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interactions between organisms
if organisms of 2 species interact with each other, there can be these outcomes (forms of symbiosis)
both benefit
one benefits, other isn’t affected
one benefits, one is harmed
one is harmed, other is not affected
symbiosis: mutualism
both benefit (+/+)
ex. bees get nectar from a plant, plant gets a way to spread pollen
bacteria in gut that help you break down your food
symbiosis: commensalism
one species benefits, other not affected
ex. burrs that get stuck in sheep’s wool get dispersed elsewhere
sheep does not mind, plant benefits
symbiosis: parasitism and predation
parasitism
one organism benefits, other is hamred
pathogens causing disease
viruses take over cellular function, frequently killing the cell
predation
predator eat prey
symbiosis: amensalism
one is harmed, one doesn’t benefit
ex. large pine trees shed needles on the ground and those needles decompose the soil is acidified so grass can’t grow in that soil
the nature of a relationship can change
some organisms that are beneficial or harmless can become harmful
opportunistic pathogens
commensal gut bacteria can become pathogenic
ex. staphylococcus aureus usually non-harmful but given right conditions → severe skin infections
ex. C difficile exists at low levels in large intestine
if normal gut flora is reduced, C difficile can grow excessively, leading to a chronic infection
conditions that can provide opportunities
compromised immune system
malnutrition
excessive antibioitic treatment
microbiology and humans
human body is mostly non-human
more bacterial cells than human cells
more viruses than bacterial cells
microbes are everywhere
On the skin
10 4 -10 6 CFU/cm2
Varies by surface
In the nose
10 4 CFU/nasal swab
In the lungs
10 4 CFU/ml
In the urogenital tract
10 6 -10 8 CFU/ml
microbes in digestive tract
microbes differ by location on the body, age, and from person to person, geography, dietary lifestyle, antibioitic use, health
toxic shock syndrome
cause: staphylococcus aureus
how/mechanism: opportunistic pathogen
produce set of toxins that cause massive immune reaction
toxins → bloodstream
can occur through wounds getting infected
symptoms: fever, vomiting, rash, rapid blood pressure loss, loss of skin, FATAL (5% of cases)
virulence factors
beta-lactamase
make it resistant to penicillin antibiotics
toxic shock syndrome toxin
cause immune reaction
treatments
prevention of organ failure
antibiotics (are not beta-lactams)
challenging b/c of abx resistance genes
MRSA is resistant to methicillin
VRSA is resistant to vancomycin
pharyngitis
cause: streptococcus pyogenes
anaerobic hemolytic gram + bacterium -→ scarlet fever, rheumatic fever, and pharyngitis (strep throat)
how/mechanism
symptoms
swollen lymph nodes, inflammation of back of pharynx, pus-filled abscesses covering the tonsils
virulence factors
capsule that contains hyaluronic acid
camouflage against immune system
M-protein (membrane protein)
protects bacterial cell from being targeted by immune cells
treatments
long-term antibiotics
anti-inflammatories
botulism
cause: clostridium botulinum
rod shaped, gram +, spore forming, obligate anerobe found in soil
ingestion of the toxin rather than live cells in adults
children: ingestion of spores
how/mechanism
produce toxin that acts as muscle relaxant → paralysis
symptoms
blurred vision, dizziness, dry mouth
virulence factors
most toxic proteins
binds to ends of muscle-controlling neurons → stops neuron from transmitting message to muscle -→ paralysis
endospore
small doses of toxin can be directly injected into specific muscles for desirable effect (Botulinum toxin = botox)
treatments
repeated washing of intestinal tract to remove clostridium
antibodies to neutralize toxin
antibiotics in infant infections
may be permanenet or last for years
pseudomembranous colitis (AKA c-diff)
cause: clostridium difficile
gram-positive, spore forming rod
GI tract
how/mechanism
becomes pathogen following broad spectrum antibiotics treatment
normal gut microbiome dies off, c-diff survives and reproduces rapidly
symptoms
leads to colitis, inflammation and possible ncerosis of the colon walls → internal bleeding and possibly death, especially in elder patients
virulence factors
produces toxins and enzymes that cause hemorrhagic death of the intestinal walls
spores are resistant to antibiotics such as cephalosporin and penicillin
treatments
stronger antibiotics such as vancomycin or metronidazole kill vegetative cells
repopulation of the GI tract with healthy community of microbes
fecal transplants from healthy colons are effective against recurring infection
tuberculosis
cause: mycobacterium tuberculosis
gram-positve, acid-fast, aerobic bacillus
how/mechanism
symptoms
persistent productive cough, frequently with blood in the sputum
fever, weakness, and more
lungs are affected but more organs can be affected
virulence factors
low virulence (people can be carriers but rate of tuberculosis is low)
mycolic acid (makes cells acid-fast)
protects cell from the immune system
won’t be digested in the lysosome
protects from dehydration
cells can survive outside the body for months
treatments
long-term antibiotics WHICH ONES?
