treatment: non-compliance for more than 2
 Treatment: give antitoxin months
 Clostridium tetani – tennis-racket shape;
tetanospasmin (toxin) III. GRAM NEGATIVE
 MOT: inhibition of GABA and glycine = ↑Ach  Spirochetes
 Clinical Manifestations: spastic paralysis  trismus o Treponema pallidum – MOT: sexual contact, child birth;
(lock jaw), sardonic smile, dysphagia/dyspnea, incubation period: 3 weeks; clinical manifestations: syphilis,
muscle stiffness, opisthotonus congenital syphilis
 Treatment: antibiotic (metronidazole) – DOC  Syphilis
 Prevention: tetanus toxoid; antitetanus serum  Stages:
 Clostridium perfringens – alpha toxin (toxin); clinical o Primary – appearance of hard chancre (painless
manifestations: gas gangrene genital lesion/ulcer); inflammation of groin area;
 Clostridium difficile – clinical manifestations: resolves after 1 week
pseudomembranous colitis; treatment: metronidazole o Secondary – latency period: asymptomatic;
(DOC) reactivation: rashes all over body
o Tertiary – multiorgan involvement; gumma
II. ACID-FAST formation
 Mycobacterium – 1o component  mycolic acid (waxy)  Congenital Syphilis – ToRCHes; transmitted during 2nd
o Mycobacterium leprae trimester of pregnancy
 Clinical Manifestations: leprosy; Hansen’s disease;  STI Work Up: - Venereal Disease Research Laboratory
cutaneous tuberculosis (VDRL); Rapid Plasma Reagin (RPR); HIV test; Hepatitis
 Forms: B Surface antigen (HBsAg)
TUBERCULOUS LEPROMATOUS  Clinical Manifestations: still birth; intrauterine growth
Description small number of depressed cutaneous restriction (IUGR); congenital defects (saddle nose;
microorganisms sensation; large number of
microorganisms; Treatment:
hutchinson teeth; mulberry molars; scaphoid scapula;
dapsone (DOC); rifampicin; saber skin)
clofazimine  Diagnosis: Serological Methods
Skin Lesion erythematous; flat nodular skin lesions found in
skin lesions well-ventilated parts of body o Non-Treponemal – screening: Veneral Disease
(ex. nose) Research Lab Method (VDRL); Rapid Plasma Reagin
Lepromin Test positive negative (RPR)
o Mycobacterium tuberculosis o Treponemal – confirmation: Treponema Pallidum
 Clinical Manifestations: pulmonary TB; extrapulmonary TB Hemagglutination Assay (TPHA); Fluorescenth
 Diagnosis: Treponemal Antibody Absorption (FTA-Abs)
 Clinical Diagnosis – based on signs and symptoms   Treatment: penicillin (DOC)
cough (> 2 weeks); unexplainable weight loss; low o Leptospira interoggans – MOT: direct contact with
grade fever; night sweats; chest pain/back pain; leptospire infected urine; clinical manifestation:
hemoptysis leptospirosis
 Laboratory Diagnosis  Classifications:
o Direct Sputum Smear Microscopy (DSSM) – gold  Suspected Leptospirosis
standard; submit 2 samples (consecutive days);  Anicteric Leptospirosis – mild
positive result = at least 1 sample has acid-fast  Icteric Leptospirosis – severe; aka Weil’s Disease;
bacillus triad: jaundice, hemorrhage, proteinuria
o Chest X-Ray (PAIL)

