The flashcards below were created by user
on FreezingBlue Flashcards.
-Types of DNA mutations:
Permanent changes in DNA
- Types of DNA mutation:
- 1. Frameshift
- 2. Point Mutation (silent mutation or nonsense mutation)
- 3. Missense Mutation
- 1. Induced mutation: Known chemical
- ex: Radiation, carcinogens (cancer), chemical or physical causes
- 2. Spontaneous mutation: DNA polymerase errors that are not connected.
To test if a chemical is a mutagen (causes mutation) by using a bacteria
- When a base is added OR removed; major changes to protein occurs.
- --> enzyme wont work properly.
*because of the addition or subtraction to the mRNA coding, the whole thing gets shifted and the amino acids get changed COMPLETELY**
Point Mutations: Silent and non-sense
When a base is changed
- 1. Silent mutation: change in DNA (and RNA) but NO change in the protein.
- ex: mRNA: UUU (PHE) becomes UUC (STILL PHE)
- 2. Non-Sense: Change in DNA creates stop codon; creates an incomplete protein.
- Ex: UUG (Leu) becomes UAG (now a stop codon)
Change in DNA (And RNA) which leads to change in amino acid; codon before and after are just fine.
ex: UUU(Phe) becomes UUA (NOW Leu)
Horizontal Gene Transfer:
--> two types: Recombiant?
Bacteria can pass their genes not only to their offspring but also LATERALLY
to other microbes of the SAME generation.
-transfer involves a DONOR cell that gives a portion of its total DNA to the RECIPIENT cell (aka "recombinant
"-incorporation donor's dna into its own dna)
1. Genetic exchange:
DNA fragment/plasmi is transferred to bacteria
2. Genetic (homologous) recombination:
DNA fragment is integrated into the chromosome
- Some effects of Horizontal gene transfer:
- 1. Increased ability to cause disease
- 2. Antibiotic resistance
Three types of Horizontal gene transfer?? (pg 233-239)
1. Transformation: gain DNA "naked" dna from environment; DNA fragment/plasmid is gained
2. Conjugation: DNA transferred from donor to recipient through pillus (straight hair-like structure)
3. Transduction:DNA carried from donor to recipient by bacteriophage (virus)
Transformation (Horizontal Gene Transfer)
- Griffith's role?
Gain DNA "naked" dna from environment; DNA fragment/plasmid is gained
--> Recipient cell is "competent" (due to alternation in cell to make it permeable to large dna molecules) when it is in a physiological state to uptake the donor DNA.
--> Frederick Griffith 1928: Streptococcus Pneumoniae; mixed dead encapsulated bacteria (non-virulent) with live non-encapsulated bacteria and injected into mice==>died. In blood: living encapsulated bacteia!! Found out that genes of dead bacteria entered the live cells; changing them genetically to become virulent.
--> Avery and colleagues: discovered DNA is the hereditary material in 1944 (rather than previously thought protein)
Conjugation (Horizontal Gene Transfer):
-what kind of dna?
-compared to transformation?
-F Factor & E.coli
-Rolling Circle replication
transferred from donor to recipient through pillus (straight hair-like structure)
-->mediated by one kind of plasmid (a circular piece of dna that replicates independently from cell's chromosome); get transmitted during conjugation.
-->unlike Transformation: Requires direct cell-to-cell contact; AND the donor cells must carry the plasmid while the recipient cell shouldn't (opposite mating type)
-->E.Coli & F Factor : conjugative plasmid that carries genes for sex pili and for the transfer of the plasmid to another cell.
--> Rolling circle replication: describes a process of unidirectional nucleic acid replication that can rapidly synthesize multiple copies of circular molecules of DNA or RNA, such as plasmids, the genomes of bacteriophages, and the circular RNA genome of viroids
Transduction (Horizontal Gene Transfer)
- DNA carried from donor to recipient by bacteriophage (virus)
- --> generalized or specific transduction
- --> accidental; transducing particle lacks viral genetic material
-->bacterial DNA transferred from a donor cell to a recipient cell inside a virus that infect bacteria called a bacteriophage (generalized)
The process of transferring a piece of cell DNA adjacent to a prophage to another cell.
Plasmids (pg 234)
--> F Plasmid
--> R Plasmid & two groups of genes?
self-replicating, gene-containing circular pieces of dina; found mainly in bacteria and sme eukaryotic microbes: saccharomyces cerevisiae.
