Infectious Diseases and Microbes - Vocabulary Flashcards (Lecture Notes)
Scope and purpose
This lecture reviews general principles of pathogenesis of infectious diseases and the characteristic changes caused by different microbes across various body sites.
It provides a broad overview of how viruses, bacteria, fungi, protozoa, helminths, prions, and ectoparasites cause disease, with emphasis on structure, replication, and clinical implications.
Visuals contrast viral and bacterial particles at the microscopic level.
Real-world relevance includes global health burden, vaccine/antibiotic use, and contemporary examples such as COVID-19.
General principles of microbial pathogenesis
Infectious diseases are a major global health problem, despite vaccines and antibiotics being widely available in many regions (not universally accessible).
A key question: what gives microbes advantages in causing disease (viruses vs parasites vs fungi) and how they interact with different body sites.
Cellular vs acellular microbes
Cellular: organisms with cells (bacteria, fungi, protozoa, helminths, ectoparasites).
Acellular: nonliving infectious agents (viruses) that require host cells to replicate.
Viruses as an ongoing debate in microbiology: are viruses living? They are often considered nonliving because they require a host cell to replicate.
Important epidemiological statistics (global/in US context):
Influenza and pneumonia combined are the 8^{\text{th}} leading cause of disease in the US. \text{(8th leading cause of disease in the US)}
In low-income countries, limited healthcare access, unsanitary living conditions, and malnutrition contribute to a large burden of infectious diseases. The top three causes of death in developing countries include lower respiratory infections, HIV/AIDS, and diarrheal disease; malaria and tuberculosis are among the top 10.
Infectious diseases are especially important as causes of death among children, older adults, and individuals with chronic debilitating diseases or immunodeficiency (inherited or acquired).
Special/sensitive groups concept in public health and vaccination strategies during crises (e.g., COVID-19 prioritization).
Categories of infectious agents (scope of the lecture)
Broad classes discussed: prions, viruses, bacteria, fungi (endemic and opportunistic), protozoa, helminths, ectoparasites.
Size range example: prion proteins (< 20\text{ nm}) to tapeworms (up to 10\text{ m}).
Note on prions: prions are abnormal forms of a protein (PRP) that cause transmissible spongiform encephalopathies (TSEs).
Prions
PRP (prion protein) is normally found in neurons; disease occurs when PRP becomes misfolded.
Structural change leads to loss of normal function and gain of harmful properties; structure determines function.
Examples of transmissible spongiform encephalopathies (TSEs): bovine spongiform encephalopathy (BSE, mad cow disease), kuru (associated with cannibalism), Creutzfeldt–Jakob disease (CDJ) variants (sporadic, hereditary, familial, and variant CDJ).
Transmission routes beyond rare meat-borne or iatrogenic exposure include medical settings: surgery, organ transplantation, blood transfusion.
Key concept: prions are a protein, so there is no genetic material to replicate in the traditional sense; they propagate by inducing misfolding of normal prion proteins.
Viruses
Viruses are obligate intracellular parasites; they depend on host cell metabolism for replication.
They are generally considered nonliving outside a host cell because they cannot reproduce independently.
Basic structure: nucleic acid genome enclosed by a protein capsid; some are enveloped by a lipid membrane.
Classification criteria include: type of nucleic acid (DNA or RNA), capsid shape, presence/absence of envelope, replication mode, target cell type, and pathology caused.
Visual diversity: viruses vary widely in shape and size; structural differences confer different mechanisms for immune evasion, cell entry, and tissue tropism.
Clinical note: different viruses can produce similar clinical pictures; similarly, the same virus can cause different manifestations depending on host status (immune competence) and level of exposure (dose).
Example concepts:
Adenovirus vs rhinovirus can both cause upper respiratory infections despite different morphology.
COVID-19 demonstrated wide variation in disease severity among individuals, influenced by host immune status and exposure level.
Bacteria
Bacteria are prokaryotes: they have cell membranes and lack membrane-bound nuclei.
Most bacteria have a cell wall composed of peptidoglycan.
