Study sets, textbooks, questions
Upgrade to remove ads
pathogenesis bacteria & other microorganisms - exam #3
Terms in this set (64)
any condition in which the normal structure or functions of the body are damaged or impaired
successful colonization of a host by a microorganism
signs and symptoms
- objective and measurable incidents. Body temperature, antibodies in blood serum, blood pressure, breathing rate, etc...
- subjective (felt or experienced) incidents. Nausea, loss of appetite, pain, etc...
specific group of signs and symptoms characteristic of a particular disease
any disease caused by the direct effect of a pathogen.
infectious disease communicable
capable of being spread from person to person through either direct or indirect mechanisms. Contagious is easily spread amongst people.
infectious disease noncommunicable
not spread from one person to another.
disease as the result of a medical procedure
disease acquired in hospital setting.
disease transmitted from animals to humans
diseases not caused by pathogen.
disease that occurs in short amount of time
disease that occurs in large amount of time.
pathogen goes dormant for extended periods of time with no active replication.
Ability of a microorganism to cause disease
Degree of pathogenicity
- Adhesion factors
- Extracellular enzymes
- Antiphagocytic factors
confined to small area of body, near portal of entry.
localized pathogen or toxins produced spread to a secondary location
infection spreads all over the body
initial infection caused by one pathogen
infection caused by a second pathogen due to body damage done by first pathogen.
number of pathogenic cells/viruses that causes infection in 50% of the sample population
number of pathogenic cells/viruses/ toxins that kills 50% of the sample population
obligate intracellular pathogens
can only reproduced inside host cells.
facultative intracellular pathogens
can reproduced inside or outside host cells.
presence of bacteria in blood is
bacteremia involving pyogens (pus-forming bacteria)
viruses are found in the blood
toxins are found in the blood
bacteria are both present and multiplying in the blood
patients with septicemia
a life-threatening decrease in blood pressure (systolic pressure <90 mm Hg), prevents cells and organs from receiving enough oxygen and nutrients
swelling of tissues
ability of microorganisms to produce toxins
metabolic products produce by fungi that are toxic to humans.
stages of infection
incubation, prodromal, illness, decline, convalescence
the period between exposure to an infection and the appearance of the first symptoms
short period after incubation; early, mild symptoms
period of illness
disease is most severe and has characteristic signs and symptoms
period of decline
signs and symptoms of the disease subside; patient is vulnerable to secondary infections
period of convalescence
the person regains strength and the body returns to its prediseased state
What stage of infection are people most contagious?
period of illness
What are Koch's postulates? How are Koch's postulates used to determine the etiological agent for diseases? What are some of the limitations, exceptions, and/or difficulties of applying Koch's postulates?
1) the suspected causative agent must be absent from all healthy organisms but present in all diseased organisms
2) the causative agent must be isolated from the diseased organism and grown in pure culture
3) the cultured agent must cause the same disease when inoculated into a healthy, susceptible organism
4) the same causative agent must then be reisolated from the inoculated, diseased organism
- These postulates states:
*The phenotype (sign or symptom of disease)
should be associated only with pathogenic
strains of a species.
*Inactivation of the suspected gene(s)
associated with pathogenicity should result in
a measurable loss of pathogenicity.
*Reversion of the inactive gene should restore
the disease phenotype.
- Used to determine what genes contribute to a pathogen's ability to cause disease. It is a proposed revision to Koch's postulates because of the existence of pathogenic strains in organisms that are usually not pathogenic
- Germ theory of disease: Infections by pathogenic microorganisms cause disease
- Exceptions to Koch's postulates
*Some pathogens can't be cultured in the
*Diseases caused by a combination of
pathogens and other cofactors
*Ethical considerations prevent applying Koch's
postulates to pathogens that require a human
- Difficulties in satisfying Koch's postulates
*Diseases can be caused by more than one
*genetic manipulation in some pathogens is not
possible at the moment and/or there are no
suitable animal models.
stages of pathogenesis
1. Exposure (contact): able to gain entry to the host
2. Adhesion (colonization): capability of pathogenic microbes to attach to body cells
3. Invasion: dissemination of a pathogen throughout local tissues or the body
4. Infection: multiplication of the pathogen leads to infection
What is the difference between primary pathogen vs opportunistic pathogen?
