MicroBiology Exam 3 Flashcards
(126 cards)
1
Q
Gram positive Medically important genus
A
Staphylococcus Streptococcus Bacillus Clostridium Listeria
2
Q
Gram negative medically important genus
A
Neisseria
Pseudomonas
Salmonella
Escherichia coli
3
Q
Staphylococcus genus traits
A
cocci: grows in clusters
staphylo: Greek for “bunches of grapes”
Adapted to acidic and salty skin
4
Q
S. aureus
Type of Staphylococcus
A
Around 20-30% of people carry S. aureus in their nasal passages (major reservoir)
Spread from -sites on body-already colonized
-other people carrying it thru direct contact
-fomites= inanimate objects carrying bacteria
Ex: gym equipment
5
Q
Diseases caused by S. aureus
A
Food poisoning
Skin and wound infections
Internal infection
6
Q
Food poisoning
S. aureus
A
- Food is inoculated with bacteria from skin infection or nasal passage
- Growth of bacteria in food (especially salty foods or custards), as cells grow, they secrete toxins.
- Consumption food containing the toxin will induce symptoms
- Vomiting & cramps (upper GI), occasionally causes diarrhea & low fever. Rarely fatal unless dehydrated~ treat by replacing lost fluids
7
Q
Skin and wound infections
S. aureus
A
- Includes boils and impetigo
- Infection usually requires a break in the skin from accidents, war wounds, and surgery
8
Q
Internal infection
S. aureus
A
-High mortality rates
-Usually spreads from skin or wound infection
Examples: Pneumonia (lungs), Septicemia (bacteria in blood)
-Treatment: for infection—20-40yrs ago, easily treated with antibiotics; NOW there are problems with drug resistance strain specific
9
Q
Streptococcus genus traits
A
cocci: cells grow in twisted chains.
Fairly common in oral cavity, most species are harmless
10
Q
S. pyogenes
Type of Streptococcus
A
“Group A strepts” and not usually found in/on healthy people
Can lead to Strept Throat, Scarlet fever, or Rheumatic fever
11
Q
Strept throat
S. pyogenes
A
- Pharyngitis caused by S. pyogenes (most sore throats are actually caused by viruses not bacteria etc ^^)
- Most common at ages 5-15
- Symptoms include fever, headache, and sore throat with pus on tonsils
- Usually self-limiting in a week, BUT may spread beyond throat to cause meningitis, pneumonia, septicemia
- May also trigger scarlet or rheumatic fever
12
Q
Scarlet fever
S. pyogenes
A
- Once typical childhood disease in the 19th century—major killer; rather rare today b/c treatment w/ antibiotics
- Usually begins as strept throat, followed by spreading bright red rash→ chest, arms, neck
- Rash due to “erythrogenic toxin” which triggers cytokines (immune system chemicals), which leads to inflammation. Big danger—can include endocarditis and kidney inflammation
13
Q
Rheumatic fever
S. pyogenes
A
- Incidence much reduced by use of antibiotics to treat strept throat
- Usually begins as strept throat, → body produces antibodies against S. pyogenes. Antibodies react w/ antigens on heart tissue causing autoimmune disease
- Immune system attacks hearth tissue—damages heart valves permanently and can be fatal.
14
Q
Skin and wound infections
S. pyogenes
A
- Impetigo: Spreading rash usually around the mouth, more common in kids
- Also caused by Staph. Aureus
- Blood poisoning: Infection of blood that starts with wound/trauma infection, leads to inflammatory response → red streaks= inflamed blood vessels
- Skin damage minimal—once entry of bacteria into blood can lead to septic shock (drop in BP), fatal septicemia
15
Q
Puerperal fever AKA “Childbed fever”
S. pyogenes
A
- Pathogenesis, can be major contributor to maternal and infant deaths
- Bacteria may be present in vagina or introduced by doctor at time of birth
- During birth bacteria is transferred up into uterus and spreads into the blood through the area where the placenta was attached
- Can cause systemic infection, infection of organs~ often fatal, once major cause of mother death at birth, much rarer today and can be treated with antibiotics
16
Q
S. pneumoniae
Type of Streptococcus
A
- Diseases usually start with colonization of nose and/or throat
- Source of bacteria may be through inhalation of aerosol with bacteria OR could be “self-bacteria” may carry S. pneumonia
- If bacteria spread→ get pneumonia
17
Q
Pneumonia: “Pneumococcal pneumonia”
Developed from S. pneumoniae
A
- Many microbes can cause pneumonia, but S. pneumoniae is most common cause
- Disease process: bacteria spread into the lower respiratory tract.
- Often results from lose of function of ciliated epithelial cells (in trachea), ciliated cells trap and sweep up (into mouth) various microbe—could lose cells if smoker—if killed by flu virus, flu opens up opportunity for bacteria (secondary infection)
- Once in lungs→capsules allow bacteria to evade phagocytosis bacteria (S. pneumoniae), can kill macrophage—macro-phagocytic WBC. Bacteria lyse→ triggers local inflammation, capillaries around alveoli become leaky, alveoli begin to fill with fluid, WBC, bacteria which inhibits gas exchange= less O2 absorbed, individuals becomes cyanotic (kyanos-blue)—blue-ish tint—too little O2 reaching tissue
- Symptoms: Blue tint, high fever, cough w/ blood in sputum (blood from capillaries). Death by suffocation~ mortality rate 30-35% cases before antibiotics. Today ~5% mostly very young and elderly
18
Q
Bacillus
Traits of the genus
A
common soil bacteria—produce durable endospore← which can survive extreme conditions~ toughest biological thing to kill.
