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Disease
a condition where normal structure and/or function are damaged or impaired
Infection
invasion of pathogen or parasite that lead to disease
Signs
things that can be directly measured by clinician (e.g. body temperature)
Symptoms
things felt by patient that cannot be clinically measured (e.g. nausea)
Syndrome
groups of signs and symptoms that help indicate a particular disease
Signs and symptoms help direct towards:
Diagnosis
Asymptomatic/subclinical
only signs can be observed through correct testing
WHO's International Classification of Diseases (ICD) is used globally to:
classify and monitor diseases
Infectious
disease is directly affected by pathogens
Communicable
capable of spreading person-to-person
Iatrogenic
acquired as result of medical procedure
Nosocomial
acquired from hospital setting
Zoonotic
acquired from animal
Non-communicable
obtained from non-living thing such as soil or contaminated object
Non-infectious
not caused by pathogen
Periods of Disease
1) Incubation
2) Prodromal
3) Illness
4) Decline
5) Convalescence
Incubation
intial entry of pathogen; replication begins
Prodromal
Replication continues; host shows signs and symptoms
Illness
signs and symptoms are most severe in host
Decline
pathogen number starts to decrease; host's immune system is weak and vulnerable to secondary infection
Convalescence
host starts to recover
Acute disease
relatively short; influenza
Chronic disease
longer time; cancer, HIV
Latent disease
comes in episodes; pathogen replicates when disease is active; herpes
Koch's Postulates
set of standards that must be met to demonstrate that X pathogen causes X disease
Koch's Postulates list
1) pathogen must be found in every case of disease; not found in healthy individuals
2) pathogen can be isolated and grown in pure culture
3) healthy test subject infected with suspected pathogen; must develop same signs and symptoms as seen in postulate 1
4) pathogen must be re-isolated from new host and must be identical to pathogen from postulate 2
Koch's (wrong) assumptions
1) Pathogens are found only in disease individuals
2) All subjects are equally susceptible to infection
3) All pathogens can be grown in culture
Molecular Koch's Postulates
1) sign or symptom of disease should be associated only with pathogenic strains of a species
2) Inactivation of suspected gene associated with patho should result in measurable loss of patho
3) Reversion of inactive gene should restore the disease phenotype
Pathogenicity
ability of pathogen to cause disease
Virulence
degree of pathogenicity; continuum among many pathogen types
Example of Highly Virulent Pathogen
Bacillus anthracis; induces severe signs and symptoms
Example of Low Virulent Pathogen
Rhinovirus; induces low signs and symptoms
Median Infectious Dose (ID50)
number of pathogens required to infect 50% of population
Median Lethal Dose (LD50)
number of pathogens required to kill 50% of population
Example of Primary Pathogen
enterohemorrhagic E. coli (due to Shiga toxin)
Example of Opportunistic pathogen
S. aureus (common cause of nosocomial infections)
What can influence susceptibility to disease?
Drugs, resident microbiota, genetics, age
Stages of Pathogenicity
1. Exposure to Host
2. Adhesion and colonization
3. Invasion
4. Infection
5. Transmission
Stages of Pathogenicity: Exposure to Host
pathogens are exposed to portals of entry to begin adhesion; Some portals are worse than others; mucosa
Describe TORCH infections
pathogens that can cross placental barrier as portal of entry
TORCH Infections: T
Toxoplasmosis; Toxoplasma gondii (protozoan)
TORCH Infections: O
Syphillis; Treponema pallidum
Chickenpox; Varicella-zoster; herpesvirus3
Hep B; hepadnavirus
HIV; Retrovirus
Fifth disease-erythema; Parvovirus B19
TORCH Infections: R
Rubella; German measles
Togavirus
TORCH Infections: C
Cytomegalovirus; herpesvirus 5
TORCH Infections: H
Herpes simplex viruses HSV 1 and 2
Stages of Pathogenicity: Adhesion
Adhesins: molecules/structures that bind to certain host receptors
Biofilm: production of community glycocalyx
Stages of Pathogenicity: Invasion
occurs when colonization is established; Pathogens produce toxins to allow further colonization into body/tissue; Helicobacter pylori urease production
Stages of Pathogenicity: Invasion: Mechanisms of Invasion
1) Endocytosis
2) Effector proteins- secreted to trigger entry; Salmonella and Shigella
3) Surface proteins allow for binding to host cell; trojan horse approach
Some pathogens are able to?
survive lysosomes that engulf; Mycobacterium TB
Stages of Pathogenicity: Infection
Multiplication leads to established host infection
Stages of Pathogenicity: Transmission
Skin, respiratory, urogenital & gastrointestinal tracts; coughing, sneezing, secretions & excretions
What does the root -emia mean?
