Looks like no one added any tags here yet for you.
list some ways infections can influence the microbiota
diarrhea reduces overall numbers of gut microbiota, intestinal pathogens occupy host binding sites and alter available nutrients, inflammation can benefit pathogens more than normal microbiota
parasite
an organism that benefits while it causes damage to the host
primary pathogens
cause disease in healthy hosts
opportunistic pathogens
cause disease only in comprised hosts or after entering unprotected sites
reservoirs
animal, bird, or arthropod that normally carries the pathogen without showing symptoms
ID50
infectious dose, amount of virus to infect 50% of the host
LD50
lethal dose, amount of virus to kill 50% of the host
direct infection
involves direct contact between people or reservoirs
indirect infection
transmission by “vehicles” such as inanimate objects
horizontal transmission
direct or indirect contact with formites or vehicles
vertical transmission
passage from a mother to her fetus during pregnancy or birth
portals of entry (5)
mouth, respiratory tract, conjuctiva and mucous membranes, wounds, injuries, and skin lesions, parental route - direct injection into blood stream
role of immunopathogenesis in disease pathology
immune response to a pathogen is a contributing cause of pathology and disease
roles of virulence factors (5)
enter a host, find their niche, avoid normal host defenses, multiply, transmit to a new susceptible host
molecular Koch’s postulates that confirm the identity of a pathogenicity gene (3)
phenotype under study should be associated with pathogenic strains of a species, specific inactivation of the virulence genes should reduce its effects and isolate the gene, reversing or replacing the mutated gene should restore pathogenicity
how are proteins involved in pathogenesis
many proteins are secreted by type III systems in pathogenicity islands
pathogenicity islands
clusters of virulence genes in bacterial pathogens that encode virulence functions and are horizontally transmitted
indicators of pathogenicity islands
unique GC/AT ratio, linkage to a tRNA gene, association with genes homologous to phage/plasmid genes
role of horizontal gene transfer in pathogen evolution
genomic sequencing has proven that epidemics are caused by new strains of the same pathogen rather than an old strain reemerging
viral and bacterial host attachment mechanisms
adhesin, capsid or envelope proteins (virus), pili or nonpilus proteins (bacteria)
type I pili assembly
adhere to carbohydrates on host membranes, produce static attachment to the host cell, grow from the outer membrane of certain gram-negative bacteria
type IV pili assembly
involved in “twitching motility”, produce dynamic attachment via assembly and disassembly, grow from inner membrane of many gram-negative bacteria
how do differences in host susceptibility occur
immunocompetence and receptor availibility
role of biofilms in infections
enable persistent adherence, resistance to host defenses, and tolerance to antimicrobial agents
exotoxins
proteins produced and secreted by various types of bacteria that kill host cells and unlock their nutrients
endotoxins
a part of a lipopolysaccharide of gram-negative bacteria and hyperactivate host immune systems to harmful levels
functional categories of bacterial exotoxins (9)
plasma membrane disruption, cytoskeleton alterations, protein synthesis disruption, cell cycle disruption, signal transduction disruption, cell cycle disruption, cell-cell adherence, vesicular traffic, inhibit exocytosis, superantigens
hemolysins
membrane-disrupting toxin that lyses red blood cells
leukocidins
membrane-disrupting toxin that lyses white blood cells
AB exotoxins
consists of a ring of B subunits and a central A subunit that work together to disrupt host cell functions, A subunit is the toxicity-associated factor, B subunit binds to the host cell and delivers the A subunit
mechanisms of host cell cAMP disruption by bacterial exotoxins