19
Q
B. cereus
Type of Bacillus
A
- Very common bacteria, found in soil, dust, hands
- Can cause food poisoning→ food can be inoculated by dust or hands
- Spores heat tolerant—may not be killed by low temperature cooking→ growth of bacteria leads to toxin production in food.
- Consumption of toxin→ symptoms, which are usually over w/in 24hrs, once toxin is out of the body.
- Types of toxin:
- Emetic type- fairly heat stable, symptoms w/in 1-6hrs mostly upper G.I. tract→ cramps and vomiting, similar to staphy poising
- Diarrheal type- heat-labile toxin (deactivates w/ heat), symptoms w/in 8-16hrs, mostly low G.I. tract→ cramps & diarrhea~ similar to food poisoning Cl. perfringen
20
Q
B. anthracis
Type of Bacillus
A
- Causes anthrax & associated with livestock and bioterrorism
- Two form:
- Cutaneous form- skin infection, black lesion (least dangerous form if stays on skin)
- Inhalation or pulmonary form- high mortality from pneumonia, and spread in blood
21
Q
Clostridium
Traits of the genus
A
- gram-positive rods
- spore formers
- found in soil
- strict anaerobes.
- Spores survive if O2, cells won’t grow if O2—they need an anaerobic environment for cells to grow
22
Q
C. tetani
Type of Clostridium
A
- Causes tetanus or lock-jaw
- Disease process: bacteria are introduced from soil into deep wound. If there is a lot of tissue death around wound= O2 free environment → bacteria can grow, they secrete toxin. Toxin prevents release of neurotransmitter: cycine & gaba. Glycine/ gaba—inhibit muscle contraction.
- So—if there is no gaba lyciene released=spastic contraction when it reaches chest muscles→ can’t breathe
- Prevention: “Tetanus shot” contains modified toxin
23
Q
C. botulinum
Type of Clostridium
A
-Causes of food poisoning botulism
-Disease process: food inoculated from soil, dust, food handlers; if there is an anaerobic environment, the spore will germinate. Bacteria secretes toxin into food. Consumption of food leads to poisoning by botulinum toxin.
Ex. Canned food.
-Toxin prevents releases of Acetylcholine in nerve-muscle junctions. Acetylcholine is stimulatory, so if no acetylcholine—no muscle contraction
-Causes flaccid paralysis= death when chest muscles paralyzed and you can’t breathe.
-Botox: treats wrinkles Botulinum toxin applied locally—paralyses facial muscles
-If taken orally—1 microgram is fatal—extremely fatal
24
Q
C. perfringens
Type of Clostridium
Causes food poisoning
A
- Causes food poisoning and gangrene
- Food poisoning associated with meats, stews, gravy
- Disease process spores in food survive in low temperature cooking
- Food cools, spores germinate somewhere in the center of food. Cells in food–cells are consumed; in body the cells form spores again; in process of sporulation—enterotoxin released—toxin acts in small intestines ~ causes release of water.
- Incubation period is roughly 8-24hrs; symptoms include nausea, cramps, and diarrhea. Rarely causes vomiting
- Usually better within 24-36hrs
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C. perfringens
Type of Clostridium
Causes Gas gangrene
-Gas Gangrene, develops when bacteria are introduced into anaerobic tissue
Ex: Diabetes, compound fracture, war wounds
-If tissue is anaerobic, spores germinate; multiply --> get spreading necrosis, more anaerobic areas to colonize
-Cells ferment. Lots of smelly products—gases, beneath skin, bubbles gives “gas gangrene” name.
-If palpate skin—hear crackling “crepitation”
-Can continue to spread and can develop into septicemia and leads to leaky blood vessels, circulatory shock (drop in BP), systemic organ failure. If untreated, has high mortality rate.
-Treatment includes surgery (amputation—only option in the past but still occurs), today-high doses of antibiotics, hyperbaric (high air pressure) chamber—give more O2 into the blood, more O2 into the tissues.
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C. difficile
"C. dif"
Type of Clostridium
- ”C. dif” causes intestinal disease, associated with use of antibiotics
- Normally C. dif has hard time colonizing in gut in large numbers—cant compete well with other bacteria in gut (“normal flora”)
- If use antibiotics, can reduce many normal flora species which opens up the habitat; allows C. dif to multiply, resistant to many antibiotics and leads to overgrowth of C. dif
- Inflammation of gut due to toxins—causes watery diarrhea, cramps, fever, too. If chronic may be fatal
- Need to replace normal flora—Ex: stool transplant~ full of normal flora
- C. dif may already be present in low numbers—but can also be spread patient to patient
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Listeria
| Traits of the genus
- gram positive rods
- Can be carried in animal's bodies—including humans
- Also can survive for long periods of time in soil and water
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L. monocytogenes
| Type of Listeria
- Psychrotrophic bacteria, can be grown at refrigeration temperature and at body temperature
- Causes listeriosis, rare compared to other food borne diseases (compared to Salmonella), maybe 2000 cases per year—high mortality rate up to 20% ~ 400-500 deaths per yr.
- Bacteria usually enter body via food, they can invade and kill white blood cells. Especially if someone already has a weak immune system. Eventually can spread to the brain and can cross placenta leading to a stillborn child.
- Associated with “pre-cooked” meat like deli meats, and unpasteurized cheese.