whooping cough
cause: bordetella pertussis
non-motile, aerobic, gram-negative coccobacillus
how/mechanism
symptoms
cold-like to persistent deep cough
frequently 40-50 coughing spels every day have consequences
difficulty breathing
broken ribs
exhaustion
vomiting
virulence factors
pertussis toxin
specific adhesin to help attach to host cell
2 toxins that increase mucus production in tracheal cells
tracheal cytotoxin prevents cilia from moving so mucus stays in place and bacteria replicate
treatments
treat individual symptoms
immune system can kill the bacteria
prevention
vaccination
mainly in infants
known as pertussis
syphilis
cause: treponema pallidum
thin gram-negative spirochete, obligate parasite
spiral shape helps it attach to epithelial cells → multiplies rapidly and penetrates into capillaries
congenital syphilis
infected individuals who become pregnants may transmit it to their embryos
how/mechanism
sexually transfmitted infection that has 3 stages
primary syphilis
a chancre (type of ulcer) forms at the site of infection
painless
goes away on its own in 3-6 wks but infection is still present
secondary syphilis
3 wks to 6 months post-infection
body rash, fever, headaches, sore throat
many go away on its own
complications can occur in the bones, joints, liver, eyes and brain
after 2ndary syphilis, 30% of infections can enter a latency that can last for years and decades
infected and can transmit it but no symptoms
tertiary syphilis
benign tumors AKA gummas form in the liver, skin, bone, and cartilage
painful but not fatal
impair function
neurosyphilis
infection of nervous sytem
blood vessels in the brain, cranial nerves, and dorsal root of spinal cord
symptoms
severe headaches
convulsions
blindness
argyll-robertson pupil
dementia
symptoms
virulence factors
treatments
antibiotics
ciprofloxacin
before, mercury and arsenic were used
prevention
contact avoidance (condoms) as well as treatment of infected before sexual contact
gonorrhea
cause: neisseria gonorrheae
gram-negative aerobic diplococcus
sexually transmitted disease with different symptoms in men and women
males
painful urination, pus, and infertility (rare)
women
50% asymptomatic
50% mistaken for bladder infection
bacteria cannot attach to vaginal cells, so it attaches to cells farther up the genital tract
cervix, uterus, fallopian tube → pelvic inflammatory disease
virulence factors
fimbriae attach to host cell
capsule
enzymes destroy host antibodies
constantly-changing surface proteins
host doesn’t develop long-term immunity
treatment
antibiotics
cephalosporins
challenge: resistant strains are arising AKA super gonorrhoea
enteric diseases
cause: enteric bacteria
ex. escherichia coli, salmonella, and yersinia
subgroup called coliforms
facultatively anaerobic, gram-negative rods that don’t form endospores and can ferment lactose
associated with fecal contamination
virulence factors
capsules and fimbriae
toxins that lead to diarrhea
hemolysins
type-3 secretion systems (T3SS)
bubonic plague
cause: yersinia pestis
enteric bacterium
different strains have different severities
symptoms
high fever and buboes (very swollen lymph nodes)
if untreated, bacteremia (bacteria in blood), necrosis of tissue, and death can occur
transmitted by fleas on rodents
black death killed 1/3 of europe
squirrels in modern day
virulence factor
type-3 secretion system and its toxins
secretion system creates a link between bacterium and host phagocyte (immune cell)
toxin induces apoptosis (programmed cell death) in the immune cell, so it doesn’t attack the Y pestis cell
treatment
antibiotics, esp with early detection
prevention
control rodent populations
hepatitis
inflammatory condition of liver
liver functions to
store sugar and regulate blood
production of clotting agents
removal of toxins in body
symptoms
jaundice
accumulation of bilirubin (metabolic waste product) in the blood → yellowing of skin and eyes
abdominal distress
bleeding into skin and internal organs
chronic inflammation leading to cirrhosis
multiple causes
hepatitis B virus
partially dsDNA and ssDNA genome
replicates with RNA intermediate
infects liver cells, then is released by exocytosis
the cell doesn’t die so it continues to make more virions (billions)
viral replication releases a lot of incomplete viral particles
caspid proteins coated with surface antigens, but no genome
not infectious but recognized by the immune system → overwhelms the immune system
hepatitis B epidemiology
transmission via bodily fluids
infectious
high viral load in infected individuals, infective dose is relatively low
treatment is harder than prevention
vaccination is effective (95%)
disease in populations
epidemiology
study of the frequency and distribution of disease and other health-related factors in a population
how frequent are outbreaks?
who is susceptible?
where does the disease come from?
multiple fields of biology, psychology, meterology, climatology
stages of disease
infection
acquisition of pathogen, or its transition into pathogenicity
incubation
time between infection and arrival of first symptoms
can be hours or years
prodromal period
generalized, mild symptoms arise
gradual immune response
illness
symptoms are most evident
where disease is usually identified
decline
when treatment or immune system work to combat the disease
convalescence
recovery from the disease
can be infectious at any stage
where does disease come from?
animal reservoirs
human carriers
nonliving reservoirs
animal reservoirs
zoonotic diseases
diseases spread by animals
transmission
eating infected animal
contact with animal waste
animal bites
biological vectors
control can be challenging
if there are many animals
if the animals are wild
aka tics
human reservoirs
frequently asymptomatic
may not require direct contact
contact with contaminated materials
nosocomial infections
arise when patient is hospitalized for something else → often opportunistic pathogens
nonliving reservoirs
water, food, soil
often contaminated by contact with infected individual
parasites such as giardia can be found in bodies of water where animals defecate
tetanus and anthrax spores can be found in water
methods of transmission
pathogens spread by people or by objects that people touch
direct contact: person to person
indirect contact: objects to person
droplet transmission: cough/sneeze, usually less than 1 meter
vehicle transmission: pathogens are spread by some nonliving intermediate
airborne transmission: droplets move more than 1 meter
air conditioning, wind, sweeping, shaking out clothes
waterborne transmission: contaminated water source
fecal oral route
foodborne transmission: cotnamined food
fecal oral route
bodily fluid transmission
fluids behind handled outside the body
ex. blood transfusions
vector transmission: spread of pathoen through intermediate animal
insect carries disease, doesn’t cause it
biological vectors: pathogen reproduces within a vector, usually has a step in its life cycle that requires the vector
mosquitos carrying malria, fleas carrying plague
mechanical vectors: pathogen does not reproduce within vector but vector physically moves the pathogen
houseflies land on some contaminant and then land on your food