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📚 Basic Microbiology 2026 - Complete Semester Exam Study Notes

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WHY STUDY MICROBIOLOGY?

• Cause serious infectious diseases
• Support digestion and the immune system
• Contribute to antibiotic and vaccine production

• Decompose organic matter and recycle nutrients
• Fix nitrogen in soil
• Participate in bioremediation of environmental pollution

• Food production: yogurt, beer, bread
• Biotechnology and pharmaceuticals
• Bioenergy production

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LEARNING OBJECTIVES (Exam Focus)

1. Comprehend fundamental morphological, structural, and physiological features of bacteria, viruses, fungi, and parasites
2. Recognize key characteristics of each group
3. Understand mechanisms of invasion, transmission, and disease causation
4. Compare and differentiate bacteria, viruses, fungi, and parasites - structure, reproduction, treatment approaches

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PART 1: BACTERIA - THE PROKARYOTIC MICROORGANISMS

What Are Bacteria?

• Single-celled microorganisms classified as prokaryotes
• Lack a membrane-bound nucleus - genetic material (DNA) floats freely in the cytoplasm
• Found virtually everywhere: soil, water, air, inside other organisms
• Thrive in extreme environments (hot springs to arctic ice)
• Most bacteria are harmless or beneficial (nutrient cycling, digestion, decomposition)
• Among the oldest life forms on Earth - fossil evidence dating back 3.5 billion years

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Key Characteristics of Bacteria

1. Cell Wall Composition

• Bacteria possess a rigid cell wall containing peptidoglycan
• Gram-positive bacteria: thick peptidoglycan layer
• Gram-negative bacteria: thinner peptidoglycan layer + an additional outer membrane

2. Reproduction - Binary Fission

• Bacteria reproduce asexually through binary fission
• A single parent cell divides into two identical daughter cells
• This enables rapid growth (exponential/logarithmic)

3. Metabolic Diversity

• Autotrophs: produce their own food via photosynthesis or chemosynthesis
• Heterotrophs: obtain energy by consuming organic compounds
• This flexibility allows colonization of virtually every habitat on Earth

4. Genetic Material

• Single circular chromosome of DNA
• May contain plasmids - small, circular DNA molecules carrying accessory genes
• Plasmids often encode antibiotic resistance, virulence factors, and metabolic advantages

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Bacterial Morphology (Shape Classification)

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Bacterial Cell Structure (Detailed)

Structures Present in ALL Bacteria:

• Cell membrane (plasma membrane) - semi-permeable lipid bilayer; site of nutrient transport and energy production
• Cell wall - contains peptidoglycan; gives rigidity and shape; protects against osmotic lysis
• Cytoplasm - gel-like medium containing all cellular components
• Nucleoid region - area where DNA is concentrated (no nuclear membrane)
• Ribosomes (70S) - site of protein synthesis; composed of 50S + 30S subunits (target of many antibiotics)

Optional/Variable Structures:

• Capsule - polysaccharide/polypeptide outer layer; protects against phagocytosis; key virulence factor; present in Streptococcus pneumoniae, Klebsiella
• Flagella - whip-like protein appendages (made of flagellin); provide motility; can be peritrichous (all around), monotrichous (one), amphitrichous (both ends), lophotrichous (tuft at one end)
• Pili (Fimbriae) - short protein projections; help bacteria adhere to host surfaces; sex pili transfer DNA during conjugation
• Endospores - dormant structures formed by Bacillus and Clostridium species under unfavorable conditions; extremely resistant to heat, chemicals, radiation; germinate when conditions improve

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Gram Staining - A Critical Technique

1. Apply crystal violet (primary stain) - all bacteria turn purple
2. Add iodine (mordant) - fixes crystal violet to peptidoglycan
3. Wash with acetone/alcohol (decolorizer)
4. Apply safranin (counterstain)

• Gram-positive: retain crystal violet → appear purple/violet
  • Thick peptidoglycan (20-80 nm) retains the dye complex
  • Examples: Staphylococcus aureus, Streptococcus pyogenes, Bacillus, Clostridium
• Gram-negative: lose crystal violet, pick up safranin → appear pink/red
  • Thin peptidoglycan + outer membrane allows dye washout
  • Examples: E. coli, Salmonella, Pseudomonas, Neisseria

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Bacterial Reproduction and Growth

Binary Fission (Primary Method)

