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MMB311 Study Note

The document is a comprehensive exam study note for Medical Microbiology and Parasitology, covering topics such as classification, identification, and nomenclature of microorganisms, bacterial structure and function, bacterial growth and metabolism, and antimicrobial agents and therapy. Key concepts include the classification of bacteria, the Gram stain procedure, bacterial reproduction, and mechanisms of action for various antimicrobial drugs. The notes are prepared for nursing students at Osun State University and include essential definitions and classifications relevant to the field.
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0% found this document useful (0 votes)
10 views39 pages

MMB311 Study Note

The document is a comprehensive exam study note for Medical Microbiology and Parasitology, covering topics such as classification, identification, and nomenclature of microorganisms, bacterial structure and function, bacterial growth and metabolism, and antimicrobial agents and therapy. Key concepts include the classification of bacteria, the Gram stain procedure, bacterial reproduction, and mechanisms of action for various antimicrobial drugs. The notes are prepared for nursing students at Osun State University and include essential definitions and classifications relevant to the field.
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

MMB 311 — MEDICAL MICROBIOLOGY &

PARASITOLOGY
COMPREHENSIVE EXAM STUDY NOTE
Osun State University, Osogbo — 300 Level Nursing
Prepared for: Abdurrazaq Muslimah Alarape

SOURCES: All uploaded lecture slides + flagged standard knowledge where slides were silent
TOPIC 1: CLASSIFICATION, IDENTIFICATION & NOMENCLATURE
OF MICROORGANISMS
Source: Classification__Identification_and_Nomeclature_of_Microorganisms.pptx

1.1 What Are Microorganisms?


Microorganisms are organisms too small to be seen with the naked eye. They are observed with a
microscope.
Types of microscopes:
• Bright field
• Phase-contrast
• Dark-field
• Fluorescence
• Electron microscope

Microorganisms are ubiquitous (found everywhere). They can be:


• Normal flora (harmless/beneficial residents of the body)
• Pathogenic (cause disease)
• Types: bacteria, parasites, viruses, fungi

1.2 Bacterial Taxonomy


Taxonomy = Classification, Identification, and Nomenclature of bacteria.
Most important classification tool: Gram's Stain.
• Bacteria are divided into Gram-positive and Gram-negative groups.
• Bacteria may be motile or non-motile.

1.3 Classification of Bacteria


A. By Ancient Origin
TERM DEFINITION
Archaeobacteria Ancient bacteria — primitive, often found in extreme environments
Eubacteria True bacteria — the typical bacteria studied in microbiology

B. By Shape (Morphology)
TERM DEFINITION
Cocci (coccus) Spherical/circular. Arrangements: singly, diplococci (pairs), tetrads
(4), sarcinae (8), streptococci (chains), staphylococci (clusters)
Bacilli (bacillus) Rod-shaped. May have flagella. Arrangements: singly, diplobacilli
(pairs), streptobacilli (chains)
Spirilla (spirillum) Curved to corkscrew spiral. Rigid and motile. Spirochetes = long,
slender, flexible spirilla
Vibrio Curved like a comma. Example: Vibrio cholerae (causes cholera)
Coccobacillus Shape between a sphere and a rod

C. By Oxygen Requirement
TERM DEFINITION
Aerobic Require oxygen for respiration
Anaerobic Grow in absence of oxygen
Microaerophilic Grow in small amounts of oxygen (5% O2, 10% CO2)
Facultative Can live with or without oxygen (grow better with O2)
Obligate aerobe Grow ONLY in presence of O2
Obligate anaerobe Die in presence of O2
Aerotolerant anaerobe Grow equally well with or without O2

D. By Energy Source
TERM DEFINITION
Photosynthetic Use sunlight to produce their own carbohydrates for energy
autotrophs
Chemosynthetic Process inorganic molecules (e.g., sulfur, iron) for energy
autotrophs
Heterotrophs Depend on outside organic molecules (e.g., carbohydrates, sugars)
for energy

1.4 The Gram Stain — Procedure and Interpretation


Devised by Christian Gram. It is a differential stain — it differentiates bacteria based on cell wall
differences.

Procedure steps:
• Apply crystal violet (primary stain) — both gram+ and gram- stain purple
• Apply Lugol's iodine (mordant) — forms a complex with crystal violet
• Decolorize with alcohol — washes off the stain from gram-negative bacteria
• Apply safranin (counterstain, light red) — stains the decolorized gram-negative bacteria pink

Interpretation:
TERM DEFINITION
Gram-positive Thick peptidoglycan + teichoic acid. Resist decolorizing. Stain
PURPLE/VIOLET
Gram-negative Thin peptidoglycan + outer membrane with LPS. Washed off by
alcohol. Stain PINK/RED

⚠ NOTE: Teichoic acid is found ONLY in gram-positive bacteria. This is commonly tested.

1.5 Nomenclature of Microorganisms


System used: Binomial nomenclature (two names: generic + species name).
• Generic name: starts with a CAPITAL letter
• Species name: lowercase
• Both names are italicized or underlined
• Example: Vibrio cholerae (causes cholera)

Virus nomenclature does NOT follow standard binomial rules. Viruses are named by:
• Disease they cause — e.g., Measles virus, Smallpox virus
• Place of first report — e.g., Ebola virus, Norwalk virus
• Discoverers — e.g., Epstein-Barr virus
• Latin/Greek words — e.g., Coronaviridae = 'crown'; Parvoviridae = 'small'
• Route of infection — e.g., Influenza virus ('influence of bad air')
TOPIC 2: BACTERIAL STRUCTURE AND FUNCTION
Source: Bacterial_structure_and_function.pptx

2.1 General Features of Bacteria


• Bacterium = single cell organism; Bacteria = plural
• Found in soil, water, air, human body, arctic ice, deserts — ubiquitous
• Smallest cells: ~0.35 µm diameter; largest common bacteria: ~2 µm long
• Capable of independent respiration and can complete life cycle without other cells
• Bacteriology = the study of bacteria

2.2 Cell Envelope


The cell envelope = plasma membrane + cell wall. Functions:
• Provides structural integrity
• Protects against internal turgor pressure (inside has higher protein concentration than outside)

2.3 Peptidoglycan (Murein)


Unique to bacteria — not found in any other organism. Located immediately outside the cytoplasmic
membrane.
• Made of: polysaccharide backbone of alternating N-Acetylmuramic acid (NAM) and N-
Acetylglucosamine (NAG) in equal amounts
• Responsible for: rigidity of cell wall and determination of cell shape
• Relatively porous — not a permeability barrier for small substrates
• Attacked by: lysozyme (breaks bonds between NAM and NAG)

2.4 Gram-Positive vs Gram-Negative Cell Walls


TERM DEFINITION
Gram-Positive THICK peptidoglycan (up to 95% of wall). Contains TEICHOIC
ACIDS (ribitol and glycerol types). No outer membrane. Stains
PURPLE.
Gram-Negative THIN peptidoglycan (5-10% of wall). Has OUTER MEMBRANE
containing LPS (lipopolysaccharide). LPS is responsible for
antigenic properties. Stains PINK.