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Neisseria
| Traits of genus
Gram neg: dilococci
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N. meningitidis
| Type of Neisseria
- One causes of meningitis; called “meningicoccal meningitis”
- Most common cause in young adults
- Bacteria may be carried by 10% of population (healthy people), often find it inside the nose or throat
- Meningitis is rare—kept in check by barriers and immune system
- Disease occurs when bacteria enters the blood, much more likely if the respiratory lining is damaged
- Bacteria multiply in blood (septicemia); in some cases it can cross blood-brain barrier and causes inflammation of meninges lining of CNS
- Symptoms: High fever, vomiting, severe headache, very painful stiff neck*
- Initially, similar to the flu~ can die within 24hrs; high mortality rate
- Treatment: Antibiotics can kill N. meningitis. Problem may progress too quickly. Bacteria may be passed to others—important to treat contacts with antibiotics.
- Prevention: vaccine available
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N. gonorrhoeae
| Type of Neisseria
aka “Gonococcus”
- Causes sexually transmitted Urethritis, urinary tract infection (UTI)
- Made possible by attaching via Pili
- Painful urethritis with pus-filled discharged
- “gonorrhea”--means “flow of seed”
- Usually more apparent in males
- Treatment was easily treated with penicillin, many penicillin resistant strains; can be treated with other drugs that work
- “The Clap” from French “Clapier” also means a “Brothel” “Clapoir” -genital sore
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Pseudomonas
| Traits of the genus
- Usually thin gram-negative rods
- Adapted to many habitats.
- Can find cells in soil, in water, on bodies.
- Many species produce pigments
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Ps. Aeruginosa
| Type of Pseudomonas
- Fluorescent yellow green pigment
- ****Of all medically important bacteria—most consistently resistant to antibiotics
- Diseases- mostly opportunistic—difficult to avoid it, but actual infections are rather uncommon if healthy
- To get infection, need break in the barrier (skin) OR debilitating disease
- Examples: -Cystic Fibrosis related lung infections, get build-up of mucus in lungs, Ps. aeruginosa is most persistent infecting agent. In CF patients, accounts for most deaths w/CF
- Burn infections—burn removes significant barrier to infect. Ps. aeruginosa can infect burned tissue. Once in skin—can move into blood. Accounts for most deaths among burn patients who survive initial trauma
- Folliculitis- inflammation of hair follicles, see lots of pus-filled pimples, associated with whirlpools/Hot tubs
- Outer ear infection- among swimmers “swimmers ear”
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Salmonella
| Traits of genus
-Gram negative rods
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Salmonellosis
Type of Salmonella
Sources
- gastroenteritis caused by many types of Salmonella
- Bacteria spread by fecal-contamination of water or food
- With modern wastewater treatment—water transmission is rare; in U.S. today—will almost always be food-borne
- Sources: Food is contaminated by food handlers; Spinach, Peanut products. Feces from pet reptiles. Food contamination by bacteria from animals that are the food—contaminant during slaughter- guts can break open; Eggs- contaminant by passage through Cloaca.
- Cook your eggs,can have some bacteria inside the egg—but mostly on the outside. ~Don't eat raw cookie dough
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Salmonellosis
Type of Salmonella
Disease info
- Disease process: bacteria enter with food. Bacteria can invade mucosal cells, lining small intestines
- Results: intense inflammatory response from release of LPS, and cytokines by damaged cells. Leads to water loss.
- Symptoms: initially in upper G.I. Tract, nausea, vomiting. Later-abdominal pain, diarrhea, low fever (maybe)
- Timing of symptoms at least 12-48 hours after ingestion, may last up to 1 week.
- Normally self-limiting so usually not treated with antibiotics—main thing (w/ diarrhea) is to replace fluids
- Prevention—detect bacteria in food, proper food handling. Care not to spread bacteria to raw foods (not going to be cooked). Cook foods to proper temperature.
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Salmonella typhi
| Type of Salmonella
- TYPHOID fever or “Enteric fever” -Rare in U.S.--but also much more dangerous than Salmonellosis
- During the infection, the bacteria spread to spleen, liver, to blood--> systemic infection w/out antibiotics. Mortality rate: 10=30%
- Good water sanitation plus discovery (early 20th century) of “carrier state” led to decline in incidence
- Shift in types of Salmonella infections to food-borne
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Escherichia
| Traits of genus
- Gram neg. rods
- Escherichia coli very common gut species
- Huge number of strains, most strains are relatively harmless residents of colon.
- But some strains are pathogenic—carry additional genes, capacity to cause disease. Many genes acquired by transfer from plasmids or phages
- Transmission: by both food or water in U.S. today—mostly by food.
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ETEC or Enterotoxigenic E. coli
| Pathogenic strain of Escherichia
- Typically enter through food, bind to lining of small intestine. Usually don't invade lining, but do secrete toxins~ cause movement of water into lumen.
- Symptoms: Diarrhea, usually w/out fever. No invasion of lining.
- Timing: 8-12 hrs after ingesting the food. Need time for bacteria to multiply and secrete toxins.
- May last about a week. Usually self-limiting. Replace fluids—better in a few days. More dangerous if you are an infant—they can dehydrate fast.
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EHEC or Enterohemorrhagic E. coli
| Pathogenic strain of Escherichia
- Includes much-publicized E. coli O157:H7
- Linked to raw milk, under cooked hamburger, unpasteurized cider
- After infection the cells may invade the lining of the gut and they also may produce toxins that will circulate through the blood.
- Creates a progression of symptoms—cramps, diarrhea at 2-5 days.
- Could develop into hemorrhagic colitis: inflammation of the large intestine—bloody diarrhea. OR could turn into Hemolytic- uremic syndrome (HUS) in about 5% of kids with O157:H7.