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  Treatment: doxycycline (DOC  prophylaxis and mild);
pen G (severe)
o Borrelia
 Borrelia burgodoferi – vector: tick; clinical manifestations:
Lyme Disease – bull’s eye appearance (tick bite)
 Borrelia recurrentis – clinical manifestations: relapsing
fever
 Forms:
o Epidemic – body louse (vector); humans (host)
o Endemic – ticks (vector); rodents (host)
 Neisseriae
o Neisseriae gonorrhea – gram (-); intracellular; diplococcic
 MOT: sexual contact (1o); child birth
 Risk of Infection:
 Men – 20%; asymptomatic
 Women – 50%; symptomatic
 Clinical Manifestations: Pelvic Inflammatory Disease
(PID); opthalmia neonatorum – blindness: < 24 hours; STI
– urethritis, epidydimitis, cervicitis
 Treatment: ceftriaxone; cefixime; azithromycin
o Neisseria meningitides – gram (+); diplococci; coffee
bean/kidney shape; clinical manifestations: meningitis;
meningococcemia – fulminant stage (purpura fulminans –
large ecchymoses  bullae)
 Bordetella Pertussis – strict aerobe
o Selective Media: Bordet-Gengou Media; colony: mercury
drop colony
o Clinical Manifestations: pertussis – whooping cough
 Stages: (1) paroxysmal; (2) catarrhal – infectious; toxin
production
o Treatment: macrolides (ex. azithromycin)
o Prevention: DPT vaccine
 Haemophilus
o Haemophilus infuenzae
 Humans: Type B (Hib)
 Clinical Manifestations: pneumonia (infants); meningitis;
sepsis; osteomyelitis
 Prevention: H influenza b conjugate vaccine
 Treatment: vaccination
 Complete – penicillin (pen G)
 Incomplete – penicillin (ampicillin)
o Haemophilus ducreyi – appears like a school of red fish;
MOT: sexual contact; clinical manifestations: soft
chancre/chancroid – painful genital ulcer/lesion; treatment:
ceftriaxone (DOC), cefixime
 Chlamydia
o Chlamydiae
 Chlamydia trachomatis
 MOT: sexual contact (1o); child birth
 Risks of Infection: men  symptomatic; women 
asymptomatic
 Clinical Manifestations: pelvic inflammatory disease;
ophthalmia neonatorum; blindness: > 72 hours;
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trachoma; lymphogranuloma vencreum (LGV); STI:
urethritis, cervicitis, precititis, epidydimitis
 Treatment: tetracycline (ex. doxycycline)
o Chalmydophila
 Chlamydia psittaci – clinical manifestations: psittacosis
 Chlamydia pneumoniae
 Mycoplasma and Ureaplasma
o Mycoplasma pneumoniae – wall-less; pleomorphic
 1o component – sterols
 Staining Method: Diene’s Staining; colony: fried egg
colony
 Clinical Manifestations: walking pneumonia
 Treatment: tetracycline (DOC)
o Ureaplama urealyticum – clinical manifestation: non-
gonococcal urethritis in men
 Enterobacteriaceae
o Shigella
 Causative Agent: shigella dysenteriae; s. flexneri; s. sonnei;
s. boydii
 MOT: fecal-oral (associated with improper hand washing)
 Clinical Manifestation: bloody dysentery – scanty stool
with blood and mucus
 Treatment: ampicillin (DOC)
o Salmonella typhii
 MOT: ingestion of contaminated poultry products (ex.
chicken; eggs)
 Clinical Manifestations: bacterial gastroenteritis ot
salmonellosis; typhoid fever – enteric fever  rose spots
– samon colored; blanching maculopapular rashes
 Treatment: empirical therapy – ceftriaxone;
azithromycin; severe typhoid fever – ciprofloxacin (1st
line)
o Escherichia coli – most common cause of UTI
 Strains:
 ETEC – enterotoxigenic; associated with Traveller’s
Diarrhea
 EPEC – enteropathogenic; associated with infantile
diarrhea in 3rd world countries
 EIEC – enteroinvasive; associated with shigella-like
diarrhea
 EAEC – enteroaggregative; associated with diarrhea in
immunocompromised individuals
 EHEC – enterohemorrhagic; aka O157:H7 strain;
hemolytic uremic syndrome (HUS)
 Pseudomonas aeruginosa – obligate aerobe; oxidase (+)
o Clinical Manifestations: wound infection/burn wound
infection (pigment: pyocyanin, pyoverdin; odor: grape-
like/sweet-taco-corn like); sepsis – skin lesion: ecthyma
gangeonosum; pneumonia  atypical
o Treatment: penicillin (ex. carbenicillin; ticarcillin;
piperacillin); cephs (ex. ceftazidine; cefoperazone)
© MANOR REVIEW CENTER NOTES (K.L)
 Campylobacter and Helicobacter CAUSATIVE
AGENT
MOT CLINICAL
MANIFESTATION
TREATMENT

o Campylobacter jejuni – j-shape/gull-wing shape; MOT: Amebiasis Entamoeba fecal-oral amebic dysentery; Metronidazole
histolytica amebic liver abcess (DOC);
fecal-oral; clinical manifestation: bloody diarrhea; Entamoeba Tinidazole;
dispar Iodoquinol
treatment: macrolides (ex. azithromycin) Fresh Water Naegleria fowleri Primary amebic meningoencepalopathy
Amoeba (PAM)
o Helicobacter pylori – urease (+) Acanthamoeba castellani Granulomatous amebic encephalopathy
 Clinical Manifestations: gastric carcinoma; peptic ulcer (GAE)
Giardiasis Giardia fecal-oral traveller’s diarrhea; Metronidazole
disease (gastric – 70%, nocturnal pain; duodenal – 90%, lamblia gay bowel syndrome (DOC)
abdominal pain; foul
pain is relieved by food  obese patients) –smelling diarrhea;
malabsorption of
 Diagnosis: endoscopy – gold standard; urea breathe test adek (steatorrhea)
Cyclosporidiasis Cylcospora ingestion of abdominal pain; Co-Trimoxazole
– urea –(urease)-> ammonia cayetanensis cyst- nausea and vomiting; (DOC)
 Treatment: contaminated diarrhea
fruits and
 Monotherapy vegetables
Trichomoniasis Trichomonas sexual contact dysuria; burning Metronidazole
 Double Therapy vaginalis sensation during (DOC)
urination; severe
 Triple Therapy – PPI + 2 ABX (clarithromycin; vaginal pruritis;
yellow-green/yellow
amoxicillin; metronidazole) curdy vaginal
 Quadriple Therapy – PPI + 2 ABX + surface coating discharge with fishy
odor
agent (sucralfate; rebamipide) Toxoplasmosis Toxoplamsa inhalation of cervical Sulfadiazine +
gondii cyst from cat’s lymphadenopathy; Pyrimethamine
 Vibrionaceae feces; ingestion retinitis (DOC);
of raw pork Clindamycin
o Vibrio cholerae (Alternative)

