Comprehensive Microbiology Study Guide: Eukaryotes, Viruses, Archaea, and Pathogens

Domain Features and Eukaryotic Characteristics

• Domain Classification and Structures:

  • Bacteria: Cell walls contain peptidoglycan with $\beta(1 \rightarrow 4)$ glycosidic bonds that are vulnerable to enzymatic cleavage by lysozyme.

  • Archaea: Distinct prokaryotic domain with unique cell membrane and cell wall chemistries.

  • Eukaryotes: Domain comprising protists, fungi, plants, and animals.

    • Eukaryotic cells may possess cell walls or flagella.

    • Eukaryotes are the only domain of life that possesses cilia.

Fungi: Characteristics, Structure, and Mycoses

• General Fungal Distribution and Traits:

  • Ecology: Found in both terrestrial and aquatic environments.

  • Nutritional Strategy: Many are saprophytes (saprotrophic decomposers that feed on dead organic matter).

  • Pathogenicity: Numerous fungal species act as human, animal, or plant pathogens.

  • Growth Temperature: Optimal growth temperature for fungi is generally lower than that of bacteria.

  • Medical Applications: Penicillin is an antibiotic derived directly from a fungal compound.

• Fungal Cellular Structure:

  • Cell Wall: Contains chitin, a structural polysaccharide similar to N-acetylglucosamine (NAG).

  • Morphological Types:

    • Yeast: Single-celled fungal organisms.

    • Mold: Multicellular fungal organisms.

  • Thallus Structure:

    • The vegetative body of a fungus is the thallus, which consists of filament networks called hyphae.

    • Septate Hyphae: Hyphae containing internal cross-walls (septa) dividing the cells.

    • Aseptate Hyphae: Continuous hyphal filaments lacking internal cross-walls (septa).

  • Dimorphic Fungi:

    • Fungi capable of altering their growth form depending on environmental temperature.

    • Mold Form: Exists at room temperature ($25^\bullet\text{C}$).

    • Yeast Form: Exists at human body temperature ($37^\bullet\text{C}$).

• Classification of Mycoses (Fungal Infections):

  • Superficial Mycoses: Infections localized exclusively to the outermost layer of the skin.

  • Cutaneous Mycoses: Infections affecting the deeper epidermis and skin layers.

  • Subcutaneous Mycoses: Infections located beneath the skin layer.

  • Systemic Mycoses: Deep-seated infections that disseminate into the host bloodstream.

  • Opportunistic Mycoses: Infections caused by fungi that become pathogenic only when specific host conditions are favorable (e.g., in immunocompromised individuals lacking effective immune resistance).

• Medically Important Fungal Infections:

  • Histoplasmosis:

    • Etiologic Agent: Dimorphic fungus.

    • Pathology: Respiratory disease affecting the lungs.

    • Transmission: Inhalation of fungal spores originating from bird and bat droppings.

  • Cryptococcosis:

    • Etiologic Agent: Cryptococcus neoformans (an encapsulated yeast).

    • Pathology: Systemic fungal infection.

    • Transmission: Inhalation of airborne spores from dried pigeon droppings.

  • Nosocomial Candidiasis:

    • Definition: Hospital-acquired fungal infection.

    • Etiologic Agent: Candida albicans (extremely prevalent fungal pathogen).

    • Clinical Manifestation: Oral thrush and opportunistic systemic infections.

Protozoan Pathogens and Parasitic Infections

• General Characteristics of Protozoa:

  • Single-celled eukaryotic microorganisms.

  • Apicomplexa: Group of parasitic protozoa characterized by an apical complex structure at the cell apex used to penetrate host cells, along with specialized reproductive structures.

• Key Protozoan Pathogens and Clinical Conditions:

  • Primary Amoebic Meningoencephalitis (PAM):

    • Etiologic Agent: Free-living "brain-eating" amoebae.

    • Pathology: Invades the central nervous system (CNS) causing rapid neural destruction.

  • Amoebic Dysentery:

    • Etiologic Agent: Intestinal protists/amoebae.

    • Transmission: Fecal-oral route via contaminated food or water.

  • Giardiasis:

    • Etiologic Agent: Giardia species (flagellated protozoan).

    • Transmission: Zoonotic transmission (spread from animals to humans); ingested in cyst form.

    • Pathology: Forms cysts and physically interferes with nutrient absorption in the small intestine.

  • Malaria:

    • Etiologic Agent: Plasmodium species (including Plasmodium falciparum and Plasmodium vivax).

