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302 Cards in this Set
- Front
- Back
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what is the gram stain reaction of campylobacter and helicobacter
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gram negative
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when were campylobacter and helicobacter recognized as being responsible for major human infectious disease
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1980s
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Describe 4 ways in which campylobacter and helicobacter are related
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1. spiral shape
2. low guanosine and cytosine content 3. unable to ferment or oxidize carbohydrates 4. microaerophilic growth |
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What two species of campylobacter are responsible for gastroenteritis? Where are they most prevalent?
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C. jejuni-most important common cause of bacterial gastroenteritis in the US
C. coli-frquent cause in Asia and Africa |
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what diseases arise from infections wit hC. fetus fetus
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-systemic infections like bacteremia, meningitis, septic abortions
-causes septic abortion in sheep and cattle |
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Describe campylobacter
motility |
highly motile by way of polar flagella
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describe campylobacter's unique morphology
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often two cells are attached at their ends which leads to a seagull appearance
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what is important to recognize about campylobacter's size?
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-they are relatively thin bactera and thus are diffficult to visualize by gram stain
-they can pass through .45um filters but not 0.2um |
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Describe campylobacter's growth and nutritional requirements
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-difficult to grow/ fastidious
-require microaerophilic conditions (reduce oxygen tension) but are NOT anaerobes -better growth at 42C than 37C |
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Describe the role of C. jejuni flagella in its pathogenesis
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the flagella plays a role in pathogenesis, non flagellated mutatns are much less virulent in animal models. The flagella undergo both phase and antigenic variation
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Describe the intestinal damage caused by C. jejuni
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-destruction of the mucosal surfaces of the lower small intestine and colon
-diarrheal stools due to malabsorption of fluids -stools contain leukocytes and blood in a dysentery phase -organisms invade to the sub-epithelial layers (lamina propria) of the intestine -rare bacteremia |
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What roles does the C. jejuni capsule play
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-highly vraiable
-virulence -epithelial cell adhereance -cell invasion |
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What is LOS (C. jejuni)
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LOS=lipooligosaccharide
highly variable role in serum resistance, epithelial cell adherance, and cell invasion -molecular mimicry of neuronal gangliosides linked to Guillian Barre syndrome |
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What roles does the C. jejuni flagella play in its virulence
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-colonization
-virulence -epithelial cell invasion -secretion apparatus for invasion antigens |
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Describe the modification of C. jejuni flagellin
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modified by O linked glycosylation which is requried for flagellar assembly
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What is the purpose of the C. jejuni N -linked-glycosylation systen
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-modifies some periplasmic and outer membrane proteins
-N linked glycan is important for colonization, epithelial cell adherence and invasion but the exact role is unclear |
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List the 4 unique structures of the C. jeuni cell surface
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-capsule
-LOS -flagellum -N linked glycan Remember "Campylobacter Loves Funny Nuns" |
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T/F campylobacter is normal flora of many animals
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true
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What are the significant reservoirs of camplylobacter that can transmit the bacteria to humans when there is fecal contamination of food or water
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-dogs, particularly puppies
-poultry products -natural food products such as unpasteurized milk |
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What is the infectious dose of camplylobacter
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Low for C. jejuni and C. coli ~1000 organisms
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Describe Gullian Barre syndrome and the role that camplyobacter plays
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-immune mediated sequelae of bacterial and viral infecitions/ vaccines
-often assocaited with campylobacter infections -the myelin sheath of multiple peripheral nerves is damaged resulting in paralysis -LOS may be similar to neural gangliosides and the immune system cross reacts -recovery can take up to 6 months, affects 1-2/ 100,000, most common cause of rapidly acquired paralysis in the US today |
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What disease does Helicobacter pylori cause
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chronic gastric inflammation (gastritis), discovrered only 20 years ago, originally thought to be commensal
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What is the reservoir of H. pylori
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-NOT animals
-infections appear to cluster among family members, suggesting person to person spread |
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Who figured out that H. pylori could cause gastritis, peptic ulcers, and gastric cancer? How did they do it?