2.5 Plasma Membrane


Also called cytoplasmic membrane.
• Composed of a phospholipid bilayer
• Functions: permeability barrier for most molecules; transport of molecules into the cell
2.6 External Structures
Fimbriae (Attachment Pili)
• Short protein tubes extending from outer membrane
• Present in high numbers over the entire bacterial surface
• Function: attachment of bacteria to surfaces

Pili
• Longer than fimbriae; present in low numbers
• Sex pili (conjugation pili): allow exchange of genetic material between bacteria (conjugation)
• Other pili: attach bacteria to plant or animal cells
• Loss of pili = bacteria cannot establish infection
• All gram-negative bacteria have pili

Flagella
Whip-like structures responsible for bacterial motility.
TERM DEFINITION
Monotrichous Single flagellum
Lophotrichous Tuft of flagella at one pole
Amphitrichous Single flagellum at each of two opposite poles
Peritrichous Multiple flagella at several locations around the cell

2.7 Internal Structures


Bacterial DNA / Nucleoid
• NOT enclosed in a membrane-bound nucleus — resides in cytoplasm (prokaryote feature)
• Most bacterial chromosomes are circular (some linear exist)
• Plasmids: small, independent, circular pieces of DNA; encode traits that are advantageous but
not essential; can be gained or lost; transferred between bacteria (horizontal gene transfer)

Ribosomes
• Site of protein synthesis
• Prokaryotes: 70S ribosomes (made of 50S + 30S subunits)
• 50S subunit contains 23S and 5S rRNA
• 30S subunit contains 16S rRNA
• Eukaryotes: 80S ribosomes — this DIFFERENCE is exploited by antibiotics

Inclusions
• Non-living, non-metabolic, non-membrane-bound cytoplasmic components
• Volutin granules: contain inorganic polyphosphate; also called metachromatic granules
• Appear red or blue when stained with methylene blue or toluidine blue (metachromatic effect)
TOPIC 3: BACTERIAL CELL GROWTH AND METABOLISM
Source: Bacterial_cell_Growth.pptx

3.1 Key Definition


Microbial growth = increase in the NUMBER of cells (population growth), NOT increase in size of
individual cells.

3.2 Bacterial Reproduction


• Method: Binary fission (primitive cell division)
• Process: bacterium doubles in size, replicates chromosome, two chromosomes attach to
separate sites on plasma membrane, cell wall forms between them, two daughter cells
produced
• Generation time: time taken for bacteria to reproduce itself (double its number)

3.3 Phases of Bacterial Growth (Growth Curve)


Bacteria in culture medium pass through 4 sequential phases:

TERM DEFINITION
1. Lag Phase Initial phase. NO increase in cell numbers. Bacteria adjusting to
new medium. High metabolic activity as cells prepare to grow.
2. Log Cell numbers increase exponentially — doubles every generation
(Logarithmic/Exponential time. Condition is favourable. Nutrients abundant. This is the phase
) Phase of maximum growth rate.
3. Stationary Phase Population does NOT increase OR decline. Equilibrium between
new cells and dying cells. Caused by: depletion of critical nutrients
OR accumulation of waste products (metabolic byproducts),
overcrowding.
4. Death Phase Cells begin to die exponentially (but at a low rate). Caused by
depletion of intracellular ATP reserves. NOT all cells die in this
phase.

⚠ NOTE: Lag phase = no growth. Log phase = maximum growth. Stationary = equilibrium. Death =
decline. These are frequently tested in MCQs.

3.4 Conditions Required for Bacterial Growth


A. Temperature
TERM DEFINITION
Psychrophiles Cold-loving. Optimum temperature: 10°C
Mesophiles Moderate temperature: 25°C – 35°C (most pathogens including
human pathogens are mesophiles)
Thermophiles Heat-loving. Optimum: 60°C
Extreme thermophiles Optimum: 80°C – 100°C

B. pH
TERM DEFINITION
Acidophiles pH 0–6 (acidic environments)
Neutrophiles pH 7–9 (neutral environments — most pathogens)
Alkalophiles pH 10–14 (alkaline environments)

C. Water and Osmotic Pressure


• Bacteria grow best in areas saturated with water
• Increase in osmotic pressure causes the cell to burst (lyse)
• Optimum pressure is required for best growth

D. Oxygen Requirements (detailed classification)


TERM DEFINITION
Obligate aerobes Grow ONLY in the presence of O2
Facultative anaerobes Grow with or without O2, but better WITH O2
Aerotolerant anaerobes Grow equally well with or without O2
Obligate anaerobes Die in presence of O2
Microaerophilic Grow in 5% O2 and 10% CO2
TOPIC 4: ANTIMICROBIAL AGENTS AND THERAPY
Source: ANTIMICROBIAL_AGENTS_AND_THERAPY-[Link] — Dr. A. R. Ojewuyi

4.1 Key Definitions


TERM DEFINITION
Antimicrobials Substances that kill or inhibit the growth of microorganisms. May be
natural, semi-synthetic, or synthetic.
Antimicrobial therapy The use of antimicrobial substances to treat infections.
Chemotherapy Use of chemicals for therapy in diseases (infections or
malignancies).
Antibiotics Natural substances produced by microorganisms (or semi-
synthetic) that selectively kill or inhibit bacteria at low
concentrations WITHOUT considerable harm to the host.
Bacteriostatic INHIBITS the growth of bacteria (does not kill).
Bactericidal KILLS bacteria.
Selective toxicity Property of a drug to kill/inhibit the target organism without injuring
host cells.

⚠ NOTE: All antibiotics are antimicrobials, but NOT all antimicrobials are antibiotics.

4.2 Brief History


• 1928: Alexander Fleming discovered penicillin — extracted from the fungus Penicillium spp.

4.3 Classification of Antimicrobials by Target Organism


TERM DEFINITION
Antibacterial Active against bacteria
Antiviral Active against viruses
Antifungal Active against fungi
Antiprotozoal Active against protozoa
Anthelmintic Active against helminths (worms)

4.4 Mechanisms of Action of Antibacterial Drugs


1. Cell Wall Synthesis Inhibitors — Beta-Lactams
Beta-lactams include: Penicillins, Cephalosporins, Monobactams, Carbapenems.
• Interfere with cross-linking of peptidoglycan in cell wall
• Effectiveness depends on concentration exceeding MIC (Minimum Inhibitory Concentration) and
continuously saturating active sites of PBP (Penicillin-Binding Protein)

Penicillins:
• Penicillin G, Penicillin V — natural penicillins
• Ampicillin, Amoxicillin — aminopenicillins
• Methicillin, Nafcillin, Oxacillin, Cloxacillin, Dicloxacillin — penicillinase-resistant
• Ticarcillin, Carbenicillin, Piperacillin, Mezlocillin — anti-pseudomonal
• Beta-Lactamase inhibitors: Clavulanic Acid, Sulbactam, Tazobactam

Cephalosporins (generations):
TERM DEFINITION
1st generation Cephalothin, Cephapirin, Cefazolin, Cefadroxil, Cephalexin
2nd generation Cefuroxime, Cefaclor, Cefamandole, Cefoxitin, Cefotetan
3rd generation Ceftriaxone, Ceftazidime, Cefotaxime, Cefixime, Cefoperazone
4th generation Cefepime
5th generation Ceftaroline

• Monobactam: Aztreonam — active against gram-negative rods only; NO activity against gram-
positive or anaerobes
• Carbapenems: Imipenem, Meropenem, Ertapenem

2. Cell Membrane Function Inhibitors


• Polymyxin B and Colistin (Polymyxin E) — inhibit gram-negative bacteria
• Mechanism: competitively displace Mg2+ or Ca2+ from negatively charged phosphate groups
on membrane lipids
• Activity antagonized by Mg2+ and Ca2+

3. Protein Synthesis Inhibitors


Exploit the difference between bacterial 70S ribosomes and mammalian 80S ribosomes.
TERM DEFINITION
30S subunit inhibitors Aminoglycosides (e.g., Gentamicin, Streptomycin), Tetracyclines
50S subunit inhibitors Macrolides (e.g., Erythromycin), Lincomycins (Clindamycin),
Chloramphenicol, Streptogramins, Oxazolidinones
Chloramphenicol Inhibits peptidyl transferase on 50S subunit
Oxazolidinones Inhibit fMet tRNA binding to P site

4. Nucleic Acid Synthesis Inhibitors


TERM DEFINITION
Rifampin Binds to beta subunit of DNA-dependent RNA polymerase.
Prevents RNA synthesis.
Quinolones Inhibit bacterial DNA gyrase (prevents DNA replication)
Sulfonamides Structural analogs of PABA. Compete with PABA for active site of
DHPS, blocking folic acid synthesis. Folic acid is required for
nucleotide precursors.