- Primary pathogen: cause disease in host regardless of the host's resident microbiota or immune system.
- Opportunistic pathogen: only cause disease when host's defenses are compromised (body's protective barriers, immune system, or normal microbiota).
What are the portals of entry of pathogens?
Sites through which pathogens enter the body
- Outer layer of dead skin cells acts as a barrier
- Some pathogens can enter through openings
- Others enter by burrowing into or digesting
outer layers of skin
2) Mucous membranes
- Line the body cavities that are open to the
- Provide a moist, warm environment hospitable
- Respiratory tract is the most common site of
- Gastrointestinal tract may be route of entry
- Typically forms effective barrier to pathogens
- Pathogens may cross the placenta and infect
*Entry via the parenteral route circumvents the usual portals
What pathogens are capable of crossing the placental barrier?
Toxoplasma gondii (protozoan) - Toxoplasmosis
Treponema pallidum (bacterium)- Syphilis
Varicella-zoster virus (human herpesvirus 3) - Chickenpox
Hepatitis B virus (hepadnavirus) - Hepatitis B
Parvovirus B19 - Fifth disease (erythema infectiosum)
Togavirus - Rubella (German measles)
Human herpesvirus 5 - Cytomegalovirus
Herpes simplex viruses (HSV) 1 and 2 - Herpes
What are the portals of exit of pathogens?
Pathogens often leave hosts in materials the body secretes or excretes
- skin (flakes)
- broken skin (blood)
- insect bite
- anus (feces)
- vagina (secretions, blood)
- placenta (transmission to fetus)
- urethra (urine, semen, secretions)
- mammary glands (milk, secretions)
- eye (tears)
- nose (secretions)
- mouth (saliva, sputum)
- ear (earwax)
- injection (blood)
Why is adhesion important for infection? What molecules are used by pathogens to bind to host cells? How can host cells prevent infection by preventing adhesion? How is adhesion important for biofilm formation?
- Process by which microorganisms attach themselves to cells
- Required to successfully establish colonies within the host
- Adhesins (ligands): glycoproteins or lipoproteins; bind to host receptors, interaction can determine host cell specificity.
- Changing/blocking a ligand or its receptor can prevent infection
- Inability to make attachment proteins or adhesins renders microorganisms avirulent
- Some bacterial pathogens attach to each other to form a biofilm
How do capsules and components of the cell wall are used by bacteria to resist host defenses?
- Glycocalyx firmly attached to bacterial cell wall.
- Impairs phagocytosis.
- Not only cause of virulence; nonpathogenic
bacteria produce capsules.
Components of cell wall
- Fimbriae allows for attachment to host cell.
- Waxes resist digestion by host phagocytes
- M protein mediates attachment to host's
epithelial cells and resists phagocytosis
by host's white blood cells
How do pathogenic enzymes disrupt the host defenses? What host molecules are disrupted for each type of enzyme?
Enzymes: disrupt host proteins used for defense.
- Coagulases: coagulase blood by forming fibrin
- Kinases: dissolve clots formed by the body.
- Hyaluronidase: dissolves hyaluronic acid in
- Collagenase: breaks down collagen.
- IgA proteases: breaks down IgA antibodies
What is antigenic variation? How do viruses and bacteria use it to avoid the host's immune system?
Changing surface antigens to avoid recognition by host's antibodies
- can occur by altering a variety of surface molecules including proteins and carbohydrates.
How do using the cytoskeleton of the host cell helps pathogens avoid host defenses?
Invasins produced by pathogen rearrange actin filament of cytoskeleton to promote phagocytic-like, thus pathogen enters the host cell.
What are toxins?
Poisonous substances produced by some microorganisms
What are exotoxins? What are they made of? How do exotoxins damage host cells? How are exotoxins transferred from one bacteria to another?
- Produce inside bacteria and secreted to the surrounding environment or released due to lysis.
- Proteins molecules, most are enzymes. Destroy particular parts of host cell or inhibit particular metabolic functions.
- Small amounts can be harmful.
- Genes for toxins are carried on plasmid or phages.
- Antitoxins: antibodies made against toxins.
- Toxoids: inactivated exotoxins used for vaccination.
- Responsible for signs and symptoms in diseases.
- Three major types based on structure and function: A-B toxins, membrane-disrupting toxins, & superantigens.