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Barry Marshal and Robin Warren
swallowed a culture of H. pylori and did follow up studies |
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Describe the gram stain of H. pylori
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gram negative bie electron microscopy but is very thi and difficult to visualize by light micro
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Describe H. pylori growth requirements
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-requires enriched meida
-microaerophilic -grows best at 37C not 42C (contrast to campylobacter) -slow growth, 4-7 days for colonies |
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Describe H. pylori motility and what is unique about it
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highly motile due to polar flagella which are unusual in that they are sheathed within a membrane covering
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What staining method can be used to detect H. pylori in biospsy material of diseased induviduals
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Giemsa
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Urease is a key virulence determinate of H. pylori. Why?
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-breakdown of urea to ammonia leads to an alkaline microenvironment that protects the organism from stomach acid
-ammonia and CO2 produced are toxic to host cells aiding in local tissue destruction and persistent infection -most active ureas known among pathogenic bacteria |
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Describe the CagA pathogenicity island that leads to H. pylori strains with increased pathogenicity
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-Encodes a type IV secretion system (TFSS)
-the genes of the type IV secretion systems are related to conjugal transfer genes -CagA is an effector molecule that is translocated into the host cell and then phosphorylated on tyrosine kinase residues by members of teh Src-kinase family. This induces signaling pathways that lead to dramatic mophological changes of the host cell |
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What changes result when cagA is phosphorylated on tyrosine kinase residues by members of the Src-Kinase family
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-actin polymerization
- hummingbird phenotype -growth factor like stimuli - IL-8 transcription |
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What do type IV secretion systems secrete and what processes are they involved in
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protein or DNA and protein
involved in conjugation, DNA uptake and release, effector translocators |
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describe the VacA virulence factor of H. pylori
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VacA= vacuolating cytotoxin
cuases production of large cacuoles throught host cell cytoplasm, leads to cell damage |
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list the virulence factors of H. pylori
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1. Cag pathogenicity island (CagA, type 4 SS)
2. VacA 3. LPS 4. Flagella 5. Nitrogen metabolism (urease and arginase) 6. Adherance factors Remember "Currently Vaginal Love Fun is Not Allowed" |
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What secreted proteins make up the virulence factors of H. pylori? what do they cause
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VacA and paralogs
CagA cause gastric epithelial cell damage, IL-8 induction, Tyr phosphorylation |
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what are the two nitrogen metabolising enzymes of H pylori
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urease, arginase
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Do Helicobacter and Campylobacter infections show seasonality? What ages groups are most affected
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Helicobacter infections are not seasonal but C. jejuni infections are most common during the summer (May-Sept)
helicobacter infections are most common in older induviduals especially those about 50 Campylobacter infections are more common in young adults ages 20-40 and very young children less than 5 years old |
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what is the gram stain and oxygen relationship of Pseudomonas aeruginosa
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gram negative rod, aerobe (but do oxidative degradation of sugars in the absence of oxygen, not fermentation)
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what type of pathogen is pseudomonas aeruginosa
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oppotunistic
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Where is P. aeruginosa found
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throughout the environment
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What patients are most at risk for infection with P. aeruginosa
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burn, leukemia, cycstic fibrosis
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Describe P. aeruginosa motility
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motile by way of polar flagella
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Describe P aeruginosa metabolism and its relationship to it's oxygen relationship
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-non fermentative
-gets energy from odixative degradation of sugars, they are aerobes NOT facultative anaerobes it is capable of growing in the abscence of oxygen but its energy is not gained by fermentation -readily grows on normal media |
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Describe Pseudomonas in terms of its metabolic diversity
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capable of using a wide range of different organic compounds as carbon sources, can grow at a wide range of temperatures 4-42C
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Describe Pseudomonas pigmentation
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-diffusible pigments
-P. aeruginosa on clear agar produces green halos to to the release of blue pyocyanin and yellow fluorescein pigments -the pgiments fluoresce with a long wave length UV lamp -burn wounds infected with P. aeruginosa can glow in the dark |
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Describe the odor of P. aeruginosa
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fruity grape like small, can be detected on patient's breath
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what molecule serves as a quorum signal for P. aeruginosa
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Acyl-homoserine lactone
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Describe the strain of P. aeruginosa that infects CF patients
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-mucoid pheontype
-production of extracellular polysaccharide material made of alginate -difficult to treat with antibiotics |
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List the 6 virulence factors of P. aeruginosa
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1. Adhesive pilli
2. Cap on Flagella 3.Toxins 4. Elastases (LasA, LasB) 5. Cytolysins 6. Pigments (pyocyanin) Remember"All Creey fat Truckers Enjoy Corny Porn" |
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How does the P. aeruginosa flagellum function as a virulence mechanism
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the tip of the flagellum has a cap protein that binds mucin
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What is the function of elastases LasA and LasB, virulence factors of P. aeruginosa
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proteolytically degrade different tissue proteins leading to frank tissue destruction
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how do P. aeruginosa pigments serve as virulence factors
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pyocyanin pigment catalyzes superoxide and peroxide production leading to oxidative damage to tissues
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List the 5 extracellular product categories of P. aeruginosa
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1. proteases (LasB, LasA, alkaline protease)
2. hemolysins (phospholipase C, rhamnolipid) 3. exotoxin A 4. exoenzyme S 5. pyocyanin pigment |
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What toxin does P. aeruginosa produce
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exotoxin A
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how does exotoxin A of P. aeruginosa work?