- Toxins affect kidneys-leads to clots in capillaries—lysed red blood cells—ultimately kidney failure, death in 5% of HUS cases
- Can treat with antibiotics, but rapid diagnosis is key.
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Viruses are:
- Acellular life form: Latin word—means “poison” or “venom”.
- Discovered in late 1800's, can't see viruses with light microscope.
- Found, filters that removed all the bacteria, didn't remove all infectious agents.
- Eventually seen in the 1940's w/ invention of electron microscope.
- Acellular (non cells) called “particles” or “virions”
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Viruses: differences from cellular life
- Much smaller than cells. Bacteria: 2000 nm (2 microns). Viruses: 10-200 nm
- Given type of virus contains either DNA or RNA—not both.
- Some types of viruses use RNA for genome (genetic material)
- Obligate intracellular parasites—outside of host cell—cannot replicate or evolve, inactive. -Only active (replicating) when they are inside host cells. Direct cell's machinery to make virus.
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Viruses: difficulties
- Blocking viral replication difficult to do w/out harming host cell.
- Difficult to find anti-viral drug that stops virus, but don't harm host. Need to find unique target only virus needs.
- Ex. Tamiflu, for influenza--- blocks unique enzyme nevraminidase which is needed to release the virus.
- Better approach has been vaccination. Vaccines stimulation immune system, immune system stops virus
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Viral Structure:
Capsid
Envelope
Genetic Material
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Capsid
Structure and shapes
(Part of viral structure)
- Protein coast that surrounds nucleic acids
- Observed shapes—helical coils of sub-units. Get flexible rods
- Icosahedral shape sub-unit arranged into 20 triangular faces.~roughly spherical (mostly helical or icosahedral shaped)
- Bullet-shaped—odd shape, ex: rabies.
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Capsid
Function
(Part of viral structure)
- Protects genomes, attachment to specific most proteins.
| - Only infects cell, if capsid protein fits receptor.
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Envelopes
Structure
(Part of viral structure)
- Found on some viruses, surrounds the capsid
| - Part phospholipid, derived from host cell membrane, part protein, usually project as “spikes” coded for by virus
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Envelopes
Function
(Part of viral structure)
-Attachment viral proteins lock onto host receptors, entry of virus—helps with fusion of envelope w/ host membrane
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Genetic material
Types
(Part of viral structure)
- Unlike w/ cells—some viruses will use RNA for the genome
- Double stranded DNA
- Single stranded DNA
- Single stranded RNA
- Double stranded RNA
- Almost all human viruses are DS DNA or SS RNA
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Genetic material
Function
(Part of viral structure)
- Code for viral proteins
- About 10-100 genes total.
- They are parasites—they use host for other needs) (humans: 25,000-30,000 genes)
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Virus Classification
- Terms used in classification: divisions into families—names end in -viridae,
- “genus” often end-virus, species or type names~ variable—may be “latinish” often uses disease name.
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Basis for division
| viral classification
- Nucleic acid composition: type (DNA or RNA), # of strands (DS or SS), sense of strand (+ or -), # of base size
- Capsid structure: shape, size, site of capsid assembly- cytoplasm or nucleus
- Envelope- yes or no
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Double stranded DNA viruses:
- Herpesviridae
- Papillomaviridae
- Hepadnaviridae
- Poxviridae
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Herpesviridae
| Double stranded DNA viruses
Species:
- Herpes simplex 1—cold sores,
- Herpes simplex 2- genital herpes,
- Epstein-Barr—mononucleosis (infection of WBCs);
- Varicella-Zoster—chicken pox(varicella) and shingles (zoster)
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Papillomaviridae
| Double stranded DNA viruses
Species:
- HPV-6
- HPV-16
- Many type of warts
- Some species of HPV linked to cervical and other cancer
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Hepadnavirida
| Double stranded DNA viruses
Species:
| -Hepatitis B—(spread by contact with blood, other body fluids)
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Poxviridae
| Double stranded DNA viruses
Species:
- Variola virus-human small pox
- Vaccinia virus—virus in small pox—related to cow pox, Cow pox virus—cow pox.
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Double-stranded RNA viruses:
-Reoviridae
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Reoviridae
| Double-stranded RNA viruses
Species:
| -Rotavirus A, B, C, etc—water, and food-bore diarrheas dangerous to infants
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Single-stranded RNA virus, positive-sense
- Calciviridae
- Picornaviridae
- Retroviridae
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Calciviridae
| Single-stranded RNA virus, positive-sense
Species:
| - Norwalk Agent—water, food-borne diarrheas
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Picornaviridae
| Single-stranded RNA virus, positive-sense
Species:
- Rhinovirus A, B, C etc—common cold,
- Human Enterovirus C—polio (begins as gut infection, but may cause paralysis),
- Hepatitis A—usually food-borne
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Retroviridae
| Single-stranded RNA virus, positive-sense
Species:
| -HIV virus—AIDS
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Single-stranded RNA viruses, Negative-sense
- Paramyxoviridae
| - Orthomyxoviridae
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Paramyxoviridae
| Single-stranded RNA viruses, Negative-sense
Species:
- Measles virus—measles
- Mumps virus—mumps
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Orthomyxoviridae
| Single-stranded RNA viruses, Negative-sense
Species:
- H1N1 flu virus
- H5N1 virus-- influenza flu
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Identification of virus
- May be by symptoms ALONE
| - Culturing viruses is difficult to grow—need live host cells (can be done-but is expensive-time)
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Non-culture ID methods of virus
- Serology—use specific virus proteins to look for specific antibodies; or use specific antibodies to look for specific virus proteins.