1. DNA replication - circular chromosome is duplicated
2. Cell elongation - cell grows in size
3. Septum formation - cross-wall forms at the center
4. Cell division - two identical daughter cells produced

Growth Phases:

1. Lag phase - adaptation; no increase in cell number; bacteria synthesize enzymes and adjust to environment
2. Log (exponential) phase - rapid, exponential growth; most metabolically active; most susceptible to antibiotics
3. Stationary phase - growth rate = death rate; nutrient depletion, waste accumulation
4. Death (decline) phase - death rate exceeds growth; cells die due to nutrient exhaustion and toxic metabolite accumulation

Genetic Variation Mechanisms:

• Transformation: uptake of free DNA from the environment
• Transduction: DNA transfer via bacteriophage (virus)
• Conjugation: direct cell-to-cell DNA transfer via sex pilus; main mechanism of antibiotic resistance spread

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Bacterial Pathogenesis

How Bacteria Cause Disease:

• Bacteria use adhesins (surface proteins), pili, and fimbriae to attach to host tissues
• Prevents removal by mechanical defenses (mucus flow, peristalsis)

• Penetrate host cell barriers via enzymes (hyaluronidase, collagenase, proteases)
• Some invade intracellularly (e.g., Mycobacterium, Listeria)

• Capsule resists phagocytosis
• Biofilm formation protects bacterial communities
• Some bacteria suppress immune responses

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Bacterial Classification Systems

By Oxygen Requirements:

• Obligate aerobes: require O₂ (e.g., Mycobacterium tuberculosis)
• Obligate anaerobes: killed by O₂ (e.g., Clostridium tetani)
• Facultative anaerobes: grow with or without O₂ (e.g., E. coli, most pathogens)
• Microaerophiles: require low O₂ (e.g., Campylobacter)

By Temperature Preference:

• Psychrophiles: cold (0-15°C)
• Mesophiles: moderate (20-45°C) - most human pathogens
• Thermophiles: hot (45-80°C)

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Bacterial Diseases and Treatments

Common Bacterial Diseases:

• Tuberculosis - Mycobacterium tuberculosis - lung infection
• Pneumonia - Streptococcus pneumoniae, Klebsiella
• Foodborne illness - Salmonella, E. coli, Staphylococcus aureus
• Sexually transmitted - Neisseria gonorrhoeae, Treponema pallidum
• Wound infections - Staphylococcus, Clostridium

Antibiotic Classes and Mechanisms:

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Antimicrobial Resistance (AMR) - Critical Exam Topic

• 2019 data (Lancet, AMR Collaborators): AMR is one of the leading causes of death globally
• Bacterial resistance is tracked by infection syndrome and by species
• Key resistant organisms: MRSA (Staphylococcus aureus), drug-resistant Mycobacterium tuberculosis, carbapenem-resistant Enterobacteriaceae
• Mechanisms of resistance:
  • Enzymatic inactivation (e.g., beta-lactamase destroys penicillins)
  • Target modification (altered penicillin-binding proteins in MRSA)
  • Efflux pumps (pump antibiotic out of cell)
  • Reduced permeability (less uptake)

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PART 2: VIRUSES - OBLIGATE INTRACELLULAR PARASITES

What Are Viruses?

• Unique acellular entities existing at the boundary between living and non-living matter
• Obligate intracellular parasites: absolutely require a living host cell to replicate
• Lack cellular structure; cannot perform metabolic functions independently
• Consist of genetic material (DNA or RNA) enclosed in a capsid (protein coat)
• Once inside a host, they hijack the cell's machinery to produce new viral particles

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Viral Nomenclature - How Are Viruses Named?

• The disease they cause: Poliovirus, rabies virus
• The body system affected: Respiratory viruses, enteroviruses
• Type of disease: Murine leukemia virus
• Geographic locations: Coxsackievirus, West Nile encephalitis virus, Venezuelan equine encephalitis virus, Russian spring-summer encephalitis virus, California encephalitis virus
• Their discoverers: Epstein-Barr Virus (EBV)
• How they were originally thought to be contracted: Dengue (meaning "evil spirit"), Influenza (from "influence of bad air"), Herpes (from Greek "herperin" = crawling)
• Combinations: Rous Sarcoma virus
• Names can change (German measles = rubella) or be abbreviated (HIV, EBV = HHV-4, HSV-1 and -2, hCMV)