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-identical to diphtheria toxin
-NAD is split and ADP ribose is attached to EF-2 -EF 2 is necessary for translocation of nascent proteins on eukaryotic ribosomes -modifying EF2 stops protein synthesis and kills the cell -a single molecule of exotoxin A is sufficient to kill the cell |
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What are the 11 most common clinical situtations where P. aeruginosa is encountered?
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1. cystic fibrosis pts (mucoid strain)
2. burn pts (leading to septicemia) 3.osteomyelitis following trauma 4. pts with indwelling catheters (IV or urinary) 5. eye infection (scratched cornea infected) 6. folliculitis 7. bed sores (decubitus) 8. diabetic wound/ ear infection 9. IV drug user endocarditis and septic osteomyelitis 10. neutropenic pts 11. UTI/ urosepsis/ septic shock Remember "Can Boys Ovulate? Certainly Every Fun Boy Does. It's Not Unimpossible." |
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Why is it difficult to treat P. aeruginosa infections
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1. resistant to many antibiotics
2. organism is not growing intimate association with pts cells 3. difficult to get systenmic anitibiotics at high concentrations to the site of bacterial growth |
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Describe the complications associated with the Pertussis vaccine
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rare but serious nerological problems
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what is the goal of pertussis vaccine research
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to identifiy the apporpriate subcellular element which when administered as a vaccine will cause no side effects yet adequate protective immunity.
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who cultivated pertussis for the first time
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Jules Bordet
also played a role in establishment of Pasteur institiute, descovered complement system |
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describe the gram stain of Bordetella pertussis
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small gram negtaive bacilli
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what is they oxygen relationship of B. pertussis
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aerobic
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Describe the cultivation requirements of B. pertussis
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-does not grow on normal media
-must use Bordet- Gengou media, given special instructuions -slow gorwth, colonies @ day 3 |
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What is the reservoir of B. pertussis
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strict human parasite so reservoir is other induviduals disease can spread from clinically ill children and subclinically ill adults (larger rerservior)
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Who discovered the adjuvant effect of combining the pertussis vaccine with diphtheria and tetanus toxoids and aluminum
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Pearl Kendrick
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How does B. pertussis pathogenesis differe from Haemophilus influenzae
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H. influenzae is capable fo systemic spread from the respiratory system. B. pertussis colonizes only the tracheobronchial epithelium
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Describe B. pertusis pathogenesis
Where does it colonize? Virulence? How does death occur? |
colonizes the tracheobronchial epithelium
systemic spread of exotoxins secreted from the organism at the site of infection death occurs most often from pneumonia caused by secondary invaders like S. pneumoniae |
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how is B. pertussis/ whopping cough infection initiated
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inhalation of aerosol droplets produced by sneezing, infected induviduals
high contagious |
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What are the three stages of Whooping cough disease
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1. catarrhal
2. paroxysmal 3. convalescence |
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When does the first stage of whooping cough become evident?