cholera toxins target a host cell with A subunit ADP-ribosylates and can cause sharp increases in cAMP levels, resulting in ion transporters carrying water out of the cell and causing diarrhea
toxins that disrupt protein synthesis (2)
shiga toxin, diphtheria toxin
shiga toxin
exotoxin produced by shigella and e. coli whose A subunit cleaves the 28S rRNA in ribsomes to cause acute kidney failure
diphtheria toxin
exotoxin produced by corynebacterium diphtheriae twhose A subunit ADP-ribosylates eukaryotic elongation factor 2, causing cell death and pseudomembrane formation in the trachea
type II secretion
a modification of the same system used for type IV pilus biogenesis with extendable and retractable secretion structures that secrete proteins
type III secretion
reengineered flagellar synthesis mechanism normally located within pathogenicity islands that typically is triggered by cell-cell contact and injects proteins from the bacterial cytoplasm into the host cell through a molecular syringe
pore-forming proteins
exotoxins that disrupt host cell membranes by inserting themselves into the membrane by binding cholesterol and membrane receptors
phospholipase enzymes
exotoxins that disrupt host cell membranes by hydrolyzing phospholipids into fatty acids
type IV secretion system
evolutionary modification of a conjugation pilus that secretes proteins and sometimes proteins and DNA directly from the cytoplasm or periplasm
bacterial toxin secretion system 1
SecA dependent, one effector per system (E. coli alpha hemolysin)
bacterial toxin secretion system 2
SecA dependent, similar to type IV pili (pseudomonas aeruginosa exotoxin A)
bacterial toxin secretion system 3
SecA independent, multiple effectors secreted, syringe mechanism injects effectors into target cells (Yersinia Yop proteins)
bacterial toxin secretion system 4
related to conjugational DNA transfers, multiple effectors secreted, some systems inject effectors into target cells (B. pertussis toxin)
bacterial toxin secretion system 5
autotransporter, SecA dependent to periplasm, self-transport through outer membrane, one effector per system (Gonococcal)
bacterial toxin secretion system 6
related to phage tails, single effector, harpoon mechanism (burkholderia)
steps of toxin secretion through Type II secretion system
proteins secreted into periplasm, get folded, secreted through outer membrane pore
examples of Type III secretion system
salmonella, yersinia, shigella, escherichia
mechanisms pathogens use to determine their location
two-component signal transduction systems that monitor magnesium and pH levels and quorum sensing to detect exotoxins made by other cells
ways pathogens avoid extracellular immune detection
secrete thick capsule, produce proteins that bind to antibodies, induce apoptosis of phagocytes, alter surface antigens
strategies intracellular pathogens use to prevent phagolysosome induced death
learn to grow in acidic conditions of the phagolysosome, prevent phagosome-lysosome fusion, escape the phagosome
mechanisms used by pathogens to avoid intracellular immune detection
mimicry by changing antigens, flipping cytokine profiles, stopping apoptosis, redirecting host ubiquitylation signals that tag proteins for destruction
salmonella virulence factors
type III secretion systems invade host cell and replicate within the host cell, has 14 pathogen islands
genomic tools that have proven pathogen biology
genomic sequencing and bioinformatic analysis can identify potential pathogenicity islands and virulence genes, compares sequences of virulent and attenuated strains, and reveals how to grow obligate intracellular pathogens in the lab
how to use RNA sequencing to understand host-pathogen interactions
monitors pathogens’ transcripts during infection and views the host’s transcriptional response to it
fluorescence resonance energy transfer
identifies which host cells have been targeted by the pathogen proteins by constructing translational fusion between a gene encoding a bacterial effector protein and a ß-lactamase gene, once expressed a fusion protein can be translocated from the pathogen directly into host cells using one of the secretion systems.