4.5 Antifungal Agents


Fungi are difficult to eradicate because:
• Mammalian cells lack enzymes to degrade fungal cell wall polysaccharides
• Both mammals and fungi are eukaryotic with similar cell membranes (contain sterols)
TERM DEFINITION
Ergosterol Found in FUNGAL cell membrane
Cholesterol Found in MAMMALIAN cell membrane

Antifungal mechanisms:
• Interact with ergosterol and punch holes in membrane: Polyenes — Amphotericin B, Nystatin
• Inhibit ergosterol synthesis: Azoles (Imidazoles: Cotrimazole; Triazoles: Fluconazole),
Allylamines (Terbinafine/Lamisil)
• Inhibit synthesis of glucan in cell wall: Echinocandins (Caspofungin)
• Inhibit DNA and RNA synthesis: Flucytosine
• Accumulate in stratum corneum to block fungal penetration: Griseofulvin
• For superficial mycoses: Benzoic Acid (fungistatic), Gentian Violet (for Candida)

4.6 Antiviral Agents


Viruses are obligate intracellular parasites — replication depends on host cell.
Antiviral drugs:
• Must be active INSIDE host cells
• Are VIRUSTATIC — do not eliminate non-replicating or latent virus
• May need activation by viral or cellular enzymes before exerting effect
To inhibit viral replication, drugs either:
• Block viral entry
• Block viral exit
• Inhibit any step in between
• Single nucleotide mutations in target viral protein may cause drug resistance

4.7 Antibiotic Susceptibility Testing


Purpose: determine which antibiotics a bacterial isolate is sensitive to.
• Broth macro dilution (Tube dilution test)
• Broth micro dilution / MIC panels
• Agar dilution tests
• Disk diffusion testing / Etest

Minimum Inhibitory Concentration (MIC):


• The lowest concentration of antibiotic that visibly inhibits growth of a bacterium
• For effectiveness: antibiotic concentration must exceed MIC
• Large zone of clearance in disk diffusion = sensitivity to that antibiotic

4.8 Resistance to Antimicrobial Drugs


Mechanisms of Resistance
TERM DEFINITION
Enzyme inactivation Beta-lactamases cleave beta-lactam ring of
penicillins/cephalosporins
Reduced permeability Changes in bacterial membrane prevent antibiotic entry into cell
Target mutation Alters binding characteristics of antibiotics to their target
Altered metabolic Some resistant bacteria acquire PABA from environment (bypass
pathways sulfonamide block)
Efflux pumps Molecular pumps export antibiotics faster than the rate of import

Non-genetic Origins of Resistance


• Low replication rates (antibiotic metabolized before it acts) — e.g., Mycobacteria
• Bacterial L forms — cell wall-free bacteria; cell wall inhibitors useless
• Colonization of sites where antibiotics cannot reach — e.g., Gentamicin cannot enter cells;
Salmonella resistant to gentamicin

Genetic Origins of Resistance


Chromosomal Resistance:
• Mutations in RNA polymerase render it resistant to rifampin
• Efflux pumps with specificity for antibiotics — found in all bacteria

Extrachromosomal Resistance — accounts for interspecies acquisition; contributes to MDR (multi-drug


resistance):
• Plasmids — carry resistance genes
• Transposons — mobile genetic elements
• Conjugation — direct cell-to-cell transfer of resistance genes
• Transduction — bacteriophage-mediated transfer
• Transformation — uptake of naked DNA from environment

Dangers of Indiscriminate Antibiotic Use


• OTC availability leads to emergence of antibiotic resistance
• Wrong antibiotic selected
• Full regimen not completed
• Hypersensitivities (e.g., penicillin anaphylaxis)
• Hepatotoxicity
• Changes in normal flora
TOPIC 5: STERILISATION AND DISINFECTION
Source: Sterilisation_and_Disinfection.pptx

5.1 Key Definitions


TERM DEFINITION
Sterilization Any process by which ALL forms of microbial life (bacteria, spores,
fungi, viruses) are COMPLETELY DESTROYED. 'Sterile' =
complete absence of all living microbes.
Disinfection Any process (chemical or physical) that destroys harmful microbial
agents. Does NOT necessarily destroy spores. Applied to
INANIMATE objects only.
Antiseptic Chemical agent applied to LIVING tissue to inhibit or kill
microorganisms.
Bacteriostatic Chemical agent that INHIBITS growth or multiplication of bacteria.
Action is REVERSIBLE.
Bactericidal Agent that KILLS bacteria.

⚠ NOTE: Disinfection is for inanimate objects. Antiseptics are for living tissue. Sterilization is the
highest level — kills everything including spores.

5.2 Physical Methods of Sterilization


A. Dry Heat
Preferred for glassware, oils, and powders that cannot be penetrated by water or steam.
TERM DEFINITION
Flaming Articles passed through Bunsen flame (need not become red hot).
Used for scalpels, culture tube mouths, glass slides, forceps points.
Limited immediate use.
Red heat Inoculating wire loops and needles heated in Bunsen flame until
RED HOT. Limited immediate use.
Incineration Microorganisms exposed to open flames are burned. Ideal for
infected animal carcasses.
Hot Air Oven Electrically heated, thermostatically controlled with built-in fan and
ventilator. Times: 3 hours at 140°C, 1 hour at 160°C, 30 minutes at
180°C. Ideal for dry glassware, non-absorbent cotton wool, paraffin
oil, powder.

B. Moist Heat
TERM DEFINITION
Pasteurization 60–65°C. Used for milk pasteurization and heat-killed bacterial
vaccines.
Boiling 100°C. Emergency use — syringes, scissors, forceps. Kills most
vegetative bacteria in 5–10 min. Some spores survive for hours.
Steam at 100°C (Koch Kills all vegetative organisms but NOT spores. Used for large
steamer) equipment, dairy industry. Tyndallisation (named after Dr. John
Tyndall): steam on 3 successive days to kill spore-forming bacteria.
Autoclave (121°C) Most effective moist heat method. 121°C at 15 psi pressure for 15
minutes. HIGHER pressure = HIGHER temperature = SHORTER
time. Used for culture media, surgical dressings.

⚠ NOTE: Autoclave is the GOLD STANDARD of sterilization. Pressure, not just heat, is the key
mechanism.

C. Radiation
TERM DEFINITION
Non-ionizing: UV Damages DNA. Used for surface sterilization, air disinfection in
radiation operating rooms.
Non-ionizing: Infrared Low energy electromagnetic rays. Kills by oxidation (heat
radiation generated). Used for large batches of syringes. Temperature:
190°C for 10 minutes.
Ionizing radiation High energy (gamma rays, X-rays). Penetrate packaging. Used for
sterilizing heat-sensitive items like plastics, sutures, prosthetics.