What are the sxs? How long does it last? Can the organism be recovered from the patient |
-first stage becomes evident 7-10 days post infection,
-Catarrhal, characterize by runny nose, sneezing, fever, malaise, anorexia -last 1-2 weeks -organism can be recovered |
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What is the second stage of whooping cough
What are the sxs? How long does it last? Can the organism be recovered from the patient |
-Paroxysmal coughing state
-multiple coughs followed by inspiratory gasp (whoop), vomiting, leukocytosis -lasts 2 to 4 weeks -organism is difficult to recover |
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What is the third stage of whooping cough
What are the sxs? How long does it last |
-third stage is convaescence stage
-sxs fade but this is when secondary infections occur (penumonia, seizures, encephalopathy) lasts 3-4 weeks or longer |
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list 4 virulence factors of B. pertusis
what do they do? |
1. Pertussis toxin (Ptx)-ADP ribosylatin toxin, modified G protein, messes up immune effector cells
2. Filamentous Hemagglutinin (FHA)-attachment and adherence 3. Adenylate Cylase toxin-low [ ] increases cAMP messup up signaling, high [ ] cytolytic toxin 4. Tracheal cytotoxin-destroys ability of tracheal epis to move cells material upwards remember "PFAT" |
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Describe the Pertussis toxin of B. pertussis
What type of toxin is it? What does it do? What is it's target What is the net effect? |
type= AB toxin
action= ADP ribosylation of host cell protein target = G protein (different than cholera toxin) net effect= block the function of different immune effector cells in the host (macrophage, neutrophils, etc) |
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What is the role of the filamentous hemagglutinin (FHA) virulence factor of B. pertussis
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cell surface attachment factor that is believed to promote adherance of the bacteria to tracheal ciliated cells
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What are the two roles of the adenylate cyclase toxin of B. pertussis
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1. internalized into a host cell and causes a toxin medaited derailment of signal transduction by enzymatically increasing the [cAMP] inside the cell
2. at high [ ] it possesses a cytolytic activity (hemolysin) |
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What is the role of the tracheal cytotoxin virulence factor of B. pertussis
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after B. pertussis attaches to the cilia tips of tracheal epithelial cells, it destroys the ability of those cells to move materials upwards, including the bacterial cells.
-the toxin consists of the basic subunit of peptidoglycan |
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Describe what happens to the peptidoglycan fragments of B. pertussis
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instead of being recycled they are secreted extracellularly
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T/F antibiotics treat whooping cough
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false
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How is whoopoing cough treated
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no antibiotics, treatment is purly supportive in terms of trying to relieve the sxs and prevent secondary pneumonia
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What components are included in the DPT vaccine
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-Diphtheria toxoid
-Pertussis- crude cell envelope fraction, adverse reactions with 1:100,000 injections -tetanus toxoid |
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during aprox what year was the DPT vaccine implemented
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late 1940s
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What are the componets fo the DPT vaccine?
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diphtheria= toxoid
Pertussis= crude cell envelope fraction tetanus= toxoid |
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What it the rate of adverse reactions with the DPT vaccine
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1:100,000
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What are the three medically important genera in the family Pasterurellaceae
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Hameophilus, Actinobacillus, Pasteurella
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What is the gram stain morphology of the family pasterurellaceae
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small gram negative bacilli or coccal-bacili
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What is the oxygen relationship and nutrtional requirements of the family pasterurellaceae
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facultative anaerobes, nutritionally fastidious
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T/F members of the family pasterurellaceae are free living in the environment
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false. They are obligate parasites of mucosal membranes
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What is unique about Haemophilus endotoxin
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It differs from enteric LPS in that it is Lipooligosaccharide (LOS) which lacks repeating O antigen carbohydrates
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Is H. influenzae incapsulated?
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Many but not all have polysaccharide capsules
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How are H. influenzae strains differentiated? Which strains cause the most serious disease?
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capsular types A-F
Type B causes the most serious systemic disease |
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What is important about non-encapsulated H. influenzae strains? What are they called
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these are the non-typeable strains. They are associated with otitis and sinusitis
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Which H. influenzae strains are associated with otitis and sinusitis
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the non typeable strains/ non-encapsulated
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Describe in detail the media needed to culture H. influenzae. What specific factors are required
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- requires enrich media with blood components
-hematin (X factor) -NAD (V factor) -commonly grown on chocolate agar |
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Describe how chocolate agar is made and why it is used to grow H. influenzae
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Chocolate agar is made by addding blood that has been heated to the point of cell lysis to a rich media. Lysis of the cells releases hematin and NAD which are required for H. influenzae growth.
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Describe the unquie colony morphology that occurs when throat cultures with H. influenzae are observed
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H. influenzae is seen as a haze of small colonies satelliting around the colony of an organism such as Staph which secretes or causes the release of growth factors from erythrocytes .