- Nucleic acid hybridization—use probes w/ specific base sequence, complement and bind to specific, unique viral nucleic acid base sequences (probe sticks—virus is there), need different probes for different viruses
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Virus types by host types
- Plant viruses
- Bacteriophages
- Animal Viruses
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Plant viruses
- Causes significant crop loss—most are vectored by insects.
| - Control diseases by controlling insects
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Bacteriophages
-Viruses infecting bacteria, mostly DS DNA viruses.
Two types:
-Virulent or Lytic
-Temperate or Lysogentic
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Bacteriophages
| Virulent or Lytic Type
—Kill the host cells immediately during replication.
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Bacteriophages
| Temperate or Lysogentic Type
—Viral DNA is incorporated into bacteria chromosome genes copied, cells NOT immediately killed...Later—may become lytic
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Animal Viruses
Typical virus replication cycle—for a single cell:
1. Adsorption or attachment
2. Entry of nucleic acids
3. Release or uncoating of genetic material
4. Synthesis of new virus protein
5. Synthesis of new virus genomes
6. Assembly of new progeny
7. Release of particles (progeny virus)
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1. Adsorption or attachment
| Animal virus infection process
-Adsorption or attachment of specific virus particle to specific host cell receptor.--required for infection, suggest that you can block infection by blocking attachment.
-Antibodies bind to viruses, block attachment.
-Attachment is a product of the virus attachment protein (in a naked virus—capsid protein; in enveloped virus—spike protein); host cell receptor usually host proteins or glycoproteins on host cell surface.
(WHY ARE THESE RECEPTORS THERE?)
-Host receptors have normal beneficial function for host cell.
-Virus evolved to use receptors.
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Benefit and Interaction w/ attachment
| 1. Adsorption or attachment
Animal virus infection process
- Benefit—some may be transferred protein, some may have receptors for hormones, ex: EGF receptor small pox uses EGF receptors to attach.
- Interaction is very specific—virus protein must fit receptor, if specific receptor is absent--> no infection.
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Variation in
Adsorption or attachment
(Animal virus infection process)
- Variation in presence/ absence of receptor. Variation among animal species (in presence/ absence), partly explains the host species range
- Variation among individual within species variation in susceptibly within population,
- Ex: CCR5 receptor on white blood ells for HIV
- Variation among cell types within a body—partly explains differences among viral diseases.
- Ex: acetylcholine receptor (ACh R) found on nerve cells, muscle cells, important in neuron-neuron communication, neuron-muscle cell. E: Rabies virus binds to ACh R infection of CNS.
- Ex: CD155 Protein found on gut cells, neurons normal role, involved in cell-cell adhesion—also acts as polio virus receptor. Polio virus causes gut infection, causes paralysis.
- Ex: CDY found on certain WBC, important in interaction w/ other WBC, also a HIV receptor—HIV kills WBC's.
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2. Entry of nucleic acids
| Animal virus infection process
-Entry of nucleic acids usually means entry of capsid many mechanism (depends on presence of envelope)
Ex: if there is an envelope—could enter by fusion of envelope phospholipid w/ cell phospholipid
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3. Release or uncoating of genetic material (Animal virus infection process)
- Release or uncoating of genetic material from protein capsid by proteolytic enzymes.
- Source of proteases could be from a host cell or viral enzymes.
- Location—most RNA viruses in cytoplasm; most DNA viruses in nucleus.
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4. Synthesis of new virus protein
| Animal virus infection process
- In all cases, viral mRNA translated by HOST ribosomes.
- Making viral protein always takes host ribosomes.
- Variation depends on viral nucleic acid.
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-DNA viruses
| 4. Synthesis of new virus protein
Animal virus infection process
- Viral DNA is used to transcribe viral mRNA
- Viral mRNA leaves nucleus binds to ribosomes
- Translation to viral protein.
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-RNA viruses
| 4. Synthesis of new virus protein
Animal virus infection process
- Genomic RNA is usually in cytoplasm throughout.
- (+ plus sense) single strand RNA viruses
- (- minus sense) single stranded RNA
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-(+ plus sense) single strand RNA viruses-RNA viruses
4. Synthesis of new virus protein
(Animal virus infection process)
- (+ plus sense) single strand RNA viruses genomic RNA can act as mRNA
- No need for transcription, genomic RNA (mRNA) can be directly translated-->protein.
- Translation of +RNA produces new viral protein.
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-(- minus sense) single stranded RNA
-RNA viruses
4. Synthesis of new virus protein
(Animal virus infection process)
-(- minus sense) single stranded RNA, genomic RNA (-RNA)
-Transcribed to make complement +RNA. RNA is template for making RNA, uses RNA-dependent(<--means RNA is used as template) RNA polymerase.
-Virus must bring enzymes.
-Complement +RNA=mRNA for translation.
((minus needs extra step—plus sense can use RNA as mRNA w/out extra step))
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5. Synthesis of new virus genomes
| Animal virus infection process
- Must make more copies of genes
- DS DNA viruses use viral DNA as templates similar to copying DNA in cells, prior to cell division.
- SS RNA viruses use single genomic RNA strand to create complementary RNA strands w/ assistance of RNA-dependent RNA polymerase.
* If genome is +RNA, complement is -RNA, then -RNA is template to make +RNA, back to genomic RNA.
* If genomes is -RNA, the complement is +RNA, +RNA is a template to make genomic -RNA.
* ***making LOTS of copies of genomes--> get LOTS of particles per round of replication.
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6. Assembly of new progeny
| Animal virus infection process
- Capsid proteins migrate to assembly sites, DNA-in nucleus, RNA-in cytoplasm.