folliculitis symptoms and causative agents
(skin disease) boils
staph aureus
necrotizing fasciitis symptoms and causative agents
rapidly progressive cellulitis
staph aureus
strep pyogenes
clostridium perfringens
scalded skin syndrome symptoms and causative agents
peeling skin on infants, systematic toxin
Staph aureus (G+ cocci)
rubella symptoms and causative agents
discolored, pimply rash, mild disease unless congenital
rubella virus
measles symptoms and causative agents
severe disease, fever, conjunctivitis, cough, rash
rubeola virus
chickenpox and shingles symptoms and causative agents
discolored lesions
herpesvirus
varicella-zoster
nosocomial infections
infections caught from the hospital
staph aureus vs strep pyogenes
s. aureus - gram positive organism that is normally found in nostrils
s. pyogenes - gram positive coccus best known for causing sore throats and immunological sequelae (ie. rheumatic fever) and can also cause necrotizing fasciitis and cellulitis
fungal respiratory infection
typically requires immunocompromised host to cause disease
viral respiratory infections
localized, influenza and rhinovirus, SARS, RSV
bacterial respiratory infection
most deadly, mycobacterium tuberculosis is leading cause of death by microbe
anthrax symptoms and causative agents
hypotension, respiratory failure
bacillus anthracis
whooping cough symptoms and causative agents
violent cough inhalation “whoop”
bordetella pertussis
pneumonia symptoms and causative agents
sore throat, chest pain, nonproductive cough
pseudomonas aeruginosa
mycoplasma pneumoniaeRSV
tuberculosis symptoms and causative agents
cough, bloody sputum, fatigue, weight loss
mycobacterium tuberculosis
RSV disease symptoms and causative agents
cough, chest pain
respiratory syncytial virus
severe acute respiratory syndrome symptoms and causative agents
cough, chest pain
SARS virus
why is tuberculosis a reemerging disease
primary tuberculosis is typically latent/dormant as the body walls the bacilli off in a granuloma and secondary is caused by reactivation of the pathogen (typically in immunocompromised people)
infection defense mechanisms of the lung
mucociliary escalator
mucociliary elevator
cilia moves mucus out of the respiratory tract into the mouth, where inhaled respiratory infections caught in the mucus will be swallowed and killed in stomach acids. as long as pathogens can’t stick to the lung cilia or wall, infection will not occur
most common causes of diarrheal diseases
viruses, specifically rotavirus, and salmonella enterica and campylobacter
osmotic diarrhea
water absorption in intestines
secretor diarrhea
secreted water in intestine exceeds absorption
inflammatory diarrhea
the epithelium gets disrupted and serum and blood are released into the intestine, destroying the intestinal epithelium
motility-related diarrhea
any condition that increases the time necessary for nutrients and water to be exposed to the intestinal epithelium for absorption
gastritis
inflammation of the stomach lining (ulcers)
gastroenteritis
nonspecific term for any inflammation along the GI tract
enteritis
inflammation mainly of the small intestine
enterocolitis
inflammation of the colon and small intestine
colitis
inflammation of the colon (large intestine)
best treatment plan for diarrheal disease patients
rehydration therapy
symptoms and causes of food poisoning
immediate diarrhea and/or vomiting
staph aureus
clostridium difficile
caused when antibiotic treatment of GI diseases causes competing bacteria to die and allows pathogen to thrive. can overgrow and cause pseudomembranous and may lead to ulcerative colitis and/or sepsis
enterohemorrhagic E. coli (EHEC)
do not invade intestinal cells, attachment and effacing lesions produced cause bloody stool
effects of diarrhea in gut microbiome
reduces diversity of microbiome
heliobacter pylori stomach survival
secretes enzyme urease, which converts urea into ammonia to neutralize stomach acids, followed by enzymes collagenase and mucinase to soften the mucous lining of the stomach and allow for the bacteria to burrow into the protective mucous layer where they’ll grow and divide, damaging the tissue
disease caused by heliobacter pylori
gastric cancer
Hep A (HAV)
-sense ssRNA virus that takes the fecal-oral route and is not a chronic illness
hep B (HBV)
dsDNA virus in the blood that is a chronic illness
hep C (HCV)
+sense ssRNA virus in blood that is chronic
urinary tract organ system
kidneys, uterus, urinary bladder, urethra
ways that UTI-causing bacteria enter bladder or kidney (4)
infection from urethra to bladder, deposition of bacteria from blood to kidney, descending infection from kidneys, ascending infection to kidneys
etiological agents of UTIs
uropathogenic E. coli, klebsiella, proteus, pseudomonas, enterobacter, certain gram positive bacteria and fungi
difference between uropathogenic e. coli and other strains of e. coli
the other strains cause GI disease
gonorrhea symptoms and causative agents
purulent discharge, burning urination, potential sterility
neisseria gonorrhoeae (G-)