    • Vector: Transmitted to humans via the bite of infected mosquitoes.

  • African Sleeping Sickness:

    • Vector: Transmitted by tsetse flies.

    • Reservoir Host: Domestic cattle and wild animals.

    • Immune Evasion Mechanism: Demonstrates Variant Surface Glycoprotein (VSG) switching, rapidly altering surface antigens to prevent immune clearance.

  • Toxoplasmosis:

    • Etiologic Agent: Toxoplasma gondii.

    • Transmission: Fecal-oral route; commonly acquired from exposure to infected cat feces.

    • Clinical Significance: Poses severe health risks and congenital damage when contracted by pregnant women.

Acellular Microbes: Viruses, Viroids, and Prions

• General Nature of Acellular Agents:

  • Acellular entities include viruses, viroids, and prions.

  • They are non-living biological structures lacking cellular organization and intrinsic metabolic activity.

• Viruses:

  • Virion: The complete, fully assembled infectious viral particle capable of existing outside host cells.

    • Virions are metabolically inert and cannot reproduce independently outside of a host cell.

  • Bacteriophages (Phages):

    • Viruses that exclusively infect bacterial host cells.

    • Do not infect or harm humans due to strict host-cell receptor specificity.

  • Viral Genome and Structure:

    • Core nucleic acid: DNA or RNA (single-stranded or double-stranded; linear or circular).

    • Protein Coat: Capsid surrounding the nucleic acid core.

    • Spike Proteins: Surface projections utilized for host-cell identification, attachment, or enzymatic activity.

  • Retroviruses:

    • RNA viruses that utilize reverse transcriptase to synthesize DNA from an RNA template.

    • Major Example: Human Immunodeficiency Virus (HIV), which causes Acquired Immunodeficiency Syndrome (AIDS).

  • Viral Multiplication Cycle:

    1. Attachment: Binding of virion to host cell surface receptors.

    2. Entry and Uncoating: Injection or uptake of the viral genome into the cytoplasm (note: uncoating of capsid does not occur in most bacteriophage infections, where only nucleic acid enters).

    3. Synthesis: Viral gene expression and replication of nucleic acids and proteins.

    4. Assembly: Packaging of nucleic acids into capsids.

    5. Release: Departure from the host cell.

       • Non-enveloped viruses lyse the host cell.

       • Enveloped viruses exit via budding (predominant in mammalian viruses).

  • Bacteriophage Infection Pathways:

    • Virulent Phages: Perform exclusively the lytic cycle, terminating in host cell lysis and death.

    • Temperate Phages: Capable of undergoing both lytic and lysogenic cycles.

    • Prophage: Integrated viral DNA residing stably within the host bacterial genome during lysogeny.

    • Lysogenic Conversion (Transduction):

      • Process wherein a temperate prophage imparts new genetic traits to the host bacterium, converting a non-pathogenic bacterium into a pathogen.

      • Examples: Production of Diphtheria toxin by Corynebacterium diphtheriae and Botulinum toxin by Clostridium botulinum.

  • Infections in Eukaryotic Cells:

    • Cytocidal: Direct destruction and death of host cells.

    • Latent: Viral genome remains dormant; e.g., Varicella-zoster virus (causes chickenpox, remaining latent to later reemerge as shingles).

    • Chronic: Continuous, low-level viral production over extended periods.

    • Transformation: Integration causing malignant host cell changes; e.g., Epstein-Barr Virus (EBV, causing mononucleosis and lymphoma) and Human Papillomavirus (HPV, causing cervical cancer).

  • Influenza Virus vs. Bacterial Respiratory Pathogens:

    • Influenza Virus: Enveloped single-stranded RNA virus causing the flu. Contains surface spike proteins Hemagglutinin ($H$) and Neuraminidase ($N$).

      • Antigenic Drift: Small, gradual point mutations in $H$ and $N$ genes causing seasonal flu strain variations.

      • Antigenic Shift: Major genetic reassortment resulting in novel spike protein combinations, leading to global pandemics.

    • Haemophilus influenzae: A bacterium capable of causing bacterial meningitis; it does not cause the flu.

  • Common Cold and Coronaviruses:

    • Common Cold Etiology: Rhinoviruses, coronaviruses, and parainfluenza viruses.

    • Coronaviruses: Enveloped single-stranded RNA viruses (e.g., SARS-CoV, MERS-CoV, SARS-CoV-2 causing COVID-19).