--> F Plasmids/ F Factor:
conjugative plasmid that carries genes for sex pili and for the transfer of the plasmid to another cell.
- -->R Plasmids (resistance factors): medically significant' resistant to a different number of antibiotics; R factors carry genes that confer upon their host cell resistance to antibiotics, heavy mentals or cellular toxins.
- -Have two groups of genes:
- (1) Resistance transfer factor-RTF: includes genes for plasmid replication and conjugation.
- (2) R-determinant: has resisstance genes that codes for enzyme production which inactivate certain drugs or toxin substances.
small dna segments that can move from one region of a dna molecule to another
--> example of chem and what things?
--> Degerming, antiseptics and sanitization
--> "-Static" agents & "-cidal" agents
Control directed at destroying harmful microbes; involves destruction of vegetative (non-endospore forming) pathogens destroy most of the vegetative cells and pathogens, but endospores and cysts may survive.
Ex of Disinfectant chemical: bleach (anything non-living)
On things: Kitchen counter, restaurant dishes,diaper changing towel
--> degerming: mechanical removal of most microbes (rather than killing)
--> antiseptics: chemical directed at living tissues.
--> sanitization: intended to LOWER microbe counts to safe public health levels to minimize chances of disease transmission from one person to another (ex: restaurant dishes)
*note*: "-Static" agents: inhibit microbe growth and "-cidal" agents kill microbes.
Halogens (chemical control of microbes)
--> bleach (chem name) and Iodine?
--> Iodine & chlorine
compounds very effective on a variety of microbes, many endospores; alters cell membrane, inhibits protein function and cellular components
a) Sodium hypochlorite
(aka BLEACH): disinfects surfaces, water, corrodes metal & affects clothing
- b) Iodine compounds: can stain; disinfectant for water and surfaces
- -can be antiseptic when mixed with detergent for hands, and mixed with alcohol: for wound treatment
Phenolics (chemical control of microbes)
--> O-Phenyl Phenol: found in two places?
--> Related to phenol; effect against a variety of microbes
a)O-Phenyl Phenol: now found in Amphyl (hospital disfectant) and Triclosan (antibacterial soap=antiseptic)
Quaternary Ammonia Compound (chemical control of microbes)
--> what microbe grows IN this chem?
--> cleansing ability due to positively charged part of molecule (cation); modification of the NH4+
--> ex: 409 Cleaner
a. Benzalkonium Chloride: antiseptic (handwipes and woundare)
**NOTE: Pseudomonas aeruginosa can grow in Quat Ammonia Compunds -.-
Different modes of action of antimicrobial drugs:
--> 6 ways??
• Inhibit DNA synthesis
• Inhibit RNA synthesis /transcription
• Inhibit protein synthesis/ translation (drugs that act at the ribosome)
• Inhibit cell wall synthesis ( penicillin, cephalosporins, vancomycin)
• Inhibit enzyme--> inhibit metabolite synthesis by targeting enzymes (sulfanilamide, trimethoprim)
• Damage cell membrane (polymyxin B)
Two groups of Synthetic antibacterial drugs:
Sulfonamides (synthetic antibacterial drug group)
--> discovered how?
--> bacteria results?
--> How is it bacteriostatic?
--> “sulfa-” drugs:
--> synergy example and use?
- • Synthetic
- • Discovered in 1927 by scientists in labs
- • Bacteriostatic: bacteria won't grow, though alive, rely on host immune system to get rid of it.
- • Competitive inhibitors (enzymes) of folic acid synthesis
- • “sulfa-” drugs: Sulfonamides inhibit binding of PABA (substrate); affect folic acid synthesis
- -Synergy (greater effect by combination of drugs) example: Sulfamethoxazole and trimethoprim (not sulfa drug, but acts on same pathway) --> used for bladder infection (cystitis)
Fluoroquinolones (synthetic antibacterial drug group)
--> example and what it treats?
- • Synthetic; Broad spectrum
- • Inhibits DNA replication by inhibiting enzyme
- • Example: ciprofloxacin “Cipro” can treat UTI, prevent anthrax
ANTIBIOTICS: ANTIBACTERIAL DRUGS GROUPS/CLASSES
- 1. Beta lactam antibiotics:
- Penicillins, Cephalosporins, Carbapenems
- 2. Chloramphenicol-only one drug
- 3. Aminoglycosides
- 4. Tetracyclines
BETA LACTAM ANTIBIOTICS
--> what does it inhibit?