D. Filtration
• Used to sterilize HEAT-SENSITIVE fluids, air, solutions containing toxins, enzymes, drugs,
serum, sugars
• Sugar solutions caramelise during autoclaving — best filter-sterilized
• Used extensively in beer and wine industries
• Filter with known pore sizes sufficiently small to hold back bacteria
Types of filters:
• Candle-type filters
• Porcelain filters
• Sintered Glass filters
• Membrane filters — Seitz filter, Hemming filter

5.3 Chemical Sterilization


Chemical agents act on microorganisms by:
• Interfering with the enzymatic system of the organism
• Coagulation of proteins
• Disruption of cell membrane
• Oxidative damage
Common chemical agents:
TERM DEFINITION
Alcohols Denature proteins. Ethanol 70% commonly used.
Aldehydes — Supplied as 40% solution. Highly bactericidal. Active against
Formaldehyde (Formalin) spores.
Phenolic compounds Disrupt cell membranes. E.g., phenol, cresol.
Heavy metal salts Disrupt enzyme function (e.g., mercury, silver compounds).
TOPIC 6: THE IMMUNE SYSTEM
Source: THE_IMMUNE_SYSTEM_____.pptx — Dr. A. R. Ojewuyi

6.1 Overview
The immune system is a complex of interrelated structural, molecular, cellular, and humoral
components that provides the host's defense against pathogens, foreign substances, and aberrant
native cells.
An immune response = aggregate of different reactions mounted by the immune system against a
potential pathogen.

6.2 Two Arms of the Immune System


TERM DEFINITION
Innate Immunity First line of defense. Rapidly mobilized. NONSPECIFIC (does not
target specific pathogens). No immunologic memory.
Adaptive (Acquired) SPECIFIC for a pathogen. Slower to respond first time. Has
Immunity IMMUNOLOGIC MEMORY — responds rapidly and vigorously to
second exposure.

Both arms interact and collaborate to destroy pathogens. All immune cells develop from pluripotent
stem cells in the bone marrow.

6.3 Innate Immunity


Recognizes:
• Complex lipids and carbohydrates in peptidoglycan
• Lipopolysaccharides (LPS) of gram-negative bacteria
• Lipoteichoic acid in gram-positive bacteria
• Mannose-containing oligosaccharides found in many microbial molecules
• Double-stranded RNA (found in replicating viruses)
• Recognizes NON-SELF structures only — avoiding autoimmunity

Mechanisms of Innate Immunity


• Mechanical barriers and surface secretions
• Humoral defense: Lysozyme, Basic polypeptides, Acute-phase proteins, Interferon
• Complement (Classical pathway, Alternate pathway, MBL pathway)
• Cells: Neutrophils, Macrophages, NK cells, Dendritic cells
• Temperature
• Inflammation

Skin and Mucous Membranes


• Intact skin: physical barrier + fatty acids from sebaceous glands (antibacterial/antifungal activity)
• Acidic pH of skin (pH 3–5) has antimicrobial effect
• Mucous membranes of respiratory tract: lined with CILIA and covered with MUCUS
• Mucociliary apparatus ('ciliary elevator'): coordinated beating of cilia drives mucus up to
nose/mouth to expel trapped bacteria
• Damaged by: alcohol, cigarette smoke, viruses — predisposes to bacterial infections
• Defensins: positively charged peptides in GI and lower respiratory tract that create pores in
bacterial membranes, killing them
• Normal flora: harmless residents that prevent pathogens from multiplying in their niche

Cellular Components of Innate Immunity


TERM DEFINITION
Monocytes and Monocytes circulate in blood; mature into macrophages in tissues.
Macrophages Engulf and kill pathogens (phagocytosis), process and present
antigens, produce cytokines (TNF, IL-1). In liver = Kupffer cells; in
nervous tissue = Microglial cells.
Neutrophils Short half-life. Important phagocytic cells. Destroy pathogens within
(Granulocytes) intracellular vesicles. Attracted by IL-8 (chemokine).
Eosinophils and Less abundant. Store granules with enzymes and toxic proteins
Basophils released upon activation.
Dendritic cells Phagocytic. Main role: activate T cells in adaptive immunity by
acting as APCs (antigen-presenting cells). Produce regulatory
cytokines (e.g., IFN-alpha).
Natural Killer (NK) cells Large granular lymphocytes (10–15% of blood leukocytes). Kill
virus-infected cells and tumor cells. Critical in ADCC (antibody-
dependent cellular cytotoxicity). Have Fc receptors.

Phagocytosis — Steps
• 1. Pathogen enters blood or tissue
• 2. Tissue cells, endothelial cells, neutrophils, and macrophages release CHEMOKINES
(chemotactic cytokines)
• 3. IL-8 is a potent chemokine attracting neutrophils
• 4. Neutrophils attach to endothelial cell surface via adhesion molecules (P-selectin)
• 5. Neutrophils migrate from circulation through endothelium to infection site
• 6. Pathogen is recognized, engulfed, internalized into a phagosome
• 7. Pathogen is killed inside the neutrophil

6.4 The Complement System


• About 30 serum and membrane-bound proteins
• Synthesized mainly by the liver
• Many components are proenzymes — must be cleaved to form active enzymes
• Three activation pathways: Classical, Alternative, MBL (Mannose-Binding Lectin)
• ALL three pathways converge to form the Membrane Attack Complex (MAC): C5b, C6, C7, C8,
C9
• MAC forms a pore in the membrane causing CYTOLYSIS (free passage of water across
membrane)

Functions of activated complement — 4 major outcomes:


TERM DEFINITION
1. Cytolysis MAC punches holes in bacterial/cell membranes
2. Chemotaxis C5a attracts phagocytes to site of infection
3. Opsonization Complement fragments coat bacteria to enhance phagocytosis
4. Anaphylatoxins C5a triggers mast cell degranulation and inflammation

6.5 Adaptive Immunity


Highly specific. Takes several days first time. Has immunologic memory — second response is rapid
and vigorous.
Two components:
• Cell-mediated immunity (CMI) — mediated by T lymphocytes
• Antibody-mediated (humoral) immunity — mediated by B lymphocytes and antibodies

Antigens
• Substance that induces production of an antibody AND reacts with the antibody it induced
• Recognition of self vs non-self: achieved by MHC (Major Histocompatibility Complex) molecules
• MHC Class II molecules: present exogenous antigens (extracellular) to CD4+ T cells via APCs
• MHC Class I molecules: present endogenous antigens (intracellular) to CD8+ T cells

Superantigens
• Bacterial/viral antigens that activate large numbers of T cells through a special pathway
• Do NOT require processing — bind to MHC molecules OUTSIDE the peptide-binding cleft
• Stimulate ~25% more T cells than standard antigens
• Examples: Staphylococcal enterotoxins, Toxic shock syndrome toxin, Group A Streptococcal
pyrogenic exotoxin A
• Consequence: massive cytokine storm — IFN-gamma, IL-1, IL-6, TNF-alpha — causing shock
and multiple organ failure

6.6 B Cells and Antibodies


• Each individual has ~10^11 unique B lymphocytes
• Found in blood, lymph, bone marrow, lymph nodes, tonsils, Peyer's patches, appendix
• Each B cell displays a single specific BCR (B-cell receptor = immunoglobulin)
• Immature B cells carry IgM and IgD on surface
• When antigen binds BCR: B cell divides (clonal selection) → plasma cells → secrete antibodies
Immunoglobulin Structure
• All Ig molecules: 2 identical LIGHT (L) chains + 2 identical HEAVY (H) chains linked by disulfide
bridges
• Light chains: MW ~25,000; can be kappa (κ) or lambda (λ)
• Heavy chains: MW ~50,000; designated γ (IgG), μ (IgM), α (IgA), δ (IgD), ε (IgE)
• Fab fragment = antigen-binding fragment
• Fc fragment = crystallizable fragment (participates in complement activation and other biologic
activities)