Gram staining differences (clinical relevance):
Gram-positive: thick peptidoglycan layer, retains crystal violet stain.
Gram-negative: thinner peptidoglycan layer and an outer membrane containing lipopolysaccharide (LPS).
Structural components
Capsule: polysaccharide layer outside the cell wall.
Nucleoid region inside the cytoplasm (no true nucleus).
Cytoplasmic membrane, cytoplasm containing ribosomes and genetic material.
Flagella for motility; Pili for attachment to host cells.
Clinical implications
Bacteria are classified by Gram staining and by shape (e.g., rods, spirals).
Some antibiotics target the cell wall; differences between Gram-positive and Gram-negative bacteria influence antibiotic choices due to the outer membrane in Gram-negatives that can reduce drug access.
Visual note: cross-section images show differences in outer layers, periplasmic space, and outer membrane.
Fungi
Eukaryotic organisms with thick, complex cell walls containing carbohydrates.
Infections can be superficial (skin, hair, nails) or deep/systemic.
Endemic fungi — restricted geographic distribution:
Valley fever (Coccidioides spp.) in the Southwestern US; dust-borne exposure.
Histoplasma in the Ohio River Valley.
Opportunistic fungi — ubiquitous organisms that typically do not cause disease in healthy hosts but can cause life-threatening infections in immunocompromised individuals (e.g., AIDS patients).
Basic fungal cell morphology image: nuclei and organelles in a single cell; multicellular fungi also exist.
Protozoa
Single-celled eukaryotes; major disease burden in developing countries.
Intracellular replication possible in urogenital system, intestines, or blood.
Examples (stress the diversity):
Entamoeba histolytica; Giardia lamblia (intestinal pathogens).
Trichomonas vaginalis (sexually transmitted; flagellated).
Toxoplasma gondii (toxoplasmosis): acquired via contact with cat feces or ingestion of undercooked meat; cats are common reservoirs.
Concept: protozoa display diverse life cycles and host interactions, requiring different treatment strategies.
Helminths
Parasitic worms; multicellular and highly differentiated with complex life cycles.
Capable of alternating between sexual and asexual reproduction (in some species) — a feature that complicates control.
Forms in humans may include adult worms, immature stages, or asexual larval forms.
Transmission and impact
Eggs are typically shed in stool and spread via contaminated water/food or poor sanitation.
Disease severity is often proportional to worm burden (infecting parasite load).- Example: 10 hookworms may cause mild or no disease; 1000 hookworms could cause severe anemia due to blood loss.
Major groups: roundworms (nematodes), tapeworms (cestodes), and flukes (trematodes); thorny-headed worms noted as a smaller category.
Note on anemia: the transcript includes a probable misprint “amnesia”; intended meaning is anemia due to helminth burden.
Ectoparasites
Insects (lice, bed bugs, fleas) and arachnids (mites, ticks) that inhabit or bite the skin.
Can act as vectors for pathogens (e.g., Borrelia burgdorferi, Lyme disease, transmitted by deer ticks).
Clinical relevance: head lice outbreaks in school settings; fleas and ticks in various settings; Lyme disease recognition.
Microbiome
The diverse microbial population (bacteria, fungi, viruses) found on and in the human body (gut, skin, upper airway, vagina).
Most microbiota are harmless or beneficial; some can cause disease (e.g., Staphylococcus aureus or Streptococcus pyogenes causing skin/soft tissue infections; dental caries).
Roles in normal health and development
Intestinal flora: digestion/absorption, maintenance of epithelial integrity, regulation of intestinal immune function, competitive inhibition of pathogens.
Microbiome diversity as a marker of nutritional status and overall health.
Diversity patterns
\text{>1000} bacterial species may reside in the normal intestinal flora.
Greatest diversity: oral cavity and stool; intermediate diversity on skin; least diversity in the vagina.
Bacterial populations at various sites tend to be similar across different individuals, though some variability exists.
Dysbiosis (microbiome imbalance) and disease associations
Antibiotics can disrupt normal flora, leading to overgrowth of pathogens such as Clostridioides difficile (C. difficile).