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Viral Structure - Key Terminology

• Capsid is usually symmetrical in shape
• Enveloped viruses (e.g., HIV, influenza) are generally more sensitive to disinfectants
• Non-enveloped viruses (e.g., adenovirus) are more resistant to environmental conditions

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Main Characteristics of Viruses

1. Obligate Intracellular Parasites

• Non-living outside the host: cannot reproduce or carry out metabolic activities independently
• Considered the "boundary between the living and non-living"

2. DNA or RNA Genome

• Each virus contains only one type of nucleic acid (either DNA or RNA, never both)
• Can be single-stranded (ss) or double-stranded (ds)
• Can be linear or circular

3. Capsid Protection

• Capsid proteins protect the viral genome from enzymatic degradation
• Determine host cell specificity (surface proteins bind specific receptors)

4. Lack of Ribosomes

• Viruses do NOT have ribosomes
• They completely depend on host cell ribosomes for protein synthesis

5. Smaller Than Bacteria

• Generally 20-300 nm (bacteria are 0.5-5 µm)
• Require electron microscopy to visualize

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Viral Replication Cycle

Step 1 - Attachment (Adsorption)

• Viral surface proteins bind to specific receptors on the host cell surface
• This determines host range and tissue tropism (which cells can be infected)
• Example: HIV binds CD4 receptors on T-helper lymphocytes

Step 2 - Penetration (Entry)

• Entry via:
  • Endocytosis (receptor-mediated)
  • Membrane fusion (enveloped viruses fuse with cell membrane)
  • Direct injection of genetic material into cytoplasm (bacteriophages)

Step 3 - Uncoating

• Capsid is removed; viral genome is released into cytoplasm or nucleus

Step 4 - Replication and Assembly

• Viral genome is replicated using host cell machinery
• New viral proteins and nucleic acids are synthesized
• Components are assembled into new virions

Step 5 - Release

• New viruses exit the cell through:
  • Lysis - cell is destroyed; viruses released all at once (non-enveloped viruses)
  • Budding - enveloped viruses bud from cell membrane without killing the cell immediately

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Lytic vs. Lysogenic Cycles

Lytic Cycle (Immediate Replication)

1. Virus invades host cell
2. Hijacks cellular machinery
3. Replicates rapidly
4. Ruptures the cell (lysis) to release hundreds of new virions
5. Causes immediate host cell death

Lysogenic Cycle (Delayed Replication)

1. Viral DNA integrates into host chromosome → forms a prophage
2. Prophage is replicated along with host DNA across many generations
3. Host cell is NOT immediately killed
4. Under stressful conditions (UV light, chemicals), prophage can switch to lytic cycle
5. Example: Bacteriophage lambda; human analog: latent HIV infection

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Viral Pathogenesis - How Viruses Cause Disease

1. Cell Destruction (Cytopathic Effect)

• Viruses hijack host cell machinery for replication
• Cells die through lysis, apoptosis (programmed cell death), or functional disruption
• Visible changes = cytopathic effects (CPE) used in lab diagnosis

2. Immune-Mediated Damage

• Immune response to viral infection itself can damage host tissues
• Inflammatory responses, fever, tissue destruction from immune cells
• Example: liver damage in hepatitis is largely immune-mediated

3. Immune Evasion

• Some viruses evade detection by:
  • Hiding inside cells (latency)
  • Mutating surface proteins rapidly (influenza antigenic shift/drift)
  • Directly attacking immune cells (HIV destroys CD4+ T cells)

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Viral Transmission Routes

Direct Contact and Airborne:

• Transmitted through skin contact, bodily fluids, or respiratory droplets from coughing/sneezing
• Examples: Influenza, COVID-19, Herpes

Vector-borne and Fecal-Oral Routes:

• Via insect bites (mosquitoes, ticks) or contaminated food/water
• Examples: Dengue fever, Hepatitis A, Rotavirus

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Medically Important Viruses

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Antiviral Treatments

• Antivirals do NOT kill viruses - they inhibit replication or viral entry
• Examples:
  • Acyclovir - inhibits herpes virus DNA polymerase
  • Oseltamivir (Tamiflu) - inhibits influenza neuraminidase
  • Antiretrovirals (HAART) - multiple drug combinations targeting HIV at different stages
• Vaccines remain the primary prevention strategy for many viral diseases

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PART 3: FUNGI

What Are Fungi?