Five Classes of Immunoglobulins


TERM DEFINITION
IgG MAJOR serum immunoglobulin. 4 subclasses (IgG1-4). IgG1 = 65%
of total IgG. ONLY Ig to cross the placenta — most abundant in
newborns. Mediates opsonization. IgG3 activates complement.
IgG4 does NOT activate complement.
IgM FIRST Ig produced in response to antigen. Secreted as
PENTAMER (5 units, J chain, 10 antigen-binding sites). Most
efficient in agglutination and complement fixation. Does NOT cross
the placenta — presence in fetus/newborn = evidence of
intrauterine infection.
IgA MAJOR immunoglobulin for MUCOSAL IMMUNITY. Found in
secretions: milk, saliva, tears, respiratory, intestinal, genital tracts.
In serum: monomer. In mucous secretions: DIMER = secretory IgA
(with J chain and secretory component). Neisseria spp. can destroy
IgA1 via a protease.
IgE Present in very low quantities. Fc binds to mast cells, basophils,
eosinophils. Triggers ALLERGIC (anaphylactic) responses by
releasing histamine and other inflammatory mediators.
IgD Present in trace amounts in serum. Major surface-bound Ig on
mature naive B lymphocytes. Function unclear.

Primary vs Secondary Immune Response


TERM DEFINITION
Primary Response First exposure to antigen. Antibody detectable within days to weeks.
First antibodies = IgM, then IgG/IgA. Antibody levels eventually
decline.
Secondary (Anamnestic) Second exposure to same antigen. MORE RAPID and HIGHER
Response levels than primary. Due to immunologic memory cells. Mainly IgG
(higher levels, persists longer, higher affinity). IgM level similar to
primary.
TOPIC 7: IMMUNIZATION
Source: IMMUNIZATION___.pptx — Dr. A. R. Ojewuyi

7.1 Definition and Objective


Immunization: Protection of susceptible individuals from communicable diseases by administration of:
• Living modified agent (live attenuated)
• Killed organisms
• Part (sub-unit) of a pathogen
• Inactivated toxin (toxoid)

Objective: Produce, without harm, a degree of resistance sufficient to prevent clinical attack of the
natural infection and prevent spread of infection to susceptible community members.

7.2 Types of Immunity Induced by Immunization


TERM DEFINITION
Active immunity Induced by vaccines. Individual ACTIVELY produces antibodies.
Long-lasting but protection is delayed until antibody levels are
sufficient.
Passive immunity Administration of PREFORMED antibodies (immune globulins).
IMMEDIATE protection. Does NOT confer long-term protection.
Useful when patient has no time to produce antibody.
Passive-active immunity Both immune globulins (immediate protection) AND a vaccine (long-
term protection) given together.

7.3 Herd Immunity


Also called community immunity. Occurs when a sufficiently large percentage of the population is
immunized, protecting even unimmunized individuals.
• Requirement: vaccine must PREVENT TRANSMISSION (not just prevent disease)
• Example: live attenuated polio vaccine (OPV) — induces intestinal IgA, prevents GI replication
of wild-type poliovirus, and is transmitted to others via stool = good herd immunity
• Killed polio vaccine (IPV) — does NOT induce secretory IgA — no herd immunity; only
immunized individuals protected

7.4 Types of Vaccines


Bacterial Vaccines
TERM DEFINITION
Capsular Polysaccharide S. pneumoniae (23 serotypes — for adults >60, chronic disease
Vaccines patients), N. meningitidis (serotypes A, C, W-135, Y), H. influenzae
type b (conjugated to diphtheria toxoid — for children 2–15
months), Salmonella typhi (one form is polysaccharide)
Toxoid Vaccines C. diphtheriae — diphtheria toxoid (at 2, 4, 6 months + boosters).
Clostridium tetani — tetanus toxoid. B. pertussis — pertussis toxoid
(acellular — first vaccine with genetically inactivated toxoid)
Killed Bacterial Vaccines V. cholerae (cholera), Y. pestis (plague), Rickettsia rickettsiae
(typhus), Coxiella burnetii (Q fever)
Live Attenuated Bacterial M. bovis BCG (tuberculosis), Salmonella Typhi (typhoid — oral),
Francisella tularensis (tularemia)

Viral Vaccines — Active Immunity


Three types:
• Live attenuated virus vaccines
• Killed (inactivated) virus vaccines
• Subunit vaccines (purified viral proteins — e.g., Hepatitis B vaccine)

TERM DEFINITION
Live vaccines Virus multiplies in host. Prolonged antigenic stimulus. Elicit both IgA
and IgG (when given via natural route). Elicit cytotoxic T-cell
response. Longer-lasting protection. Risk: may revert to virulence;
should NOT give to immunocompromised or pregnant patients.
Killed vaccines Given intramuscularly. Do NOT stimulate major IgA response. Do
NOT stimulate cytotoxic T-cell response (no viral replication).
Shorter duration. Cannot revert to virulence. More heat-stable —
better for tropical climates.

Vaccines grown in chick embryos (influenza, measles, mumps, yellow fever) — SHOULD NOT be
given to those with anaphylactic reaction to eggs.

Post-exposure Vaccines (effective when given after exposure):


• Rabies vaccine — long incubation allows post-exposure vaccination
• Hepatitis B vaccine — used after needle-stick injury

Passive Immunity in Viral Infections:


TERM DEFINITION
Rabies Immune Globulin High titer antibody from hyper-immunized humans. Given at bite
(RIG) site + intramuscularly. Given WITH killed rabies vaccine = passive-
active immunity. From humans to avoid hypersensitivity.
Hepatitis B Immune For needle-stick exposure or neonate born to HBV carrier mother.
Globulin (HBIG) From humans. Used with Hepatitis B vaccine = passive-active
immunity.
7.5 Nigerian Immunization Schedule
TERM DEFINITION
At Birth BCG, HBV-1, OPV-0
6 weeks OPV-1, Pentavalent-1 (DPT+HiB+HBV), PCV-1, Rotavirus-1
10 weeks OPV-2, Pentavalent-2, PCV-2
14 weeks OPV-3, Pentavalent-3, PCV-3
9 months Measles, Yellow Fever
15–18 months OPV, MMR (Measles-Mumps-Rubella), Chicken pox
24 months Meningitis, Typhoid fever

⚠ NOTE: Pentavalent = DPT + HiB + HBV. Previous schedule had separate HBV-2 at 6 weeks and
HBV-3 at 14 weeks.
TOPIC 8: CLASSIFICATION OF VIRUSES AND INTRODUCTION TO
VIROLOGY
Sources: classification_of_virus.ppt + DOC-20241204-WA0053_.ppt (Medical Virology)

8.1 General Properties of Viruses


TERM DEFINITION
Acellular Not made of cells — particles only
Size 20–300 nm (much smaller than bacteria)
Genetic material Either DNA OR RNA (never both)
Protein coat Capsid — made of capsomeres (protein subunits)
Envelope Some viruses have a lipoprotein membrane (derived from host cell
membrane); herpesviruses: from nuclear membrane
Obligate intracellular MUST replicate inside a host cell
Replication Unique: 1 virus → many viruses (unlike binary fission)
Nucleocapsid Genome (NA) + capsid combined

8.2 Viral Genome


RNA Viruses:
• All RNA viruses have single-stranded (ss) RNA EXCEPT Reoviruses (double-stranded RNA)
• Can be positive (+) polarity or negative (-) polarity

DNA Viruses:
• All DNA viruses have double-stranded (ds) DNA EXCEPT Parvoviruses (single-stranded DNA)
• All viruses are haploid EXCEPT Retroviruses (diploid — two copies of genome)

8.3 Viral Structure — Capsid and Symmetry


TERM DEFINITION
Icosahedral (cubic) Spherical virus. Capsomeres arranged in an icosahedron (20
symmetry faces). Examples: Adenovirus, Herpesvirus
Helical symmetry Elongated/pleomorphic virus. Nucleic acid is spiral; capsomeres
arranged around NA. Examples: Influenza, Rabies
Complex symmetry Does not conform to cubic or helical. Examples: Poxviruses
Envelope
• Derived from HOST cell membrane (during budding), EXCEPT herpesviruses (from nuclear
membrane)
• Contains glycoproteins that attach to host cell receptors
• Enveloped viruses are MORE SENSITIVE to heat, drying, and other factors than non-enveloped
viruses

8.4 Baltimore Classification (7 Classes)


Devised by David Baltimore. Classifies viruses based on genome type AND mode of
replication/transcription.