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What is the reservoir of H. inluenzae
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H. influenzae is an obligate mucosal parasite. Although it was originally thought that infection was from endogenous strains, molecular techniques have demonstrated that outbreaks of disease are due to the importation and exposure to new strains
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Describe the disease associated with Haemophilus
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--meningitis, especially children under 2
-brain damage in 1/3 of induviduals -prior to vaccine development, one of most common forms of mental retardation |
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Which strains of H. influenzae are associated with invasive, systemic disease
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encapsulated, especially type B which is also called Hibs
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What systemic diseases are associated with Hibs?
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meningitits, bacteremia, cellulitis, epiglotttis
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Aproximately what year did H. influenzae infection significantly decrease after introduction of the vaccine?
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1988-1992
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what population is most vulnerable to Hib infection
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occurs mostly in children under the age of five, with those between four and 18 months of age especially vulnerable.
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About how many deaths a year is Hib responsible for?
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The W.H.O. estimates that Haemophilus influenzae type b, or Hib, is responsible for three million serious illnesses and an estimated 386 000 deaths per year, chiefly through meningitis and pneumonia.
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Describe acute epiglottitis
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-caused by Haemophilus influenzae type b (Hib)
-sudden onset of inflammation and swelling of the top of the throat that leads to extreme breathing difficulties -can lead to suffocation and obviously it represents a medical emergency where a tracheotomy is required to keep the airway open for the patient |
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what strain of Haemophilus influenzae causes conjuctivitis? What else can cause this?
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Conjunctivitis can be caused by H. influenzae biotype aegyptius.
-Adenoviruses are another cause this type of disease |
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What is Chancroid? What casuses it?
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-Chancroid is caused by Haemophilus ducreyi. (Remember DUcreyi is DUrty.)
-sexually transmitted infection (STI) that compared to Chlamydia or Herpes is -relatively infrequent in the United States, but more common in Africa -Nearly a week after exposure, a small lesion appears that develops into a painful ulcer and there can be subsequent inguinal lymphadenopathy due to spread of the bacteria. -Individuals with genital lesions are thought to be at greater risk of contacting HIV |
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Describe the role of the capsule in Haemophilus pathogenesis
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-acts as an anti-phagocytic factor.
-needed for a process that leads to passage or the organisms through epithelial layers (needed for invasion to the meninges and the subsequent meningitis disease |
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Describe the role of IgA proetease in Haemophilus pathogenesis
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-cellular protease which has the unique ability to degrade IgA
-may facilitate colonization of a mucosal surface by destroying antibodies that would block attachment. |
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Describe the role of pili in Haemophilus pathogenesis. Which isolates does this appy to?
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-nontypeable isolates are piliated and this is thought to enhance their ability to colonize the host.
-surface proteins (HMWs, this strands for high molecular weight proteins) that appear to be homologous to the adhesions used by Bordetella pertussis. |
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T/F Haemophilus produces exotoxins
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false, There are no known exotoxins produced by H. influenzae
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Even though it does not make exotoxins, Haemophilus does produce important exoproteins. Describe one.
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One exoprotein appears to bind a host iron-binding protein called hemepexin
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Describe the role of LOS in Haemophilus pathogenesis? what is unique about it?
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The LOS form of endotoxin of H. influenzae is associated with toxicity to respiratory cilia which would facilitate colonization of the respiratory tract. LOS of this organism can undergo phase and antigenic shift.
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List several symptoms associated with Haemophilus endotoxin mediated toxicity
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fever, leukopenia followed by leukocytosis, activation of complement, thrombocytopenia, disseminated intravascular coagulation, decrease peripheral circualation and perfusion to major organs, shock ,death
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How can infection with H. influenzae be treated?
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H. influenzae is sensitive to many different antibiotics and if properly diagnosed, patients respond well to antibiotic treatment with the notable exception that approximately 5% of young children with H. influenzae meningitis will die despite appropriate treatment
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Describe the gram stain and relative size of Clostridium perfringens
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gram positive bacillus, much larger than gram negative enteric bacilli
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what is the oxygen relationship of C. perfringens
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obligate anaerobe
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T/F C. perfringens produces an endospore
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true
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T/F Clostridium is encapsulaed
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true
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What is the motility of C. perfringens
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non motile
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Describe C. perfringens growth requreiements
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-grows very rapidly on media such as blood agar
-doubling time can be less than ten minutes |
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When growing on carbohydrates, C. perfringens produces a great deal of gas. What relevance does this have to in vivo infection
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gangrene caused by this organism is accompanied by gas production in infected tissues (crepitation)
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Where can C. perfringens be found
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can be found in the intestinal tract and endospores can be found in water and soil.