- Proteins (capsid) spontaneously aggregate (can occur outside of cell).
- As protein aggregate, nucleic acids packaged inside.
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7. Release of particles (progeny virus)
| Animal virus infection process
-May release many (100's) particles per cell
Two types:
-Naked virus release
-Envelope virus released
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-Naked virus release
| 7. Release of particles (progeny virus
Animal virus infection process)
- Usually released in single burst as cell lyses.
- Lysis due to shut down of normal host activity.
- Production of viral lytic protein.
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-Envelope virus released
| 7. Release of particles (progeny virus
Animal virus infection process)
- Usually released slowly (a few particles at a time).
- Though budding host cell—not immediate lysed. Release may continue for hours.
- The particles pass through various membranes where they acquired host phospholipid membrane...RNA virus- cell membrane Phospholipid
- DNA virus get Phospholipid from nuclear and cell membrane.
- As particles pass—they pick up envelope protein.
- Envelope proteins embedded in cell membrane.
- Proteins—virus-coded proteins.
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Retrovirus:
Replication differs from others.
Family Retroviridae
Ex: HIV and Leukemia virus links.
| -Genome is single-strand (+) RNA, but... replication requires double-stranded DNA intermediate.
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Role of Transcriptase in:
Retrovirus:
Replication differs from others.
Family Retroviridae
- The DNA intermediate is created by a process called reverse transcriptase (enzyme complex).
- RT (reverse transcriptase), unique to Retrovirus= good target for anti-viral drugs.
- Inhibited by AZT—RT is essential to virus, must be carried into cell with virus~ 50-100 of RT “molecules”
- RT complex function:
- RNA-dependent DNA polymerase function= uses +RNA as template to create DNA—specifically +RNA/-DNA hybrid.
- This is unusual because it is reverse of “central dogma” of replication...usually DNA-RNA-protein, instead RNA-DNA. Hence “retro”
- Ribonuclease function—degrades +RNA strand, leaves single -DNA strand
- DNA-dependent, DNA polymerase uses -DNA to make -DNA/+DNA, result: double-stranded DNA.
- Referred to as a “provirus”
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Provirus Gene Insertion
Retrovirus:
Replication differs from others.
Family Retroviridae
- Provirus moves into nucleus, DNA is incorporated into host chromosome (gene insertion).
- Roughly similar to lysogeny. ~requires nicking chromosome, HIV has an enzyme called integrase that nicks DNA—at somewhat random locations.
- After incorporation:
- May become latent (inactive), genes will be copied when cell divides.
- Human chromosome is loaded with retrovirus sequences.
- Viral genes may be expressed which results in active infection.
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Active Infection:
Retrovirus:
Replication differs from others.
Family Retroviridae
- Protein synthesis-viral DNA transcribed to viral mRNA to viral proteins
- Genome synthesis uses -DNA strand as template to make +SS RNA, the assembly is in the cytoplasm.
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Outcome of infection by animal viruses at the level of whole organism
1: Acute active infection
2: Persistant infection
3: Cell transformation
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Outcome 1: Acute active infection
| By animal virus on whole organism
- Usually characterized by extensive, rapid cell death.
- Cell death- due to activity of virus in cell (cell lysed), or an attack on virus-infected cells by immune system.
- If enough cells are killed—then symptoms appear. Organism “has disease”.
-Possible results:
-Immune system completely eliminates the virus. Get better w/in a week or so.(more common—like flue)
OR
-Virus kills to many cells—too much damage—you don't get better—you die w/in a week or two. (maybe through small pox)
OR
-Infection could subside—symptoms could largely disappear, immune system mostly winning, BUT virus is not completely eliminated~ infection enters a persistant state.
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Outcome 2: Persistant infection
| By animal virus on whole organism
- Virus remains in some form for months, years, maybe lifetime.
- At time of initial infection—may or may not get symptoms. Immune system kicks in—largely eliminates or controls any symptoms—the virus remains.
- Requirements for persistant:
- Viruses must not kill host organism too quickly. Indicates a reduction in cell-killing activity—doesn't kill too many cells too quickly.
- Must evade the immune system—mechanisms—infect cells w/ reduced immune system activity. Ex. Skin cells—wart virus; CNS—herpes virus. (don't hangout in the blood)
- Remain in cells as genetic material only. Immune system—good at detecting foreign proteins, bad at detecting foreign genes.
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Spectrum of Persistant
| Outcome 2: Persistant infection
By animal virus on whole organism
Chromic persistantLatent persistant
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Chronic infection
| Spectrum of Persistant
Outcome 2: Persistant infection
By animal virus on whole organism
-Virus usually continues to replicate itself at low rate—may continue to be shed and infect others, may have symptoms~ depends a lot on “virus load”
- The viral load is important in chromic infection—depends on number of particles.
- Determines presence of symptoms—degree of infectiousness—how likely it can be spread.
- Examples:
- Papilloma virus—skin warts, virus shed from warts—spread by direct contact.
- Hep B, persists in liver, shed into blood, semen, spread by contact w/ fluids.
- HIV, persists in WBC, lymph tissue—spread via body fluids.
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Latent infections
| Spectrum of Persistant
Outcome 2: Persistant infection
By animal virus on whole organism
- Periods of dormancy between periods of active infection. Dormancy-no viral production, no symptoms—but genes of virus is STILL there and can become active later.
- If it becomes active, particles formed—get symptoms—can be spread.
- Maintenance of genes: integration of genes into host chromosomes
- Ex. HIV—viral DNA (via RT transcribing RNA)
- Many infected WBCs, not actively producing virus, especially if treated with AZT.