 MOT: fecal-oral Malaria Vector: anopheles mosquito (female)

Causative Agent: Plasmodium spp.
 Clinical Manifestations: cholera – osmotic type diarrhea  Plasmodium falciparum – 50%; most virulent; malignant tertian malaria
 Plasmodium vivax – 40%; benign tertian malaria
 rice watery stool  Plasmodium malaria – 10%; quartan malaria
 Plasmodium ovale – rarest form; benign tertian malaria
 Diagnosis: selective media  TCBS – colony: yellow Life Cycle:
sporozoites  merozoites (liver) ↔ trophozoites (erythrocytes)  gametocytes
colony Treatment:
 Treatment: fluoroquinolones (ex. ciprofloxacin)  chloroquine + Fansidar® (sulfadoxine + pyrimethamine) – DOC as first line
agent for P. falciparum  non-resistant and severe
o Vibrio parahemolyticus – MOT: ingestion of raw shell fish;  arthemeter + lumenfantrine – DOC as second line treatment for plasmodium
resistant to first line
clinical manifestations: cholera-like diarrhea; TCBS: green  quinine + doxycycline – DOC as third line agent for SEVERE malaria
 primaquine – radical cure; DOC to prevent transmission and relapse
colony  chloroquine – DOC for erythrocytic stage of malaria; DOC for P. vivax
o Vibrio vulnificus – clinical manifestations: mild URTI, wound Leishmaniasis Vector: sand fly
Causative Agent: Leishmania spp.
infection; TCBS: blue-green colony  Leishmania tropica, L. Mexicana – cutaneous leishmaniasis
 Leishmania brasiliensis – mucocutaneous leishmaniasis (espundia)
 Leishmania donovani, L. chagasi – visceral leishmaniasis (Kala-azar)
Treatment: Stibogluconate
VI. PARASITOLOGY Trypanosiomasis
African Trypanosoma tse-tse fly West African Non-Nervous:
 Branches  protozoology & helminthology Trypanosomiasis brucei Suramin,
gambiense Pentamidine
Trypanosoma East African Nervous:
brucei Melarsprol
I. PROTOZOAN – unicellular; free-living rhodesiens
 Phyla: American
Trypanosomiasis
Typanosoma
cruzi
kissing bug Chaga’s disease Nifurtimox;
Benznidazole
o Sarcomastigophora
 Sarcodina > Pseudopods II. HELMINTHOLOGY
 Mastigophola > Flagella  Platyhelminthes – flatworms; trematodes (flukes); cestodes
o Cillophora – cilia; (ex. Balantidium coli – spherical shape (tapeworm)
ulcer)  Roundworms – nematodes
o Apicomplexa
o Microspora I. NEMATODES
CAUSATIVE MOT CLINICAL TREATMENT
AGENT MANIFESTATION
Ascariasis – aka Ascaris ingestion of eggs Albendazole;
giant intestinal lumbricoides Mebendazole
roundworm
Strongloidiasis Stronglyoides direct massive Ivermectin
– aka thread stercoralis penetration into autoinfection
worm skin of larvae
Hookworm Necator direct iron deficiency Albendazole;
americanus penetration of anemia Mebendasone
(New World); larvae into skin
Ancylostoma
duodenale
(Old World)
Trichinellosis Trichinella ingestion of eggs muscle aches Albendazole;
spiralis encysted in raw Mebendazole
pork

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 Whip Worm Trichuris ingestion of eggs rectal prolapse Albendazole;
trichiuria Mebendazole
Enterobiasis Enterobius ingestion of eggs severe nocturnal Pyrantel pamoate;
vermicularis perianal itching Albendazole;
(Human Diagnosis: scotch
Pinworm) tape swab test
Onchocerca Onchocerca black fly (vector) river blindness Ivermectin
Volvus Volvus
Filiriasis Wuchereria mosquito bites elephantiasis; Diethylcarbamazine
bancrofti; tropical
Brugia eosinophilia
malayi

II. TREMATODES
 Schisotomiasis
o Causative Agent: Schistosoma japonicum; S. mansoni (liver);
S. haematobium (urinary bladder)
o MOT: direct penetration of cercariae into skin
o Clinical Manifestations: swimmer’s itch; katayama fever;
liver cirrhosis; portal HTN  ascites
o Treatment: praziquantel

III. CESTODES
COMMON MOT CLINICAL TREATMENT
NAME MANIFESTATION
Taenia solium pork Ingestion of raw neurocystecercosis Niclosamide;
tapeworm pork Praziquantel
Taenia saginata beef Ingestion of raw GI disturbances Praziquantel
tapeworm beef
Diphyllobothrium fish ingestions of eggs Vitamin B12 Praziquantel
latum tapeworm  raw fish deficiency
Hymenolepis dwarf ingestion of eggs Praziquantel
nana tapeworm

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