--> three subgroups:
--> discovery? Works against? Treats? Beta lactamase enzyme?
--> example and what it treats?
- Inhibit peptidoglycan crosslinking in tetrapeptides *NAM & NAG*
- --> bacteriocidal: kills the bacterium;
- -->Includes the subgroups:
- A) penicillins:
- Example: penicillin (the original)- Discovered by Alexander Fleming 1928 (an accident; mixing fungi, zone of inhibition around the growing mold)
- • Produced by Penicillium notatum (now P. chrysogenum)
- • Worked against Staphylococcus aureus
- • First antibiotic; Narrow spectrum
- • Treat strep throat (Streptococcus pyogenes)
- -Organisms make Penicillinase: A type of beta lactamase: an enzyme that works against penicillin to become resistant to it. (another broader term: beta lactamase)
-outdated and no longer works
C)carbapenems ex: imipenem
used to treat some Gram Negative bacterial infections
CHLORAMPHENICOL (ANTIBACTERIAL DRUGS GROUPS/CLASSES):
AMINOGLYCOSIDES (ANTIBACTERIAL DRUGS GROUPS/CLASSES):
--> example, treats what microbe?
--> broad spectrum:
-->Ex: Gentamicin (treat Pseudomonas aeruginosa infection)
-all broad spectrum: streptomycin, gentamicin and others...
TETRACYCLINE (ANTIBACTERIAL DRUGS GROUPS/CLASSES):
(tetracycline, doxycycline) broad spectrum
**Additional antibacterial drugs:
• Polymyxin B
• Polymyxin B- affects plasma membrane; in neosporin
• Erythromycin- inhibits protein synthesis; alternative to penicillin; Narrow spectrum; classified as macrolide
• Vancomycin-inhibits cell wall synthesis; used to treat MRSAinfections
Antifungal drugs that target ergosterol
1. Polyene: ex
2. Azole: 2 ex's
3. Allylamine: ex
-sterol molecule in cell membrane; damages plasmid membrane (mode of action)
- 1.Polyene group
- - ex: amphotericin B: Treat systemic infections; Older drug like... two systemic infections: Valley Fever and Histoplasmosis.
3. Allylamine group
- 2. Azole group
- - clotrimazole:
- - treat some cutaneous infections (athlete's foot, jock itch) & yeast infections
- -fluconazole: treat systemic infections. better than ampotericin b/c less side effects
- ex: terbinafine:
treat nail infection
-Quinine, Chloroquine, mefloquine
- • Quinine, chloroquine, mefloquine (all used to treat malaria; last two to prevent malaria when going to Africa)
- • Artemisinin: therapy combination to treat malaria
- • Metronidazole- treat giardiasis and trichomoniasis
Broth dilution test
--> MIC and MBC?
to measure MIC and MBC (minimal bacteriocidal concentration) of antibiotic.; Take bacteria with serial dilutions of drugs to know concentration of that drug
-broth: inoculated with bacteria and the wells that don't show growth can be cultured in broth or on agar plates and growth means the drug was not bacteriocidal.
Antibiotic resistance genes & Mechanisms
-->Acquiring antibiotic resistance genes
-->Antibiotic resistance mechanisms; what do reistant organisms actually do:
-From mutations or pre-existing genes
- -->Acquiring antibiotic resistance genes:
- • Natural selection - increases frequency b/c the well adapted cells are surviving & reproducing vs the ones that are not well-adapted
- • Conjugation (DNA transferred from donor to recipient through pillus (straight hair-like structure)
- • Transformation (in a lab); only certain bacteria can do this.
- -->Antibiotic resistance mechanisms; what do reistant organisms actually do:
- 1. Drug inactivation (penicillinase) to become resistant; cuts ring
- 2. Drug efflux: drug pumped out of cell
- 3. Alteration of drug target site shape (e.g. ribosome); so bacteria still works, but the drug can no longer bind.
Problems with antibiotic resistant bacteria: MRSA
--> aquired how? where did it start? carried where?
--> how is it treated?!
--> staph aureus: gram wut?
--> how to prevent?
