Chapter 4: The host's encounter with microbes Flashcards
(32 cards)
example of microbes that require small number to cause an infection
shigella Spp
levels of defense against microbes in the respiratory tract
epithelial cells bind microbes
nasal hair filter
mucus and cillia flush the particles up and out of the system (damaged in smokers such as Esma)
swallowing, coughing, sneezing
what is common in all GIT-infectious microbes
the must survive the low PH of the stomach (acid stable) as well as the peristalsis=> at some point the organism must secret a toxic or adhere then invade the mucosa, otherwise it will be flushed out by the peristalsis of the GIT
different ways that the GIT-microbes invade our cells
zipper phagocytosis: host cell membrane is zippered around the bacteria cells as it enters
membrane ruffling: rearrangement of host cells cytoskeleton causing its surface to protrude, enclosing bacteria into a vacuole or compartment within host cell
outcome of microbes after invasion of our cells
they get engulfed by macrophages, those that survive will travel to the reticuloendothelial system (liver, spleen, bones) then they can gain access to the bloodstream
an example is salmonella spp. that causes enteric fever
whats the host response against microbial intestinal invasion
decrease in water and electrolyte absorption this will cause flushing of the GI resulting in diarrhea (diarrhea also happens if GI flora is replaced by pathogens e.g Clostridium diff.)
ways of microbes going into the circulatory system
skin wounds, mucus membrane openings, microbes capable of penetrating the epithelia layer will gain access to blood from an infected organ such as pneumococcal pneumonia
features of bloodborne microbes
in order to survive, they have to circumvent antibodies, complement and phagocytic cells, once they do they can be carried by red and white blood cells to wherever (by attaching on their surfaces)
preferences of microbes in systemic spread
microbes prefer previously damaged areas, inflamed areas and quiescent and dead tissue for their growth. this is why endocarditis happens in a previously damaged valve, osteomyelitis happens in previously broken bones.
nonetheless, all organs are at risk, lungs, kidneys, liver
how does a systemic infection spread to the CNS
by crossing the blood-brain-barrier
through the choroid plexus (through the fenestrated cells)
by riding in leukocytes as “torjan horse”
viruses can enter the brain though the peripheral nerves to the meninges
from ears, mastoid bones, paranasal sinuses
subarachnoid space
how does a systemic infection spread to the skeletal system
trauma/surgery
from the blood to synovial fluid
infection spread from adjuscet infected place (untreated ear infection to the mastoid)
damage to the bone predispose to osteomyelitis
prosthetic joint are coated with proteins which are good surface for bacterial colonization
how does a systemic infection spread to the genital system
tears in mucus membranes (doing THE sex ohhhhhh 🙈)
STD
catheter
childbirth( a child can pick up microbes as he’s moving down the birth canal)
how does a systemic infection spread to the urinary system
descending via the kidney
ascending via the urethra: female urethra is shorter than males, thus more susceptible to infection, plus the anus is closer and a potential source
a site of infection from which bacteria and or other products spread to other parts of the body is
the focal infection
how do microbes cause disease, what are microbial virulent factors and where are they found
in order to cause a disease microbes must multiply, spread or secrete toxins
those genes that cause disease are found on a plasmid, transposons(mobile genetic elements) or on pathogenicity islands (genes that encode virulent factors)
whats quorum sensing
the bacteria senses others and only secrete their toxins when there is an appropriate number of bacteria, they sense each other and communicate when to release toxins though a mechanism called quorum sensing
what are the functions/benefits of bacterial cell wall
protection against the host (mycobacterium has a lipid cell wall that is resistant to antibiotics and digestive enzymes)
facilitates adhesion
enhance pathogenicity, Group A strep has an M protein on the cell wall that protects against phagocytosis and prevent the adhesion of complement system. Staphylococcus has protein A which binds Fc potion of the Ig and renders it useless
features of gram-positive bacteria cell wall bacteria
group A strep has M protein that protects against phagocytosis
staphylococcus has protein A that binds immunoglobulins and renders them obsolete
features of gram-negative bacteria cell wall
endotoxin lipid A, which causes DIC
periplasmic space with antibiotic destroying enzymes
what are exotoxins
chemicals excreted by organism that helps them spread, invade, and resist host defenses or break down substances for metabolism or allows them to live in a hostile environment (proteus and helicobacter has urease that rises the PH)
host damage by exotoxins maybe be Direct (diarrheas) or Indirect (inflammation)
difference between gram positive and gram negative release of exotoxins
Gram-postitive releases them to the environment
Gram-negative secrets them in 4 deferent secretions types
type 2: protein helps carry the exotoxin to the host cell
type 3: syringe that is injected onto the host and exotoxins are passed
which bacteria forms spores under stressful circumstances
bacillus and clostridium.
in fungus, spores are reporductive
whats the difference between flagella and pili
flagella: self moving
pili : facilitate adhesion to surfaces (type 4 pili permits crawling)
functions of a bacterial capsule and what does it consists of
protects antibody binding
protects against phagocytosis
consists of a think layer of protein and carbohydrate.. in contrast to the slime layer of loosely bound protein and polysaccharide secretion present in klebsiella spp.