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List the virulence factors of Heamophilus
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Capsule
IgA protease Pili Endotoxin-LOS Remember "Haemophilus Can Induce Penis Envy" |
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Describe Clostridium Perfringens:
gram stain oxygen relationship motility |
gram positive bacillus
obligate anaerobe non motile |
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T/F Clostridium speicies produce spores
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true
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Does Clostridium perfringens have a capsule?
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Yes
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Describe Clostridium perfringens lab growth
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-grows rapidly on common media like BAP
-can double in 10 min -produces lots of gas when growing on CHO |
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What are the sources of Clostridium Perfringens
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human intestinal tract, endospores in soil and water
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Describe gas gangrene
what causes it? How is it treated? |
-occurs when endospores of Clostridium perfringens infect traumatic muscle injuries
-causes severe muscle destruction (myonecrosis), life threatening -Tx with hyperbaric O2 |
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Describe the role of Clostridium perfringens in endometritis
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-non-living material retained in the uterus becomes contaminated with C. perfringens
-very serious, requires immediate hysterectomy -less frequent due to legalization of abortion |
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Describe Clostridium perfringes food poisoning
-Infectious dose? -Sxs? -source? -Prevalance? |
-follows ingestion of very high number of organisms
-post 8-24 hrs nausea, vomiting, ab pain, diarrhea, recover in 24 hrs -associated with hearty meat dishes like stews, soups, gravy that are not stored properly -3rd most common form of food poisoning |
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What is the gram stain of Clostridium tetani. Unique structures?
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Gram positive bacillus, terminal endospores give rise to "drumstick" morphology
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T/F Clostridium Tetani is motile
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true it is highly motile and can spread across the surface of agar like Proteus does
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What is the source of Clostridium tetani?
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-Endospores are found in the soil especially those which are contaminated by feces
-can be culture from intestine of humans without apparent disease |
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What is the oxygen relationship of C. tetani
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Obligate anaerobe, the vegetative cells are very sensitive to killing upon exposure to air however the endospores can survive in air for long periods of time
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What organism causes Tetanus
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Clostridium tetani
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Describe the conditions that must be met to get tetanus from exposure to C. tetani
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Infected tissue must be in an area with low oxidation-reduction potential because C. tetani is an obligate anaerobe. This is why puncture wounds accompanied by tissue necrosis are an ideal environment
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What specifically about C. tetani causes tetanus
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Production of exotoxin called tetanospasmin an A-B type toxin. It causes a spastic paralysis.
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Compare the two paralytic toxins of Clostridium species. What species make them? What type of paralysis do they cause?
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C. tetani= tetanus toxin aka tetanospasmin, causes a spastic paralysis
C. Botulinum ( serotypes A-G)= botulinum toxin, causes a flaccid paralysis |
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Describe the evolutionary similarity of Clostridial Tet and BoNT neurotoxins
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-Amino ends have a zinc mellanoprotease acitivity which clease differenent endocytic vesicle membrane proteins found in nerve cells
-C terminals have a domain necessary for binding neuronal cell receptors |
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Describe the mechanism of the tetanus toxin aka tetanospasmin
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-disseminates into the spinal cord
-blocks postsynaptic inhibition of spinal motor reflexes |
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How long is the period between Clostridium tetani infection and tetanus disease? How much toxin is needed to cause disease and how is it fatal?
|
-disease presents within several days to weeks
-only a small amount of toxin is needed to cause disease -untreated fatality can reach 60%, death by exhaustion and respiratory failure |
|
|
Describe neonatal tetanus
-Cause? -Signs and Sxs? |
-attacks infant during first few days of life, can present as facial spasm
-tetanus spores introduces through poor hygiene during childbirth including contaminated insturments used to cut umbilical cord and application of cow dung to umbilical stem |
|
|
How is tetanus treated?