- Named for host cells affected, diseases they caused, or bacteria that produces them.
What are AB toxins? How do they damage host cells? Be able to identify examples.
(type III toxins)
- Composed of 2 parts that are polypeptides: A and B.
- Part A: active (enzyme) component
- Part B: binding component
- Diphtheria toxin
- Botulinum toxin
- Tetanus toxin
- Vibrio enterotoxin
What are membrane-disrupting toxins? How do they damage host cells? Be able to identify examples.
(type II toxins)
- Disrupts host cell plasma membrane by forming protein channels or by disrupting phospholipid portion.
- Kills phagocytes and/or escape from phagosomes
- Leukocidins: kill phagocytic leukocytes, macrophages. Form protein channels. Produced by staphylococci, streptococci, & pneumococci pathogens.
- Hemolysins: kill red blood cells (erythrocytes).
- Form protein channels. Streptolysins produced by streptococci
- Erythrogenic toxins by Streptococcus pyogenes
What are superantigens? How do they damage host cells? Be able to identify examples.
(type I toxins)
- Antigens that provoke a very intense immune response. Bacterial proteins.
- T cells release cytokines, small protein hormones stimulate or inhibit normal host cell functions.
- High levels of cytokines in bloodstream are responsible for symptoms.
- Staphylococcal toxins in food poisoning and toxic shock syndrome
What are endotoxins? What are they made of? What are the effects of endotoxins?
- Part of outer portion of cell wall of gram negative bacteria. Lipid A from LPS.
- Released when bacteria die and cell wall breaks apart, or when bacteria multiplies.
- Stimulates macrophages to release cytokines in high concentrations which renders the cytokines toxic.
- Same signs and symptoms are produced regardless of microorganisms but not at same level.
- Can also induce blood clotting.
- Septic shock: loss of blood pressure due to bacteria
difference between endotoxins and exotoxins
- proteins produced inside pathogenic bacteria, usually gram + bacteria, as part of their growth and metabolism. They are then secreted or released into the surrounding medium following lysis
- lipid portions of lipopolysaccharides (LPSs) that are part of the outer membrane of the cell wall of gram - bacteria. They are liberated when the bacteria die and the cell wall breaks apart
How do viruses enter host cells?
- Use adhesins and receptor molecules to attach to host cells.
- Receptors are also used to penetrate host cells.
- Mimic substances needed by host cells to penetrate cells.
- Use antigenic variation to avoid the immune system:
*Antigenic drift: point mutations causing slight changes in the spike proteins.
*Antigenic shift: major change in spike proteins due to gene reassortment. This reassortment typically occurs when two different influenza viruses infect the same host.
What are the substances that contribute to the pathogenesis of fungi?
- Mycotoxins = metabolic products produce by fungi that are toxic to humans.
- Mycotoxins are not always responsible for fungi diseases.
- Secrete proteases
- Some fungi contain capsules
- Change or decrease of receptors allows fungi to become resistant to antifungal drugs.
What are the substances that contribute to the pathogenesis of helminthes and protozoans?
- For both, presence and waste products enough to cause disease and symptoms.
*Grow within host cells: Plasmodium and Toxoplasma.
*Attach to host cells to digest them and their
fluids: Giardia lamblia
*Change antigens to evade immune system:
*Use host cells and tissues for their own growth:
Recommended textbook explanations
Lehninger Principles of Biochemistry
David L Nelson, Michael M. Cox
Campbell Biology (AP Edition)
Cain, Campbell, Minorsky, Reece, Urry, Wasserman
Modern Biology: Student Edition
Janet L. Hopson, Postlethwait
Campbell Biology (AP Edition)
Cain, Jackson, Minorsky, Reece, Urry, Wasserman
Sets with similar terms
micro test 4 uab
Microbiology Exam 3 Sterling
Principles of Disease and Epidemiology
Microbiology Ch. 15 Microbial Mechanisms of Pathog…
Other sets by this creator
Intro to Antimicrobial Therapy
Unit 1 Pharmacology
NURS 3800: Final Skills Test Out
NURS 3800: Midterm Skills Lab (Oral & Parental Med…
Other Quizlet sets
Bard College; Rel 104 Creating Judaism; Spring 2017
Child and Adolescent Exam 3