- Circles of DNA outside of chromosome, circles—much less likely to be degraded.
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Herpes Family
Example of latent viruses
Latent infections
Spectrum of Persistant
Outcome 2: Persistant infection
(By animal virus on whole organism)
-Initial infection following contact.
Location:
-Herpes simplex I/II, skin, mucus membrane—leads to cold sores and genital lesions.
-Varicella-zoster (type of Hep. B)--infects upper respiratory tract—leads to chicken pox
-Epstein-Barr (EBU), oral mucosa, leads to mononucleosis.
- Initial infection contained by immune system, systems usually disappear, but viruses will persist as circles of DNA
- Location of latency simplex I/II and V-Z DNA circles in adjacent sensory nerves, movement w/in that nerve to ganglia (near spinal cord).
- EBV- latent in B cells (may remain dormant, asymptomatic for decades—or for the rest of life) OR may be re-activated by immuno-supression, or by a “stressor” ~ Ex: UV light
- Reactivation- Simplex I/II cold sores, genital lesion. Varicella-zoster appears as shingles –lesions follow path of nerve. EBV- mono-like disease.
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Outcome 3: Cell transformation
| By animal virus on whole organism
- Involves many viruses capable of persistant/latent infections.
- Transformation—part of series of events leading to cancer
- Viral genes alter nature of host cell,
- Transformations rapid cell division
- Unregulated division
- Loss of specialization
- Loss of contact inhibition—C.I.
- Keeps cells growing in sheets. Loss of C.I. leads to tumor formation—through pile up.
- Changes seen in transformed cells
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-Changes seen in transformed cells
| Outcome 3: Cell transformation
By animal virus on whole organism
- Promotion of cell division
- Driven by oncogenes (“onco”-cancer), oncogene push cell through cycle more rapidly.
- Source of oncogenes could be viral genes. OR self genes—mutation by virus DNA insertion, converts your genes into proto-oncogenes (okay, unless they mutate)--into oncogenes.
- Damage to tumor suppressor genes, Tumor suppressor genes, normally act to slow cell division, prevent tumor formation. Often work by triggering apoptosis (series of events leads to self destruction of cell=death)...Destruction of transformed cells
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Oncogenic viruses
- RNA retroviruses
| - DNA viruses
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-RNA retroviruses
| Type of Oncogenic virus
- All cancer-causing RNA viruses are retro...but not all cause cancer...
- Retrovirus-creates DS DNA, DS provirus insert into chromosome, may affect cell division rates.
- Examples:
- Rous Sarcoma virus (RSV)--causes tumors in chickens. Virus carries oncogenes, genes for an enzyme tyrosine kinase which promotes cell division.
- HTLV-1, occasional cause of leukemia
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-DNA viruses
| Type of Oncogenic virus
- Papilloma viruses
- Hepatitis B virus
- Epstein-Barr
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Papilloma viruses
-DNA viruses
Type of Oncogenic virus
- Many families—Papilloma viruses, mostly cause tumor formation by inhibition of tumor suppressor genes
- E7 protein, viral protein, binds to and inhibits Rb protein.
- Rb protein normally inhibits E2F protein.
- E2F protein involved in transcription of DNA and in DNA replication.
- Replicate DNA for cell division—sooo E2F helps cell division.
- Rb—inhibits cell division.
- E7 inhibits the Rb inhibitor= more division.
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Hepatitis B
-DNA viruses
Type of Oncogenic virus
- Causes persistant infection. Infection leads to BIG increase in liver cancer risk.
- Result of several mechanisms; chronic infection=chronic inflammation—as immune system responds—constant production of free radicals—very reactive. This can be beneficial against microbes but can damage DNA which leads to mutations= cancer.
- Insertion of viral DNA into host chromosome. Could convert proto-oncogenes into oncogenes. Oncogenes--> uncontrolled cell division—loss of regulation—tumor formation.
- Virus proteins may have direct effect, may increase DNA replication—faster cell cycle (cell divides more often). May block activity of tumor suppressor proteins.
- Hepatitis B vaccine, also prevents cancer and immediate infection.
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Epstein-Barr virus
-DNA viruses
Type of Oncogenic virus
- Herpesviridae—infects B lymphocytes, genome maintained as “episome” (circle) in cell.
- Genes (EBV) act to “immortalize” cell. Cells will divide indefinitely, in contrast with normal cells that only divide about 50x.
- Oncogenes (viral), produce proteins that promote cell division.
- Cancers include Burkitt's lymphoma (...restricted to Africa) & Hodgkin's lymphoma (cancer of WBC—lymphocytes) B-cells.
- Leads to lymph node tumors.
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Hodgkin's Link
Epstein-Barr virus
-DNA viruses
Type of Oncogenic virus
- Difficult to establish b/c 90% of the adult pop. have been infected w/ EBV at some point (can find antibodies against EBV which indicates past infection).
- Of those infected, about 70% will show few or no symptoms of disease—no formal diagnosis (of mononucleosis).
- About 30% will have acute EBV infection—develop mononucleosis.
- Of the 30% of acute, severe case of mononucleosis, about 2X increase in Hodgkin's risk.
- Viral DNA stays in B cells.
- Still a rare cancer.
- From 1 in 2000 (normal risk) if had acute EBV then 1 in 1000. Usually treatable cancer.