• Eukaryotic organisms with membrane-bound nuclei and organelles
• Cell walls contain chitin (not peptidoglycan like bacteria)
• Cannot photosynthesize - they are heterotrophs (obtain nutrients by absorption)
• Play essential roles in:
  • Decomposition: break down organic matter; primary recyclers of carbon and nutrients in ecosystems
  • Symbiosis: mycorrhizal associations with plant roots
  • Medicine: source of antibiotics (penicillin from Penicillium)
  • Food industry: fermentation (bread, beer, wine, cheese)

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Key Characteristics of Fungi

1. Cell Wall Composition

• Cell walls made primarily of chitin (a polysaccharide)
• Chitin provides structural rigidity
• This is a key target for antifungal drugs (unlike bacterial peptidoglycan)

2. Multicellular or Unicellular

• Multicellular: mushrooms and molds with complex structures
• Unicellular: yeasts (single cells)

3. Spore Reproduction

• Fungi reproduce primarily through spores
• Spores can be produced sexually or asexually
• Microscopic; spread via wind, water, animals, or contact

4. Absorptive Nutrition

• Unlike plants and animals, fungi obtain nutrients through external digestion
• Secrete digestive enzymes externally to break down organic matter
• Absorb the resulting nutrients through their cell walls

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Fungal Classification

Yeasts (Unicellular Fungi)

• Cell structure: Single-celled, oval or spherical shape; contain nucleus and organelles
• Reproduction: Primarily by budding (asymmetric division); some by fission
• Growth pattern: Form smooth, creamy colonies; grow rapidly in liquid media; prefer moist environments with sugars
• Example: Candida albicans (pathogen), Saccharomyces cerevisiae (bread/beer/wine)

Molds (Multicellular Filamentous Fungi)

• Cell structure: Multicellular with tubular hyphae forming mycelium network
• Reproduction: Sexual and asexual spore formation; spores dispersed by air, water, or contact
• Growth pattern: Form fuzzy, cottony colonies; spread across surfaces; thrive in warm, humid conditions
• Examples: Aspergillus, Penicillium, Rhizopus

Mushrooms

• Macroscopic fruiting bodies
• The visible part is the reproductive structure

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Fungal Structural Terms

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Fungal Life Cycle

1. Spore germination - Spores land on suitable substrates, absorb water; under favorable conditions (moisture, temperature, nutrients), swell and germinate to form germ tubes
2. Hyphal growth - Germ tubes elongate and branch to form hyphae; interweave to create mycelium; vegetative body absorbs nutrients
3. Reproduction - Sexual or asexual reproduction
4. Spore dispersal - Mature reproductive structures release spores; spread via wind, water, animals, or direct contact

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Fungal Reproduction - Three Main Mechanisms

Asexual Reproduction (Step 1)

• Fungi reproduce asexually through spore formation
• Common spore types:
  • Conidiospores (conidia) - produced on specialized structures (conidiophores), not enclosed in a sac; common in Aspergillus, Penicillium
  • Sporangiospores - produced inside a sporangium (sac); common in Rhizopus
• Does not require mating; allows rapid multiplication under favorable conditions
• A single fungus can produce millions of spores

Sexual Reproduction (Step 2)

• Occurs when two compatible hyphae combine
• Stages:
  1. Plasmogamy - cytoplasmic fusion
  2. Karyogamy - nuclear fusion
  3. Meiosis - produces sexual spores with genetic diversity
• Generates genetic diversity; important for adaptation

Spore Dispersal (Step 3)

• Spores dispersed by wind, water, insects, and animals
• Some fungi discharge spores with great force
• When a spore reaches a suitable environment, it germinates into a new hypha, completing the cycle

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Fungal Pathogenesis

1. Adhesion and Invasion

• Fungi attach to host tissues using adhesins
• Penetrate cells through enzyme secretion (proteases, lipases) that break down tissue barriers
• Enables colonization of host tissues

2. Immune Evasion

• Mask cell wall components
• Form biofilms (difficult to treat; resist antifungals and immune cells)
• Undergo morphological changes (yeast-to-hyphae transition) to escape phagocytosis
• Suppress immune cell responses

3. Toxin Production

• Some fungi produce mycotoxins:
  • Aflatoxins - produced by Aspergillus flavus/parasiticus; contaminate grains/peanuts; potent liver carcinogens
  • Ochratoxins - renal toxins; found in grain/coffee contamination