Used to describe presence of pathogens in bloodstream
What does the term septicemia mean?
Bacteria are present and multiplying in blood
What determines a person going into shock?
Systolic pressure is less than 90
Local infection
small area of body
Focal infection
pathogen or toxin spreads to secondary location
Systemic infection
occurs throughout body; commonly by blood stream
What can some primary infections lead to?
secondary infections of different pathogen; HIV lowers immune system and opens door for yeast and others
Virulence factors dictate:
how severe and extensive a disease is
Examples of Virulence factors:
Adhesion factors, exoenzymes, toxins, immune evasion
Adhesins
proteins that aid in attachment to host cell receptors; found in all microbial types; commonly found on fimbriae
Exoenzymes
extracellular enzymes used to invade host tissues
Types of Exoenzymes include:
glycohydrolases, nucleases, phospholipases, proteases; Hyaluronidase
Toxins
poisons that cause host cell toxigenicity
Endotoxins
lipopolysaccharides that trigger host inflammatory responses; can cause severe fever and shock
Exotoxins
proteins mostly produced by Gram positive; targets receptors on specific cells
Exotoxins: Intracellular targeting
with A&B regions for activity and binding; diptheria and botulinum toxin
Exotoxins: Membrane disrupting
aka phospholipases that degrade bilayer membrane; Bacillus anthracis and Rickettsia
Exotoxins: Superantigen
trigger excessive production of cytokines by immune cells; S. aureus and Toxic Shock Syndrome
Host Evasion
mechanisms to evade phagocytosis
Examples of Host Evasion
1. Capsules enlarge bacterial cell so phagocytes cannot engulf pathogens
2. Proteases digest host antibody molecules
3. Mycolic acid in acid fast bacteria
4. Coagulase positive microbes coagulate blood cells to keep immune cells out of reach
5. Alteration of cell surface proteins to hide from immune cell recognition
Virulence in Viruses
similar to bacteria; adhesins and antigenic variation
Examples of Virulence in Viruses
-HIV glycoprotein 20 for binding CD4 T-cells
-Influenza high mutation of envelope spikes allows for antigenic variation
Describe antigenic drift
Slight changes in spike proteins
Describe antigenic shift
Major changes in spike proteins due to gene reassortment
When does gene reassortment occur?
When two different influenza viruses infect same host
Virulence in Fungi
Many properties similar to bacteria; adhesins, proteases, mycotoxins
Examples of Virulence in Fungi
1. Capsule gram positive Cryptococcus; cause pneumoniae and meningitis
2. Mycotoxins produced by Claviceps purpurea and Aspergillus; contaminate grains and other staple crops
Virulence in Protozoans
Unique features for attachment; Giardia lamblia uses adhesive disk of microtubules to attach to intestines
Example of Virulence in Protozoans
Plasmodium falciparum changes adhesive protein for RBCs to avoid immune recognition; causes chronicity in malaria patients
Virulence in Helminths
1. Tissue penetration achieved with proteases
2. Roundworms produce cuticle to last longer against host defense assaults
3. Schistosoma degrades host antibodies to halt immune defense
Which of the following would be a sign of an infection?
fever
Which of the following is an example of a non-communicable infectious disease?
Food poisoning due to a preformed bacterial toxin in food
What type of toxin is produced by gram-negative bacteria, composed of mostly protein, has high toxicity, targets liver cells and is not heat stable.
Exotoxin
Phospholipases are enzymes that do which of the following?
degrade cell membranes to allow pathogens to escape phagosomes
Cilia, fimbriae, and pili are all examples of structures used by microbes for ____________.
adhesion
The Shiga and diphtheria toxins target ________ in host cells.
protein synthesis
What exoenzymes can be produced by Candida to invade tissue.
Protease and phospholipase