TERM DEFINITION
Class I dsDNA viruses. mRNA and genome replication as from host
genome. Examples: Adenoviridae, Herpesviridae, Poxviridae,
Papovaviridae, Hepadnaviridae
Class II ssDNA viruses. Form dsDNA intermediate for replication and
transcription. Example: Parvoviridae
Class III dsRNA viruses. Must synthesize mRNA using RNA-dependent RNA
polymerase (RDRP) carried in virion. Example: Reoviridae
Class IV Positive-strand ssRNA (+ssRNA). Genome acts directly as mRNA.
RDRP encoded in genome. Examples: Picornaviridae, Togaviridae,
Flaviviridae, Coronaviridae
Class V Negative-strand ssRNA (-ssRNA). Must first synthesize
complementary (+) strand mRNA using virion RDRP. Examples:
Paramyxoviridae, Orthomyxoviridae, Rhabdoviridae, Filoviridae,
Bunyaviridae
Class VI Retroviruses (+ssRNA — replicates via DNA intermediate). Use
REVERSE TRANSCRIPTASE to copy RNA → DNA. Examples:
Retroviridae (HIV)
Class VII dsDNA with RNA intermediate. Require reverse transcriptase.
Example: Hepadnaviridae (Hepatitis B)

⚠ NOTE: Retro = 'backward' in Latin. Retroviruses go backward: RNA → DNA (instead of normal
DNA → RNA). HIV is a retrovirus (Class VI Baltimore).

8.5 Taxonomic Naming of Viruses


TERM DEFINITION
Family Ends in -viridae (italicized)
Subfamily Ends in -virinae
Genus Ends in -virus
Species English common name
Order Ends in -virales
Example: Family Orthomyxoviridae → Genus Influenzavirus A → Species Influenza A virus

8.6 Viral Replication — Steps


TERM DEFINITION
1. Adsorption Glycoproteins on viral envelope (or folding in capsid proteins) attach
(Attachment) to specific receptors on host cell surface
2. Penetration Enveloped viruses: fusion with cell or endosome membrane. Non-
enveloped viruses: lysis of membrane or pore formation via
endocytosis
3. Uncoating Release of viral genome into cytoplasm or nucleus
4. Synthesis Transcription: viral genome → mRNA. Translation: mRNA → viral
proteins (using host ribosomes). Replication of viral genome.
5. Assembly NA + viral proteins = new virions
6. Release Enveloped viruses: BUDDING (acquires envelope from cell
membrane). Non-enveloped viruses: CELL LYSIS (rupture of cell
membrane)

8.7 Laboratory Diagnosis of Viral Infections


TERM DEFINITION
Microscopy Light microscopy: inclusion bodies (e.g., Owl's eye = CMV).
Electron microscopy: morphology and size (diagnosis of rotavirus,
adenovirus, herpes, pox). Now replaced by Ag detection and
molecular tests.
Cell culture Virus grown in PMK, HDF, or HEp-2 cells. Detects cytopathic
effects (CPE). Takes up to 5 days. Sensitive to bacterial
contamination. Some viruses (e.g., HCV) do not grow in cell culture.
Shell Vial Assay Rapid culture technique. Detects viral antigens in 1–3 days.
Serology — Antigen ELISA, Immunofluorescence (IF). Examples: Influenza
detection (nasopharyngeal aspirate), HSV (skin scrapings), Rotavirus
(faeces), HBsAg (blood)
Serology — Antibody CFT (complement fixation test), IF, ELISA.
detection
Molecular (PCR) Polymerase chain reaction. Amplifies viral genome. Used for
diagnosis and monitoring treatment response.
TOPIC 9: VECTOR CONTROL MEASURES
Source: [Link]

9.1 Definition of a Vector


A vector is an insect or any living carrier that transports an infectious agent from an infected individual
or its wastes to a susceptible individual, its food, or its surroundings. (Oxford Dictionary of
Epidemiology, 6th edition)

9.2 Types of Vectors


Invertebrate Vectors — 7 Orders:
TERM DEFINITION
Diptera — Mosquitoes Malaria, Filaria, Viral Encephalitis, Dengue, West Nile fever, Yellow
fever
Diptera — Flies Housefly: Typhoid, paratyphoid, diarrhoea, dysentery, cholera,
polio, trachoma, anthrax, yaws. Sandfly: Kala-azar, oriental sore,
Oroya fever. Tsetse fly: Sleeping sickness. Black fly:
Onchocerciasis
Orthoptera — Transmit enteric pathogens
Cockroaches
Siphonaptera — Fleas Rat flea: Bubonic plague, endemic typhus, chiggerosis,
Hymenolepsis diminuta
Anoplura — Lice Epidemic typhus, relapsing fever, trench fever, pediculosis
Hemiptera — Bugs Reduviid bug: Chagas disease
Acarina — Ticks and Hard tick: Tick typhus, viral encephalitis, KFD, Tularemia, tick
Mites paralysis, human babesiosis. Soft tick: Q fever, relapsing fever.
Trombiculid mite: Scrub typhus, Rickettsial-pox. Itch-mite: Scabies
Copepoda — Cyclops Guinea worm disease, fish tapeworm

Vertebrate Vectors:
• Mice, rodents, bats — Leptospirosis, Salmonellosis, Nipah virus disease

9.3 Types of Transmission by Vectors


TERM DEFINITION
Mechanical Transmission NO development or multiplication of pathogen in vector. Examples:
Cholera, Amebiasis (housefly)
Biological — Propagative Pathogen multiplies in vector. Example: Plague bacilli in rat fleas
Biological — Cyclo- Pathogen undergoes development AND multiplication in vector.
propagative Example: Malaria parasite in mosquitoes
Biological — Cyclo- Pathogen undergoes development WITHOUT multiplication in
developmental vector. Examples: Microfilaria in mosquitoes, Guinea worm in
cyclops
Transovarial Infected female transmits pathogen to her progeny (eggs).
Example: Tick-borne encephalitis

9.4 Integrated Vector Management (IVM)


Five components:
• Environmental Control
• Chemical Control
• Biological Control
• Mechanical and Physical Control
• Legislative Control

Anti-larval Measures:
Environmental:
• Source reduction, engineering measures (drainage, clearing stagnant water)

Chemical:
• Larvicides: Mineral oils (diesel oil, kerosene — once weekly), Synthetic insecticides (Fenthion,
Chlorpyrifos, Temephos/Abate), Paris green (stomach poison)

Biological:
• Fish: Gambusia affinis, Lebister reticulatus — one fish eats 100–300 mosquito larvae/day

