Lecture 2: Bacterial Pathogenesis Flashcards Preview

Microbio Exam 1 > Lecture 2: Bacterial Pathogenesis > Flashcards

Flashcards in Lecture 2: Bacterial Pathogenesis Deck (38):


-Microorganism capable of producing pathology (disease) in a percentage of normal, healthy non-immune individuals
-if administered in sufficient dose, will almost always cause disease, but at lower doses infection may result without overt disease (sub-clinical infection)


What is the goal of a pathogen?

-to reproduce, not cause disease per se
-disease of host is often associated with the propagation of the microorganism and/or its spread
-Ex: cough facilitates transmission


Opportunistic pathogen

-don't cause disease in a healthy host, but will cause disease only in individuals whose normal defense mechanisms have been compromised


Extracellular pathogen vs. Intracellular pathogen

-E: bacteria or parasites that replicate outside of host cells
-I: bacteria or parasites that replicate inside of host cells

-will determine the type of immune defenses it encounters


Obligate pathogens

-cannot be found anywhere but in association with their host


Obligate intracellular pathogens

-can grow only inside of host cells, and cannot be cultured extracellularly
-all viruses


Facultative pathogens

-can grow or survive in the environment as well as in their host


Facultative intracellular pathogens

-can grow inside and outside of cells and can be cultured extracellularly on agar plate in lab



-refers to the degree of disease that a pathogen can cause


T/F: the most successful pathogens are the more virulent

-False: often not the case because it doesn't pay to kill off your host before you've had a chance to successfully reach new host


Virulence factors

-components of pathogen that contribute to its ability to cause an infection
-toxins, adhesions, iron acquisition, special adaptations of metabolism


Bacterial infections can be _____, _______, or _______.

-acute, chronic, or latent


3 main ways in which bacteria breach the body's barriers and cause disease

1. intracellular growth of bacteria
2. disruption of host cell function from outside (extracellular pathogens)
3. extracellular secreted toxins that kill or alter host cells


To be successful, all pathogens have to be able to do what 3 things?

-gain entry
-establish niche and replicate
-reach new host


Routes of bacterial entry/transmission

-breathe in
-sexual contact
-vector (flea, tick bite)
-mother to fetus


Why might bacteria prefer to grow inside cells? (intracellular bacterial pathogens)

-access to nutrients
-avoid extracellular immune defenses
-cross barriers and reach deeper tissues


How and where does listeria enter a cell?

-Tips of intestinal villi because this is where E-Cadheren Receptor is transiently expressed (receptor-mediated entry)


How does listeria spread within the body?

-inside a cell, it polymerizes host actin at 1 end using a polarized bacterial surface protein (ActA)
-results in pseudopods that spread to adjacent cells
-Cytotoxic T cells are key to resolution


2 ways for bacteria to enter non-phagocytic cells:

-Zipper: receptor mediated


Ways in which extracellular bacteria can cause pathology

-secrete toxins
-damage cells of mucousal surface
-induce inflammation which can damage host cells


Mechanism of EPEC infection

-creates loose association with intestinal epithelial cells via BFP
-Then using type 3 secretion system (TTSS) injects Tir into bacterial cells
-Bacterial intimin makes tight association with Tir, now on epithelial membrane to form tight connection
-Additional effectors are injected that interact with host cytoskeleton and created attaching and effacing lesions
-Translocated effectors also disrupt tight junctions


Why is the end result of EPEC infection diarrhea?

-tight junction disruption causes disruption in sodium gradient and a flow of water into the intestinal lumen


EPEC functions are encoded on ________.

-Pathogenicity islands on EPEC chromosome


IgA protease

-method bacteria can use to not be phagocytosed
-cleave IgA between Fab and Fc so it cannot react with FcR on phagocytes


Protein A

-Another way bacteria prevent opsonization by antibodies
-bind Fc region of antibodies in "wrong direction" so they cannot react with phagocytes


Some bacteria wear a disguise from their host. One example is ________.

-Sialic acid
-minimally antigenic and serves an effective disguise for these bacteria


Bacteria can also avoid host defenses by varying antigens. Give an example of this.

-Using homologous recombination between PilE and PilS variable regions to always display different surface antigens to not be recognized by host immune system


Tetanus and botulinum toxins act through what activity/enzyme and have what final result? what about cholera and diphtheria toxin?

Tetanus and Botulin: zinc enteropeptidases that cleave synaptic SNARE proteins; result is paralysis

-Cholera toxin: ADP-ribosylates Gs; result is diarrhea

-Diphtheria toxin: ADP-ribosylates EF-2; result is cell death and organ failure


Why are bacterial toxins especially potent molecules?

-they are enzymes that can be used over and over again


How can Botulinum cause disease without colonization?

-spores germinate, grow, and produce toxin in food that is not killed off unless heated properly
-toxin itself, not bacteria, cause disease
-needs anaerobic conditions


Why don't we feed infants less than 1 year old honey?

-honey can often have botulism spores and young children don't have enough natural flora in their colon to fight off toxins that may form here due to it being anaerobic


Diphtheria toxin (DT) mechanism

-unlike, botulism usually begins by colonizing throat
-secreted by bacteria in throat, enters blood stream, binds to heart and muscle cells,
-kills cells by inhibiting protein synthesis


How does DT kill cells by inhibiting protein synthesis?

-DT is enzyme that ADP-ribosylates EF-2 thereby inactivating host cell protein synthesis
-DT is very potent and one molecule can kill a host cell


DT is a typical _________ toxin.

-originally made as one polypeptide then cleaved into A (catalytic) regions connected to B (host cell binding and translocation function) region by disulfide bonds


How does DT get into cells and have access to EF-2?

-B portions binds HB_EGF receptor on susceptible host cells
-DT internalized by receptor-mediated endocytosis
-vacuole with DT acidifies inside cell and this lower pH causes change in conformation of DT that triggers translocation of A into host cytoplasm
-In cytoplasm, disulfide bond is reduced and A is free to target EF-2


Legionnaire's disease

- caused by Legionella pneumophila that usually invades freshwater amoebae but can also infect alveolar macrophages in humans


-How does Legionella pneumophila enter host cells?

-Entry by phagocytosis
-used Type 4 secretion system to manipulate host organelle and create protected vacuole for bacteria to replicate in.
-Vacuole and host organelles are manipulated to not acidify and fuse with lysosomes
-recruits ER to increase size for bacterial growth
-once stresses, converts to transmissive form and exits host by lysing it


Humans are ________ for Legionella and are also evoluntionary dead ends in that humans do not transmit the bacteria.

-accidental hosts