- -->Methicillin resistant Staphylococcus aureus
- • Community acquired MRSA: tends to be skin infections that can spread
- • Healthcare associated MRSA in clinics, hospitals e.g. at surgical site infection -started in hospital settings;
- • Treated with vancomycin and maybe surgery or amputation to get rid of infection; used to be treated with penicillin group related drugs (oxacillin, methicillin,etc) but became resistant so must be treated with a non-penicillin drug
- -->Staphylococcus aureus: gram +
- -->Prevent transmission of MRSA skin infections:• Good hygiene
- • Don’t share towels, sports equipment, clothes
- • Get a “spider bite” checked
- • Cover an infected area
- **Note: healthy carriers can have MRSA in their noses; a third of people have S. aureus
VISA & VRSA
--> how did it originate?
- vancomycin intermediate Staph.aureus & VRSA
- vancomycin resistant Staphylococcus aureus;
So far, other drugs still work…What drugs do NOT work?
- **KNOW: MRSA gained additional resistance to vancomycin, looking for additional drugs OTHER than vancomysin
- • Problems in hospitals
pencillin groups and vancomycin..
VRE-- what microbe? found where? causes?
Vancomycin resistant enterococcus
- • Enterococcus faecalis: Gram positive coccus
- • Intestines or female genital tract (normal flora becomes resistant to vancomycin in hospitals which then spreads to other patients)
• Causes wound infections, UTI, blood infections in hospitals
Gram Positive ROD; forms endospores and produces exotoxin (**can survive most antibiotics**)
- Overgrowth due to broad spectrum antibiotic use
- -can cause life-threatening (See nosocomial infection handout)
- --causes endospores;
-gram? shows up where?
-resistant to? and what enzyme makes it resistant?
Oct. 2010 new drug resistant bacteria:
• Gram negative bacteria, Opportunistic; show up in clinical settings
• New strain is resistant to carbapenems (ibapenem used against gram neg; so now not many other drugs to treat)
• KPC or CRKP: Carbopenem resistant Klesiella pneumoniae
• Has carbapenemase-makes it resistant to carbapenems
Is MRSA resistant to oxacillin?
Methicillin-resistant Staphylococcus aureus (MRSA) have developed resistance to a wide range of penicillins, cephalosporins and other penicillinase-resistant antibiotics such as oxacillin.
Name of broad spectrum antibacterial drug that is used to treat chlamydia and rickettsia infections.
Sources of microbial infection:
-> Normal flora, reservoir, and carrier
- 1. Normal flora (candida albicans)
- 2. Reservoir: source of disease; causing microbes in nature (animals, soil, people, and water)
- 3. carrier: animal or person
Five Stages of a disease:
1. Incubation Period: no signs/symptoms; interval b/w initial infection and first appearance of symptoms; time of incubation depends on the specific microbe, it's virulence (degreee of pathogenicity) and the resistance of he host
2. Prodromal period: mild signs/symptom; short period
3. Period of Illness: Most severe signs/symptoms while generally the person overcomes the illness
4. Period of decline: signs and symptoms subside; from 24 hours to a few days
5. Period of convalescence: Body returns to prediseased state; still able to spread disease.
Disease always present in a population
Greater than expected number of cases of disease in a population in a short time.
bacterial infection spread through the blood.
--> gram? found where?
--> oxygen requirements?
Gram Negative ROD; usually part of normal flora-in intestinal coliform.
-In community settings, can cause: UTI, nosocomial pneumonia, and wound infections
--> gram? found where?
--> oxygen requirements?
Gram Positive COCCUS; can be carried in healthy people's noses & end up on skin
-->Community setting can cause: Toxic Shock Syndrome, food intoxication, skin infections (boils, impedigo) can spread to other organs.
--> MRSA: community acquired Methicillin resistant Staph. aureus; BIG problem in hospitals
--> can cause: nosocomial pneumonia
--> oxygen requirements?
--> Causes ? in what kind of patients?
Gram Negative Rod; strict aerobe; Resistant to many antibiotics & resistants
**NOTE: GENTAMICIN & Quat Ammonia...
--> Causes wound infections (especially in burn victims who are missing a skin barrier)
--> causes pneumonia (esp. in cystic fibrosis patients-forms a biofilm in CF air passages) and immunocompromised individuals.
--> Can cause nosocomial UTI & wound infections
--> oxygen requirements?
--> virulence factors:
--> Causes and life-threatening how?