Anti-adult Measures:
TERM DEFINITION
Residual sprays Insecticide on surfaces; particles remain for insects to pick up on
contact. Long period of efficacy. DDT, Lindane, Malathion (OMS-
33)
Space sprays Insecticide mist/fog sprayed into atmosphere. Pyrethrum extract 2%
(nerve poison). Ultra-low volume: Malathion, Fenitrothion
Genetic control Genetically modified Aedes OX513A by Oxitec (self-limiting genes).
Wolbachia bacteria infected male Aedes

Personal Protection:
• Mosquito nets: openings not exceeding 0.0475 inch; ~150 holes per square inch
• Screens: copper or bronze mesh, same specification
• Repellents: DEET (Diethyltoluamide)
Control of Specific Vectors:
TERM DEFINITION
Housefly Pyrethrum 0.1% residual spray, light traps, fly-proofing with mesh
Sandfly Seal cracks/holes, remove animal dung, DDT/Lindane residual
spray quarterly, personal protection
Fleas 10% DDT dust on rodents, indoor residual spray (malathion),
dusting pets, DEET repellent
Lice Good personal hygiene, 10% DDT powder or 0.5% permethrin dust,
permethrin 1% anti-lice shampoo
Ticks DDT, chlordane, malathion; environmental control; clothes
impregnated with repellent
Rodents Trapping, rodenticides: zinc phosphide, barium carbonate,
bromadiolone
TOPIC 10: INTEGRATED DISEASE SURVEILLANCE AND
RESPONSE (IDSR)
Source: [Link]

10.1 Disease Notification


Official reporting of designated diseases or disease syndromes to designated authorities.
• Disease Surveillance and Notification (DSN) introduced in 1988
• 40 notifiable diseases were initially addressed
• Regular, frequent, timely reporting is required for prevention and control

Classification of notifiable diseases:


• International
• National
• Occupational

10.2 Notifiable Priority Diseases in Nigeria


Epidemic-Prone Diseases:
CSM (Cerebrospinal Meningitis), Cholera, Measles, Viral Hemorrhagic Fever (Lassa), Human Influenza
(new subtype), Yellow fever, Diarrhoea with blood (Shigella), SARS, Smallpox, Dengue, Anthrax, SARI

Diseases Targeted for Elimination/Eradication:


Neonatal Tetanus, Leprosy, Lymphatic Filariasis, Acute Flaccid Paralysis/Poliomyelitis, Dracunculiasis
(Guinea worm), Tuberculosis

Other Diseases of Public Health Importance:


Diarrhoea (<5 years), Hepatitis B, HIV/AIDS, Malaria, Onchocerciasis, Pertussis, Pneumonia (<5
years), STIs, Trypanosomiasis, Buruli ulcer, Asthma, Diabetes, Epilepsy, Hypertension, Sickle cell
disease, Malnutrition, Plague, Trachoma, Typhoid, Human rabies, Schistosomiasis, Noma

10.3 Public Health Surveillance


Definition: The ongoing systematic collection, analysis, interpretation, and dissemination of health data.
(CDC Principles of Epidemiology, 1992)
Purpose: Provide a factual basis for setting priorities, planning programs, and taking action to promote
and protect public health.

Attributes of a Good Surveillance System:


• Simplicity
• Timeliness
• Sensitivity
• Specificity
• Completeness of information/reporting
• Representativeness
• Acceptability

Purposes of Surveillance:
• Assess public health status
• Trigger public health action
• Define public health priorities
• Evaluate programs

Uses of Surveillance:
• Detect epidemics / define a problem
• Estimate magnitude of problem
• Investigate cases and implement control measures
• Determine geographic distribution of illness
• Evaluate control measures
• Facilitate planning
• Portray the natural history of a disease
• Monitor changes in infectious agents
• Generate hypotheses and stimulate research

10.4 What is IDSR?


Integrated Disease Surveillance and Response (IDSR) is a STRATEGY (not a programme).
• Proposed in Harare, September 1998 for 46 WHO African countries
• Endorsed by Health Ministers of member states including Nigeria
• Aim: strengthen surveillance using an integrated approach
• Involves laboratory services in disease surveillance and epidemic response
• Focus: collection of data AND using the data to RESPOND to issues

10.5 IDSR Technical Guidelines — 8 Sections


• 1. Identify cases of priority diseases and conditions
• 2. Report priority diseases and conditions
• 3. Analyze and interpret data
• 4. Investigate suspected cases and outbreaks
• 5. Respond to outbreaks and other public health problems
• 6. Provide feedback
• 7. Evaluate and improve surveillance and response
• 8. Summary guideline for specific priority diseases and conditions

10.6 IDSR Forms


TERM DEFINITION
Form 001 (Immediate) 001A: Case-based form. 001B: Lab form. 001C: Line-listing of
cases
Form 002 (Weekly) Captures epidemic-prone diseases: Cholera, CSM, Lassa Fever,
Measles, Yellow Fever, HPAI
Form 003 (Monthly) Captures data on 22 priority diseases

Reporting Deadlines (Weekly — Form 002):


TERM DEFINITION
LGA to State By Monday of following week
State to Zone By Tuesday of following week
Zone to National By Wednesday of following week

Reporting Deadlines (Monthly — Form 003):


TERM DEFINITION
LGA to State By Day 7 after month-end
State to Zone By Day 10 after month-end
Zone to National By Day 14 after month-end

10.7 Types of Surveillance


TERM DEFINITION
Passive surveillance Provider-initiated reporting (health facility reports to authorities)
Active surveillance Public health system-initiated reporting (authorities seek out cases)
Sentinel surveillance Reporting from selected sentinel sites/facilities
Population-based Entire population monitored
surveillance
TOPIC 11: PARASITOLOGY — Classification, Life Cycles,
Diagnosis & Treatment
★ NOT FROM SLIDES — Standard Knowledge. This topic appeared in the course outline but no
dedicated parasitology file was uploaded. This section is based on standard
microbiology/parasitology knowledge.

11.1 Classification of Medically Important Parasites


TERM DEFINITION
Protozoa Single-celled eukaryotes. Examples: Plasmodium (malaria),
Entamoeba histolytica (amoebiasis), Giardia lamblia, Trypanosoma,
Leishmania, Toxoplasma gondii
Helminths (Worms) Multicellular organisms. Divided into: Nematodes (roundworms),
Trematodes (flukes), Cestodes (tapeworms)
Ectoparasites Live on body surface. Examples: lice, fleas, mites, ticks

11.2 Nematodes (Roundworms)


TERM DEFINITION
Ascaris lumbricoides Transmission: feco-oral (ingestion of eggs). Symptoms: intestinal
obstruction, Loeffler's syndrome (larval lung migration). Treatment:
Mebendazole, Albendazole
Hookworm Transmission: skin penetration by larvae. Symptoms: iron-
(Ancylostoma, Necator) deficiency anaemia, ground itch. Treatment: Mebendazole,
Albendazole
Enterobius vermicularis Transmission: feco-oral, autoinfection. Symptoms: perianal pruritus
(Pinworm) (especially at night). Treatment: Mebendazole
Trichuris trichiura Transmission: feco-oral. Symptoms: rectal prolapse (heavy
(Whipworm) infection), diarrhoea. Treatment: Mebendazole
Wuchereria bancrofti Transmission: mosquito bite. Symptoms: Lymphoedema,
(Filaria) elephantiasis. Treatment: Diethylcarbamazine (DEC), Ivermectin
Onchocerca volvulus Transmission: blackfly bite. Symptoms: River blindness, skin
nodules. Treatment: Ivermectin
Strongyloides stercoralis Transmission: skin penetration. Risk: hyperinfection in
immunocompromised. Treatment: Ivermectin