    • Structural Distinction: Coronaviruses lack Hemagglutinin ($H$) and Neuraminidase ($N$) spike proteins found on influenza viruses.

  • Quantification of Viruses:

    • Direct Method: Direct microscopic counting.

    • Indirect Methods: Plaque assays and hemagglutination assays.

• Viroids:

  • Structure: Small, circular, single-stranded RNA molecules.

  • Host Specificity: Exclusively infect plant species; harmless to humans.

  • Mechanism: Interfere with host cell protein translation.

• Prions:

  • Definition: Infectious misfolded protein molecules lacking nucleic acids.

  • Location and Pathology: Found primarily in the central nervous system (CNS); misfolding causes progressive, fatal neurodegenerative diseases in humans and animals (e.g., Creutzfeldt-Jakob Disease / CJD, Chronic Wasting Disease / CWD).

  • Isoforms:

    • $\text{PrP}^\text{C}$: Normal cellular prion protein present in healthy neural tissue.

    • $\text{PrP}^\text{Sc}$: Pathogenic, misfolded prion protein containing an abnormally high proportion of $\beta$-sheet secondary structures.

  • Treatment: No effective treatments exist due to resistance against standard antimicrobial and antiprotein interventions.

Comparative Biochemistry of Bacterial and Archaeal Cell Envelopes

• Metabolic Uniqueness:

  • Archaea represent the only domain of life capable of methanogenesis (creating methane gas).

• Cell Membrane Composition:

  • Bacterial Cell Membrane:

    • Hydrophobic chains composed of fatty acids.

    • Glycerol-fatty acid linkages are ester linkages.

    • Membrane structure is strictly a lipid bilayer.

  • Archaeal Cell Membrane:

    • Hydrophobic chains composed of repeating isoprene (isoprenoid) units.

    • Glycerol-side chain linkages are ether linkages.

    • Membrane structure can exist as a lipid monolayer, lipid bilayer, or a mixture of both.

• Cell Wall Composition:

  • Bacterial Cell Wall:

    • Contains peptidoglycan composed of alternating N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) residues.

    • Glycosidic bonds are $\beta(1 \rightarrow 4)$ linkages.

    • Cleaved directly by the enzyme lysozyme.

    • Peptide cross-links contain both D- and L-amino acids.

  • Archaeal Cell Wall:

    • Contains pseudomurein composed of N-acetylglucosamine (NAG) and N-acetyltalosaminuronic acid (NAT).

    • Glycosidic bonds are $\beta(1 \rightarrow 3)$ linkages.

    • Resistant to enzymatic cleavage by lysozyme.

    • Peptide cross-links contain exclusively L-amino acids.

Pathogen Etiology and Clinical Identification

• Microbial Etiology Summary:

  • Syphilis: Bacterial infection.

  • Kuru: Prion disease.

  • Anthrax: Bacterial infection.

  • Influenza: Viral infection.

  • Histoplasmosis: Fungal infection.

  • Tuberculosis: Bacterial infection.

  • Toxoplasmosis: Protozoan infection.

Case Study: Therapeutic Effects of Saccharomyces boulardii against Cronobacter sakazakii

• Organism Characteristics:

  • Saccharomyces boulardii:

    • Eukaryotic single-celled yeast.

    • Saprotrophic, spherical organism active in fermentation.

    • Possesses a standard eukaryotic lipid bilayer cell membrane.

    • Evaluated as a preventative probiotic therapeutic agent for intestinal conditions.

  • Cronobacter sakazakii:

    • Gram-negative foodborne bacterial pathogen.

    • Outer membrane contains Lipopolysaccharide (LPS) as a primary determinant of virulence.

    • Encodes outer membrane proteins via omp genes that enable invasion of human intestinal epithelial cells.

    • Causes severe, potentially fatal intestinal infections in vulnerable populations (specifically infants and immunocompromised young children).

• Experimental Findings on Intestinal Epithelial (Caco-2) Cell Viability:

  • Caco-2 cells treated with S. boulardii alone exhibit cell viability levels equivalent to untreated control cells, confirming non-toxicity.

  • Caco-2 cells exposed to C. sakazakii display a significant decrease in cell viability due to bacterial invasion and LPS-mediated damage.

  • Co-administration of S. boulardii alongside C. sakazakii results in significantly greater Caco-2 cell viability compared to cells treated with C. sakazakii alone.

  • Conclusion: S. boulardii mitigates host epithelial damage caused by C. sakazakii, though it does not entirely eliminate cell death or restore viability to $100\%$ of untreated controls.