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Fungal Diseases (Mycoses)

Superficial Mycoses

• Infections limited to skin, hair, nails, and mucous membranes
• Dermatophytosis (Ringworm):
  • Caused by dermatophytes: Trichophyton, Microsporum, Epidermophyton
  • Includes tinea pedis (athlete's foot), tinea corporis, tinea capitis
  • Highly contagious through direct contact
• Onychomycosis - nail fungal infection
• Tinea versicolor - skin discoloration by Malassezia

Candidiasis

• Pathogen: Candida albicans (most common) - an opportunistic infection
• Causes oral candidiasis (thrush), vaginal candidiasis, esophageal candidiasis
• Occurs in immunocompromised patients (HIV/AIDS, chemotherapy, corticosteroid use), diabetics, antibiotic users
• Can cause life-threatening systemic infection (candidemia) in severely immunocompromised

Aspergillosis

• Pathogen: Aspergillus fumigatus (most common)
• Spectrum:
  • Allergic bronchopulmonary aspergillosis (ABPA) - allergic reaction
  • Aspergilloma - "fungal ball" in pre-existing lung cavities
  • Invasive aspergillosis - life-threatening infection in immunocompromised patients

Systemic Mycoses

• Infections spread to internal organs; potentially life-threatening
• Pathogens: Histoplasma, Coccidioides, Blastomyces, Cryptococcus, Aspergillus
• Manifestations: pneumonia, meningitis, septicemia
• Commonly encountered in immunocompromised patients (HIV/AIDS, transplant recipients)

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Antifungal Treatments

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Beneficial Roles of Fungi

• Food Industry: Saccharomyces yeast used in bread, beer, and wine production; molds used for specialty cheeses (Roquefort, Camembert)
• Pharmaceuticals: Penicillium produces penicillin (first antibiotic); many immunosuppressants and cholesterol-lowering statins derived from fungi
• Decomposition: Primary decomposers - recycle nutrients within ecosystems by breaking down cellulose and lignin
• Symbiosis: Mycorrhizae (root fungi) assist plants in absorbing water and minerals; increase crop yields

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PART 4: PARASITES - DEPENDENT ORGANISMS

What Are Parasites?

• Organisms that live on or inside a host organism, deriving nutrients and other benefits at the host's expense
• The host-parasite relationship: parasite benefits while the host is harmed
• Cause significant global disease burden, particularly in tropical and developing regions
• Can be unicellular (protozoa) or multicellular (helminths, ectoparasites)

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Classification of Parasites

1. Protozoa (Unicellular Eukaryotes)

• Single-celled eukaryotic organisms
• Can be intracellular or extracellular parasites
• Reproduce by binary fission (asexual) or sexual stages
• Transmitted via contaminated water/food, insect vectors, direct contact
• Examples: Plasmodium, Giardia, Entamoeba, Leishmania, Trypanosoma

2. Helminths (Parasitic Worms)

• Multicellular worm-like organisms
• Three major groups:
  • Nematodes (roundworms): Ascaris lumbricoides, Enterobius vermicularis (pinworm), hookworms
  • Cestodes (tapeworms): Taenia solium (pork tapeworm), Taenia saginata (beef tapeworm)
  • Trematodes (flukes): Schistosoma, liver flukes
• Generally larger; visible to naked eye in adult stage

3. Ectoparasites

• Live on the external surface of the host
• Include lice, fleas, ticks, and mites
• Transmission: direct contact or environmental exposure
• Clinical effects: skin irritation, itching, dermatitis
• Can serve as vectors for other diseases (e.g., ticks transmit Lyme disease, Rocky Mountain spotted fever)

4. Endoparasites

• Live inside the host's body (organs, blood, tissues)
• Examples: helminths and protozoa
• Transmission: contaminated food/water, insect vectors
• Clinical effects: malnutrition, organ damage, systemic infections

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Parasite Life Cycles

Protozoan Life Cycle (Malaria - Plasmodium - Key Example)

• Infected Anopheles mosquito bites a human and injects sporozoites into the bloodstream

• Sporozoites travel to the liver and invade hepatocytes
• Undergo asexual reproduction (schizogony) to produce thousands of merozoites
• P. vivax and P. ovale can form dormant hypnozoites in the liver (cause relapses)