11.3 Trematodes (Flukes)


TERM DEFINITION
Schistosoma spp. Transmission: skin penetration by cercariae in freshwater. Types: S.
haematobium (bladder/urinary), S. mansoni (intestinal/hepatic), S.
japonicum (intestinal/hepatic). Treatment: Praziquantel
Fasciola hepatica Transmission: ingestion of contaminated watercress
(metacercariae). Symptoms: liver fluke disease, biliary obstruction.
Treatment: Triclabendazole
Clonorchis sinensis Transmission: undercooked fish. Symptoms: cholangitis, liver
disease. Treatment: Praziquantel

11.4 Cestodes (Tapeworms)


TERM DEFINITION
Taenia solium (Pork Intestinal infection: ingestion of undercooked pork. Cysticercosis:
tapeworm) ingestion of eggs → larvae in tissues (brain, muscles). Treatment:
Praziquantel (intestinal), Albendazole (cysticercosis)
Taenia saginata (Beef Ingestion of undercooked beef. Intestinal only. Treatment:
tapeworm) Praziquantel
Diphyllobothrium latum Ingestion of undercooked fish. Can cause B12 deficiency.
(Fish tapeworm) Treatment: Praziquantel
Echinococcus Hydatid disease — cysts in liver, lungs. Treatment: Albendazole +
granulosus surgery

11.5 Protozoan Parasites


TERM DEFINITION
Plasmodium falciparum Malaria — most severe. Fever every 48 hrs (tertian), cerebral
malaria risk. Treatment: Artemisinin-based combination therapy
(ACT)
Entamoeba histolytica Amoebiasis — flask-shaped ulcers in colon, amoebic liver abscess.
Transmission: feco-oral. Treatment: Metronidazole + Diloxanide
furoate
Giardia lamblia Giardiasis — steatorrhoea, malabsorption. Transmission: feco-oral,
cysts in water. Treatment: Metronidazole
Trypanosoma brucei African sleeping sickness. Vector: Tsetse fly. Treatment: Suramin,
Melarsoprol
Trypanosoma cruzi Chagas disease. Vector: Reduviid bug. Treatment: Benznidazole,
Nifurtimox
Leishmania spp. Leishmaniasis (Kala-azar, cutaneous, mucocutaneous). Vector:
sandfly. Treatment: Sodium stibogluconate, Amphotericin B
Toxoplasma gondii Toxoplasmosis. Definitive host: cats. Congenital infection →
chorioretinitis, hydrocephalus. Treatment: Pyrimethamine +
Sulfadiazine
TOPIC 12: COMMONLY CONFUSED TERMS AND CONCEPTS —
FLAGGED

12.1 Sterilization vs Disinfection vs Antisepsis


TERM DEFINITION
Sterilization Destroys ALL microbial life including spores. Applied to inanimate
objects.
Disinfection Destroys HARMFUL microbes but NOT necessarily spores. Applied
to INANIMATE objects only.
Antisepsis Destroys/inhibits microorganisms on LIVING TISSUE. Not the same
as disinfection.
Bacteriostatic INHIBITS growth — does NOT kill. Effect is REVERSIBLE.
Bactericidal KILLS bacteria.

12.2 Active vs Passive Immunity


TERM DEFINITION
Active Body PRODUCES its own antibodies. Long-lasting. Takes time.
Examples: vaccination, natural infection.
Passive PREFORMED antibodies given. Immediate. SHORT-LIVED.
Examples: antitoxins, immune globulins, placental transfer of IgG.
IgG crosses placenta The ONLY immunoglobulin class to cross the placenta.
IgA in secretions The MAJOR immunoglobulin in mucosal secretions (saliva, tears,
breast milk, etc.)
IgM — first produced First Ig produced in any immune response. Pentamer. Does NOT
cross placenta.

12.3 Innate vs Adaptive Immunity


TERM DEFINITION
Innate Non-specific. No memory. Fast. First line.
Adaptive Specific. Has memory. Slower first time, faster on repeat exposure.
Second line.

12.4 Bacteriostatic vs Bactericidal


TERM DEFINITION
Bacteriostatic Only inhibits growth — bacteria remain alive. Must be used with
intact immune system.
Bactericidal Kills bacteria outright. Used in immunocompromised patients or
serious infections.

12.5 Live vs Killed Vaccines


TERM DEFINITION
Live attenuated Replicates in host. Better immunity (IgA + IgG + cytotoxic T cells).
Longer protection. Risk of reversion. NOT for immunocompromised
or pregnant.
Killed (inactivated) Does NOT replicate. Mainly IgG response. No cytotoxic T-cell
response. No IgA. More heat-stable. CANNOT revert to virulence.

12.6 Gram Positive vs Gram Negative


TERM DEFINITION
Gram positive Thick peptidoglycan. HAS teichoic acid. NO outer membrane.
Stains PURPLE.
Gram negative Thin peptidoglycan. NO teichoic acid. HAS outer membrane with
LPS. Stains PINK.

12.7 Binary Fission vs Budding


TERM DEFINITION
Binary fission How BACTERIA reproduce — splits into two equal daughter cells.
Budding How ENVELOPED VIRUSES are released — acquire envelope
from host cell membrane as they exit.

12.8 OPV vs IPV (Polio vaccines)


TERM DEFINITION
OPV (Oral Polio Vaccine) Live attenuated. Induces intestinal IgA. Provides HERD IMMUNITY.
Risk: reversion to virulence (rare paralytic polio).
IPV (Inactivated Polio Killed. Given IM. Induces IgG only. NO herd immunity. CANNOT
Vaccine) revert to virulence. Currently used in US.
TOPIC 13: CROSS-CHECK — COURSE OUTLINE vs UPLOADED
FILES

Topics from course outline vs availability in slides:


TERM DEFINITION
Classification, ✅ COVERED — Classification pptx
Identification &
Nomenclature
Bacteria nutrition, growth ✅ COVERED — Bacterial_cell_Growth.pptx
and metabolism
Bacterial cell structure ✅ COVERED — Bacterial_structure_and_function.pptx
and function
Antimicrobial therapy & ✅ COVERED — ANTIMICROBIAL_AGENTS_AND_THERAPY-
resistance [Link]
Immunization, immunity ✅ COVERED — IMMUNIZATION___.pptx +
to microbial infections THE_IMMUNE_SYSTEM_____.pptx
Introduction to Virology / ✅ COVERED — DOC-20241204-WA0053_.ppt
general properties of
viruses
Classification of viruses / ✅ COVERED — classification_of_virus.ppt
Baltimore classification
Viral host interactions, ⚠️PARTIAL — interferons mentioned in THE_IMMUNE_SYSTEM.
pathogenicity, Detailed pathogenicity NOT in slides. Covered in Topic 8 using
interferons standard knowledge.
Laboratory identification ✅ COVERED — DOC-20241204-WA0053_.ppt
of viral infections
Sterilization and ✅ COVERED — Sterilisation_and_Disinfection.pptx
Disinfection
Vector control measures ✅ COVERED — [Link]
IDSR ✅ COVERED — [Link]
Classification of ❌ NOT IN SLIDES — Covered in Topic 11 using standard
parasites / life cycles / knowledge (flagged in purple)
diagnosis / treatment

⚠️RECOMMENDATION: For parasitology (Topic 11) — this entire topic is not in any of your
slides. Please try to source a parasitology textbook or ask your lecturer for the slides before
your exam if possible.
END OF STUDY NOTE
Good luck, Abdurrazaq. You've got this.

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