Low stool diversity is associated with disease states.
Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with altered intestinal bacterial populations and changes in viral populations in stool.
Visualization: a diverse, rainbow-like representation of microbial populations in a healthy gut vs reduced diversity in disease.
Newly emerging and reemerging infectious diseases
New agents emerge due to multiple factors:
Improved detection methods reveal pathogens that were present before.
Zoonotic transmission: animals serve as sources of new human pathogens (e.g., HIV likely from cross-species transmission).
Microorganisms acquire genes that increase virulence or alter host range via mutation or horizontal gene transfer.
Immune suppression enables infections by opportunistic organisms.
Contributing factors to emergence
Human behavior: rapid movement across borders (e.g., Ebola spread in 2014).
Environmental changes: forest regrowth and reduced farming can increase deer and mice populations, elevating Lyme disease risk.
Geographic spread via travel or movement of humans/animals (e.g., West Nile virus described in the US in 1990 after possible introduction by an infected bird).
Antibiotic use selects for resistant pathogens; resistance in tuberculosis is a notable example.
Key concept: emergence arises from interaction of pathogen traits, host susceptibility, and environmental factors.
Transmission and dissemination of microbes
Entry routes into the host (initial colonization)
Skin, gastrointestinal tract, respiratory tract, urogenital tract.
Skin as first line of defense; breaches allow infection; Skin’s role in preventing entry.
Opportunistic flora (e.g., Candida, Staphylococcus) can cause infections when barriers are breached or immunity is compromised. Iatrogenic exposure risk via needle sticks (bloodborne pathogens like HBV, HCV, HIV).
Insects or animals can introduce pathogens; some viruses invade through intact skin only with a shuttle (vector-borne transmission).
Cutaneous infections arise through breaks in the skin (wounds, incisions, burns, diabetic ulcers).
Gastrointestinal tract (GI) pathogens
Transmission via contaminated food/water; disasters (floods, earthquakes) increase risk due to water contamination.
Gastric acidity acts as a defense; acid suppression (e.g., proton pump inhibitors) can increase susceptibility to ingested pathogens.
GI defenses: thick mucus layer, pancreatic enzymes and bile detergents, defensins, secreted IgA, normal flora, secretory IgA.
Infections arise when local defenses are weakened or pathogens have effective countermeasures.
Respiratory tract
Numerous inhaled viruses, bacteria, fungi; pathogens overcome mucociliary clearance over time.
Defenses include mucus and cilia; smokers and cystic fibrosis patients have impaired mucociliary function.
Acute events can occur with intubation or aspiration of gastric contents.
Urogenital tract
Invasion usually via urethra; shorter female urethra (\sim5\text{ cm}) increases UTI risk compared with males (\sim20\text{ cm}).
UTIs can ascend to kidneys causing acute pyelonephritis if not treated promptly.
Antibiotic use disrupts normal flora, promoting yeast overgrowth (vaginal candidiasis).
Spread and dissemination within the body
Localized infection vs invasion of epithelial barrier leading to dissemination via lymphatics, blood, or nerves.
Tissue and site tropism: some pathogens stay luminal while others invade deeper tissues.
Modes of dissemination include:- Lysis and invasion: extracellular pathogens secrete tissue-damaging enzymes to invade.
Blood and lymphatic spread.
Cell-to-cell spread with intracellular replication or release of virions.
Transduction and transformation (especially for viruses sharing genetic material).
Blood-borne spread and host factors
Virulence and host immune status profoundly influence disease extent.
Transmission considerations
Direct contact via skin; oral secretions; respiratory secretions; stool; urine (less common); genital tract; vertical transmission (mother to fetus).
Vertical transmission: placental transfer is the most common route when the mother is infected during pregnancy.
Particles necessary for infection (infectious dose)
Infectious dose varies by pathogen; some viruses require very few particles to establish infection.
Norovirus example: infectious dose can be as low as 10 viral particles, contributing to its high contagiousness and notoriety on cruise ships.