• Merozoites are released into the bloodstream and invade red blood cells (RBCs)
• Inside RBCs, they mature through ring form → trophozoite → schizont stages
• Schizont ruptures, releasing more merozoites (and toxic byproducts)
• This rupture causes the characteristic cyclic fever, chills, and anemia
• Fever cycles: 48 hours (P. vivax, P. falciparum) or 72 hours (P. malariae)

• Some parasites differentiate into gametocytes (male and female)
• Mosquito ingests gametocytes during a blood meal → sexual reproduction occurs in the mosquito gut → sporozoites develop and migrate to salivary glands → cycle continues

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Helminth Transmission Pathways

Environmental Contamination:

• Helminth eggs or larvae are released into the environment through feces of infected hosts
• Contaminated soil, water, and vegetation become reservoirs for transmission
• Especially problematic in areas with poor sanitation

Intermediate Hosts:

• Many helminths require intermediate hosts (snails, fish, pigs, cattle) to complete their life cycle
• Larvae develop within these hosts before becoming infectious to humans
• Creates complex transmission chains

Human Infection Routes:

• Ingestion of contaminated food/water
• Skin penetration (e.g., hookworm larvae penetrate bare feet)
• Consuming undercooked meat containing larvae (e.g., Taenia from pork/beef)

Once Inside the Human Body:

• Helminths migrate to target organs where they mature and reproduce
• Continue the life cycle

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Ectoparasites vs. Endoparasites (Summary Table)

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Major Parasitic Diseases

Malaria

• Cause: Plasmodium species (P. falciparum, P. vivax, P. malariae, P. ovale)
• Vector: Anopheles mosquito
• Affects 200+ million people annually
• Symptoms: cyclic fever, chills, anemia, potentially fatal complications (cerebral malaria with P. falciparum)
• Treatment: Chloroquine (where sensitive), artemisinin-based combination therapies (ACT)

Amebiasis

• Cause: Entamoeba histolytica
• Transmitted via fecal-oral route (contaminated water/food)
• Causes intestinal disease (amoebic dysentery) and can spread to liver (amoebic liver abscess)
• Treatment: Metronidazole + iodoquinol

Leishmaniasis

• Cause: Leishmania species (protozoa)
• Transmitted by sandfly bites
• Forms: cutaneous (skin ulcers), mucocutaneous, visceral (kala-azar - most severe, affects liver/spleen)

Helminthiasis (Worm Infections)

• Ascariasis - Ascaris lumbricoides (roundworm); intestinal obstruction, malnutrition
• Taeniasis/Cysticercosis - Taenia tapeworms; neurocysticercosis can cause seizures
• Schistosomiasis - liver fibrosis, portal hypertension, bladder cancer (S. haematobium)
• Filariasis - lymphatic blockage (elephantiasis) caused by Wuchereria bancrofti

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Antiparasitic Treatments

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COMPARATIVE SUMMARY TABLE (Exam High-Yield)

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KEY EXAM TIPS - TOPICS MOST LIKELY TESTED

1. Gram staining procedure and interpretation - know the 4 steps, which bacteria are Gram+ vs Gram-, and why (peptidoglycan thickness)
2. Bacterial cell structures - know which are always present vs. optional, and the function of each
3. Binary fission 4 phases - lag, log, stationary, death - and which phase antibiotics work best (log)
4. Lytic vs. lysogenic cycle - key differences, what triggers the switch
5. Viral replication steps - 5 stages in order; know which step is blocked by each antiviral type
6. Fungal cell wall = chitin (NOT peptidoglycan) - this is why antibiotics don't work on fungi
7. Yeast vs. mold differences - morphology, reproduction, colony appearance
8. Malaria life cycle - all 4 stages, which organs involved, gametocyte stage (why transmission continues)
9. Ectoparasite vs. endoparasite - definitions, examples, transmission, clinical effects
10. Antimicrobial resistance - 4 main mechanisms; global burden (Lancet 2019 data)
11. Antibiotic mechanisms - which drug class targets which structure (ribosome, cell wall, DNA)
12. Major diseases per microorganism type - know the causative agent, transmission, and treatment
13. Mycotoxins - aflatoxins (liver carcinogen), ochratoxins (renal toxin)
14. Capsule function - protects against phagocytosis; key virulence factor
15. Endospores - formed by Bacillus and Clostridium; extremely resistant; germinate when conditions improve

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