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Cheese making
| Cows milk
```
%water: 88%
%fat: 3.3%
Fat(g): 8g
%Cal from Fat: 48%
Sugar(g): 12g
Protein(g): 8g
```
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Cheese making
| Goats milk
```
%water: 87%
%fat: 4.1%
Fat(g): 10g
%Cal from Fat: 53%
Sugar(g): 11g
Protein(g): 9g
```
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Cheese making
| Sheep milk
```
%water: 81%
%fat: 6.9%
Fat(g): 17g
%Cal from Fat: 57%
Sugar(g): 13g
Protein(g): 15g
```
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Antibiotics used for dairy cows
1- Used to treat mastitis(bacterial infections of the udder) and a variety of other infections--serious illness, reduction of milk yield and death.
-Important to prevent epizootics (epidemic)
2-Used as "growth promoters"--used to reduce or eliminate minor, low level infections and inflammation due to bacteria on seemingly healthy animals.
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Legality of antibiotics in milk
Practically illegal
- test milk received from dairy farmer for presence of antibiotics--if detected, milk is rejected.
- keep drug treated mastitis out of the "pool" sold to milk shippers
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Reasons why antibiotic treated milk is not used for cheese making
1. Chance that antibiotics might produce an allergic rxn in consumers who are sensitive to that drug.
2. cheese making relays on fermenting of bacteria. Lactic acid bacteria--could be inhibited or killed by anti-bacterial antibiotics like penicillin
3. Increased rates of drug-resistant bacteria and can spread from animal into humans.
- when antibiotic-resist pathogen of non-human animal origin causes human infection, disease can be very difficult to treat.
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Antibiotics commonly used in cattle
1. Beta-Lactam antibiotics
a. Penicillins (penicillin G, ampicillin, amoxicillin)
b. Cephalosporins (ceftiofur, cephapirin)
2. Tetracyclines (tetracycline, oxytetracycline, chlortetracycline)
3. Gentamicin (from the "amino glycoside" class of drugs)
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Homolactic fermentation
```
Lactose:
-Galactose-->Tagatose-1, 6-Bisphosphate
-Glucose-> Glyceraldehyde-3-Phosphate
Dihydroxyacetone-PO4
2 Pyruvate--> 2 Lactic Acid (2 Lactate)
^(Net 2 ATP per glucose )
```
Glycolysis from Glucose--> 2 pyruvate
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Primary Heterolactic Fermentation
```
Lactose--> Glucose
-CO2 or -Pentose Sugar (5 carbons)
(off sugar)
-Glyceraldehyde-3-phosphate-->(Net 1ATP per glucose)~1 pyruvate --> 1 Lactic Acid (1 Lactate)
OR
-Acetyl Phosphate-->>> Ethanol
```
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Variations on Heterolactic Fermentation
Lactose--> Glucose
-CO2 or -Pentose Sugar (5 carbons)
(off sugar)
-Glyceraldehyde-3-phosphate-->(Net 1ATP per glucose)~1 pyruvate --> 1 Lactic Acid (1 Lactate & Diacetyl).... Citrate(^1pyruvate)-->Acetic acid+CO2
OR
-Acetyl Phosphate--> Acetic acid, or Acetaldehyde--> Ethanol
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Lactococcus lactis
subsp. cremoris
Mesophilic Starter cultures: 25-40 C (77-104 F), and up to 45C (113F)
- Homolactic fermentor (More acid)
- Many types of cheese including cheddar and colby
- Old name: Streptococcus cremoris
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Leuconostoc lactis
Mesophilic Starter cultures: 25-40 C (77-104 F),and up to 45C (113F)
- Heterolactic fermentation (more flavors)
- Swiss, gouda, feta, brie, camembert, "blue" cheese, and cottage cheese
- Old name: Leuconostoc lactis
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Lactobacillus helveticus
Thermophilic Starter Cultures: 45-50 C (113-122F), and up to 55C(130F)
- Homolactic fermentor (more acids)
- Swiss, Italian cheese (parmesan, romano, mozzarella), yogurt.
- Old name: Lactobacillus helveticus
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Coloration of cheeses
- Early cheese making did not use dyes, usually pale yellow color.
- Oftern dyes or color is added around initial fermentation to produce darker yellow and orange cheese
- Marigold petal extract and carrot juice (both contain high concentrations of beta-carotene)
- Annatto-extract from red-orange seed has a bright carotenoid called "bixin"
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Cutting the curd
| Cheese making
Semi-solid curds and watery whey were converted from acidification and rennin with milk.
- reduced water content, aids storage
- Curd still contains high amount of water, but also high concentration of clotted protein and fat
- Contrastly, whey is watery solution of unclotted proteins, unfermented lactose, lactic acid and other water-soluble fermentaion products, dissolved Ca and water-soluble vitamins (B)
- Curds cut into small blocks--release more water~varying sized blocks influences cheese hardness.
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Cheddaring and milling
| Cheese making
- After whey is drained off--the remaining curds are cut and stacked on top of each other, process called cheddaring.--squeezes out more whey and by creating longer and more aligned casein filaments--changes texture.
- Drained curds (cheddared or not), are usually milled or cut by blades prior to pressing to break up casein filaments that were formed during fermentation, exposure to rennin and cheddaring.
- If a stringy or stretchy cheese is wanted--no milling occurs--casein filaments are not cute, curds are heated to 65-85C (150-185F) in hot water and then kneeded and stretched like dough
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Salting cheese
1. Salt can be mixed into curds prior to pressing, during milling--most cheddars
2. Cheese can be soaked in brine or salt water solution after the curds have been pressed into block or wheel--salt moves from outside to within--used for swiss cheese
3. Salt can be rubbed on surface of the cheese after formed in block or wheel--forms hard rind on outer surface and allows slow diffusion into the interior of cheese---hard cheeses