--> Hospital issues?
Gram Positive ROD; forms endospores and produces exotoxin (**can survive most antibiotics**)
--> grows well when normal intestinal flora is eliminated (such as antibiotics)
--> can be a life threatening diarrheal disease
--> Big problem in hospitals, nursing homes and a serious risk for the elderly and NOW recent cases have occurred in healthy individuals D:
--> ICU issues?
--> treat with with what drug group??
- Gram Negative Rod
- -->Can contaminate respiratory equipment in ICU: respirators with saline; opening up and closing tube breaks the sterility.
- -->Big problem for injured soldiers overseas (Iraq)
- --> treated with carbapenem; can become resistant.
Three Factors that contribute to Nosocomial infections? How?
1. Microbes in hospital environment: will always be there (normal flora)
2. Compromised Host: the sick patient (can't change this either)
3. Chain of Transmission: what we CAN change; "infection control" to stop microbe from traveling from patient to patient.
Infection control methods used to prevent spread of nosocomial infections:
**BEST/MOST Important way to prevent?
Gowns, sterilization of equipment used, hand-washing, minimize invasive procedures, use aseptic techniques and hand sanitizer
**MOST IMPORTANT WAY: BREAK CHAIN OF TRANSMISSION**
The 10 Virulence Factors (list)
More likely to cause severe disease; degree of pathogenicity of a microbe.
- 1. Dose
- 2. Adhesion/attachment to host cells
- 3. Invasion of host cells
- 4. Biofilms
- 5. Capsules
- 6. Enzymes
- 7. Antigenic variation
- 8. Cell to Cell Transmission
- 9. Exotoxins
- 10. Endotoxins
Dose (virulence Factor)
--> ex: poultry juice
- ex: Campylobacter jejuni
- --> only a small number of microbes needed to cause disease (in poultry-drop of juice)
Adhesion/Attachment to Host Cell (virulence Factor)
--> example of microbe:
Microbes sticking to host cells; all viruses and some bacteria
ex: E. coli : from petting zoos, raw spinach, lettuce, and hamburgers
Invasion of Host Cells (virulence Factor)
- -microbe enters/invades host cells
- -all viruses but some bacteria
- ex: Salmonella enterica serotype Typhimurium: attach to host cell, force it to swallow a bacterial cell and eventually spreads to other organs
- --seen in poultry, eggs, inside tomatoes and reptiles
Biofilms example (Virulence Factor)
Steptococcus mutans: forms cavities
any group of microorganisms in which cells stick to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS). Biofilm EPS, which is also referred to as slime (although not everything described as slime is a biofilm), is a polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides.
Capsule example (Virulence Factor)
--The capsule is considered a virulence factor because it enhances the ability of bacteria to cause disease (e.g. prevents phagocytosis). The capsule can protect cells from engulfment by eukaryotic cells, such as macrophages. A capsule-specific antibody may be required for phagocytosis to occur. Capsules also contain water which protects bacteria against desiccation.
Listeria monocytogenes causes Listeriosis
**VIRULENCE FACTOR: Cell to Cell Transmission**
in macrophages, phagocytosed==> don'[t kill but instead float through cytoplasm; travels from 1 macrophage to another
-Gram positive rod; found in soil and animal intestines; soft french cheeses, deli meats and hot dogs
-serious consequences: meningitis, Pregnancy: miscarriage, fetal brain damage, and fetal meningitis
Exotoxins vs. Endotoxins (Virulence Factor)
are secreted proteins
into the bloodstream, mostly gram positive; HIGHLY TOXIC
; gets into bloodstream and causes effect at specific sites in the body.
ex: Clostridium botulinum, Clostridium tetani, and Staph aureus
- ENDOTOXINS: Lipid A portion of LPS (in cell wall of gram negative cells); weakly toxic; causes endotoxic shock--if microbes die and exotoxins released so person goes into shock D:
- --> ex: any lysed gram negative organism
-caused by? gram? found?
-how is it destroyed?
-Infant botullism vs adult?
Caused by: Clostridium botulinum
(gram positive ROD;found in soil)
- -exotoxin causes flaccid paralysis (flabby muscles); can be destroyed by heat (can of beans, cooking)
- -Improperly canned foods (anaerobic conditions)
- -Infant botulism: caused by ingesting endospores from honey and soil;
- adults get botulism by ingestion of exotoxins --> blurry vision, difficulty swallowing and breathing
- -Treatment: antitoxin and supportive care.