Classic example: norovirus is highly hardy outside the host and can persist on surfaces for extended periods (on the order of days to up to a week, depending on conditions).
How microorganisms cause disease
Mechanisms of tissue damage and disease causation include several strategies:
Direct cytopathic effects: pathogens enter host cells and cause cell death directly.
Toxin-mediated injury: some bacteria release toxins that kill cells at a distance from the initial site of infection.
Immune-mediated collateral damage: the host immune response to the invader can cause tissue damage and clinical symptoms even as it controls infection (illustrated by complex host–pathogen interactions).
Examples and clinical implications
Viral pathogens may directly damage host cells by replication inside cells and resource sequestration.
Bacteria may adhere to and invade tissues and, in some cases, secrete toxins that disrupt tissue integrity.
The course of infections and their sequelae can be prolonged due to collateral damage or chronic inflammatory responses.
Mechanisms of viral and bacterial injury (brief recap)
Viruses
Directly damage host cells by entering cells and replicating, hijacking cellular machinery.
Bacteria
Adhere to host cells, invade tissues, and may deliver toxins that damage tissues or disrupt immune responses.
Practical and clinical implications
The COVID-19 pandemic highlighted the need for baseline understanding of viruses and infection control in clinical practice.
For practitioners such as East Asian medicine clinicians and acupuncturists, the microbiology framework helps in understanding patient presentations, infection risk, and precautions.
Ethical and practical considerations include vaccine access, antibiotic stewardship, infection prevention, and tailoring patient care to individual immune status and exposure risks.
Connections to foundational principles and real-world relevance
Structure–function principle: protein misfolding (prions) changes function and pathogenicity.
Host defense concepts: skin as a barrier; mucosal defenses (mucus, cilia, IgA); acidity of the GI tract; micrbiome’s protective role via competitive inhibition.
Dose–response concept: infectious dose (e.g., norovirus as low as 10 particles) influences transmission risk and outbreak dynamics.
Emergence and antimicrobial resistance: genetic adaptation under selective pressure from antibiotic use drives emergence of resistant strains; this shapes treatment strategies and public health responses.
Public health relevance: global burden of infectious diseases, disparities in access to vaccines and care, and the role of behavior and environment in disease spread.
Quick glossary / key takeaways
Prions: misfolded proteins causing TSEs; structure determines function.
Viruses: obligatory intracellular parasites; either DNA or RNA genomes; may be enveloped; many shapes and host ranges.
Bacteria: prokaryotes with peptidoglycan cell walls; Gram-positive vs Gram-negative differences impact antibiotic susceptibility.
Fungi: eukaryotes with thick cell walls; endemic vs opportunistic infections.
Protozoa: single-celled eukaryotes with diverse life cycles and niches.
Helminths: multicellular worms; parasite load correlates with disease severity; three major groups: roundworms, tapeworms, flukes.
Ectoparasites: insects and arachnids that bite or live on skin; vectors for pathogens (e.g., Lyme disease).
Microbiome: complex ecosystem of host-associated microbes; dysbiosis linked to disease states.
Emerging infectious diseases: influenced by detection, travel, host–pathogen adaptation, and antibiotic resistance.
Notes on transcript quality and clinical nuance
The transcript contains some phrasing that appears to be a transcription error (e.g., the word “amnesia” where “anemia” is intended). The notes reflect the intended meaning: anemia due to helminth burden.
Real-world contexts mentioned include vaccine access disparities, antibiotic stewardship, and the relevance of microbiology to clinical practice, especially in light of the COVID pandemic.
End of content
Optional study prompts
Compare and contrast prions with typical infectious agents in terms of structure, replication, and transmission.
Explain how antibiotic use can lead to C. difficile overgrowth and the clinical implications for hospital patients.
Describe how the microbiome contributes to competitive inhibition and how dysbiosis can contribute to disease states such as inflammatory bowel disease.
Discuss how the infectious dose of a pathogen influences outbreak dynamics and infection risk in closed settings (e.g., cruise ships).