-caused by? oxygen req, gram? found where?
-signs and symptoms?
Clostridium tentani: obligately anaerobic, endospore-forming, gram positive rod, common in soil contaminated with animial fecies.
-exotoxin prevents muscle relaxation; constant contracted muscles
-endospores enter wounds
-->symptoms: lock jaw, muscle stiffness/spasms
--> Treatments: antibiotic, antitoxin, and muscle relaxant. "Tetanus Toxoid Vaccine-TDaP"
--> virulence factors? how is it produced?
--> what growth conditions?
**NOTE: EXOTOXIN IS PRODUCED AND IS NOT KILLED BY HEAT**
- -exotoxin causes signs/symptoms of foodborne illness; we contaminate the food by cooking food high in protein...; good growth conditions: on a picnic table
- --> food intoxication
--> Microbes for fungus, virus?
--> signs/ symptoms: <2 years and >2 yrs?
--> Three major bacterial causes of meningitis:
- Inflammation of the meninges (the membranes that surround the brain), occurs when a microbe enters the CSF from the blood.
- **note: acute disease, communicable, not local infection
- -->Microbes: Fungus (cryptococcus neoformans), viruses (west nile) and bacteria..
- --> Signs/Symptoms: Under 2 yrs: inactivity, irritability, vomiting, maybe skin rash. Over 2 years: fever, stiff neck, headache, possible vomitting and nausea
detection of microbe from CSF or serum.
- Three major bacterial causes of meningitis:
- 1. Streptococcus pneumoniae:
- 2. Haemophilus influenzae type b:
- 3. Neisseria meningitidis:
Three major bacterial causes of meningitis:
1. Streptococcus pneumoniae:
2. Haemophilus influenzae type b:
3. Neisseria meningitidis:
**Characteristics of Bacterial meningitis:
1. Streptococcus pneumoniae:
Gram positive diplococcus; also causes pneumonia.
- --> vaccines:
- -Younger than 2 yrs:polysaccharide vaccine(PPSV)
- -pneumococcal conjugated vaccine (PCV12): children <5 yrs
- 2. Haemophilus influenzae type b: aerobic, gram negative rod.
- --> vaccines: conjugated vaccine (<5 yrs); polysaccharide + protein
- 3. Neisseria meningitidis: gram negative diplococcus (aka meningococcus)
- --> vaccines: effective against 4 out of 5 strains, can't be used in children <2 yrs; "MCV4" (conjugated), "MPSV4" (polysaccharide vaccine)
- --> other signs: low blow pressure, rash ("meningococcemia": when bacteria enter blood stream)
- **Characteristics of Bacterial meningitis: Has a capsule, transmitted by respiratory secretions, found in noses/throats of seemingly healthy carriers, college dorm students/young children/military are mostly at risk, and it's a life threatening disease.
- --> Treatment: usually antibiotics
--> Microbe info: gram, virulence factors, oxygen?
--> affected animals?
--> four types of human anthrax:
--> diagnosis and treatments?
- Microbe: Bacillus anthracis
- --> endospore forming, gram postive rod, found in soil, non-motile & aerobic, has capsule and exotoxins (virulence factors); obligate parasite.
- --> affected animals: sheep, cattle, goats.
- --> Signs/symptoms: "sudden death"
- --> Prevent: annual vaccination boosters.
- **ANTHRAX IN HUMANS:
- 1. Cutaneous skin: skin contact w/ endospores; 95% of anthrax cases in people, can get into bloodstream; treatable w/ antibiotics
- 2. Gastrointestinal: by ingesting endospores in meat; nausea, vomiting, fever, bloody diahhrea, collapse/death; 80% mortality for untreated cases.
- 3. Injectional: by injected drugs; fatal
- 4. Pulmonary: inhaling endospores; flu-like symptoms; sudden shock/death (MOST DANGEROUS FORM) and bacteria can enter bloodstream
gram stain, PCR: detect bacteria in blood/skin/resp secretions
--> Treatments: Doxycycline
(tetra) or Ciprofloxacin
(fluoroquinolone); must be started in beginning stages of disease.
attenuated (weakened) B. anthracis (animals), AVA-Anthrax vaccine absorbed (humans that work w/ animals since they can get spores from them.)