|
-toxin that has not become bound to the postsynaptic membrane can be neutralized with anti-toxin antibodies
-Tx is supportive, keep airway open -Curare-like drugs taht cause counteracting flaccid paralysis for severe cases |
|
|
How can tetanus be prevented
|
-immunization with tetanus toxoid routine for children, booster every 10 years
-active immunization of pregnant women |
|
|
Where is C. botulinum found
|
soil and in the sediments of bodies of freshwater
|
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What is the source of C. botulinum food poisoning
|
-Spores germinate in alkaline type food like seans or mushrooms that are insuffciently heated when canned
-storage in anaerobic environment leads to growth of organism and production of toxin -food does not show signs of spoilage -acidic foods such as canned fruits do not support growth |
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Where is the endospore located in C. botulinum? How does this compare to C. tetani
|
C. botulinum has sub terminal endospores, C. tetani has terminal endospores (drumstick morphology)
|
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What is the gram stain of C. botulinum
|
gram positive bacillus, subterminal endospores
|
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|
Describe the oxygen relationship and nutritional requirements of C. botulinum
|
-obligate anaerobe
-fastidious compared to other Clostridia |
|
|
How is Clostridium botulinum classified? What relationship does this have to immunization
|
Classified by BoNT type (A-G)
Immunization against one toxin does not protect against (also not that the botulinum species represents four different metabolic types) |
|
|
What types of Clostridium botulinum cuase botulism
|
A, B, E,
old ABE got boutulism |
|
|
Describe the paralysis associated with C. botulinum
|
-paralysis due to the action of botulinum toxin
-begins aprox. 1.5-4 days after ingestion of contaminated food -begins with larngeal, ocular, or respiratory muscles, then progresses to voluntary muscles to yield flacid paralysis -mortality ranges from 10-20% -note therapeutic and cosmetic uses of toxin |
|
|
What is the mechanism of the botulinum toxin
|
-toxin blocks the transmission of nerve signals at neuromuscular junction by blocking the release of acetylcholine
-AB type toxin |
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What is the genetic location of the botulinum toxin
|
-differs among antigenic types
-C and D type toxin is encoded by prophages |
|
|
Describe the botulinum toxin stability
|
-heat labile 100C for several minutes
-acid resistant, not destroyed in the stomach but acid environments do prevent germination (that's why you can get the food poisoning from canned mushrooms but not canned fruit) |
|
|
Describe infant botulism
|
-young children 3 weeks- 8 months
-organism colonizes GI tract, in vivo production of neutroxin -disease begins upon weaning when the flora of the intestine undergoes changes, insufficient competition by normal flora to block growth or organism -responsible for small precentage of SIDS -epidemiological related to sweetening of formula with honey |
|
|
How is botulism treated?
|
-supportive measures (mechanical ventillation, etc)
-antitioxin may be useful but equine origin can lead to serum sickness -antibiotics are of little value |
|
|
How can botulism be prevented?
|
Adequate cooking and reheating of foods
avoiding honey for infants |
|
|
Describe avain botulism
|
-wild migratory birs, kills estimated 10 to 50 thousand birds/ year
-ducks most suceptible -death due to drowing -motality in chickens can be 40% |
|
|
What is the gram stain of Clostridium difficile
|
gram positive bacillus
|
|
|
What is the oxygen relationship of Clostridium difficile
|
strict anaerobe, vegetative cells are very sensitive to O2
|
|
|
Describe the disease associated with Clostridium dificile
|
-diarrhea appears upon treatment with antibiotics, progressing to destructive inflammation of the colon
-pseudomembranous colitis |
|
|
How does Clostridium difficile interact with the colonic epithelium
|
-non invasive
-not entry into bloodstream -stays in hollow of intestinal spaces, causes damage by producing toxins, Toxin A and Toxin B which attack the intestinal wall |
|
|
Describe the pseudomonebranous colitis associated with Clostridium difficile infection
|
-thick, pseudomembrane on colon surface made up of fibrin, leukocytes, and necrotic colonic epithelial cells
-result of overgrowth of C. difficile due after reduction of normal flora |
|
|
Can C. difficile be found in heathly people?
|
yes, it can be culture from the intestines of about 4% of healthy adults
|
|
|
How does Clostridium difficile spread in hospitals
|
Spores are common contaminant in hospital environment, spread from pt to pt via HCW
|
|
|
Describe the mechanisms of Toxin A and Toxin B (TcdA, TcdB) of Clostridium difficile
|
-Toxin A enters epithelial cells and causes cytoskeletal rearrangements and loos of tight junctions
-This permins Toxin B to enter the lamina propria -in the lamina propria both toxins are cytotoxic and responsible for host inflammatory response |
|
|
What anibiotics are ususally associated with leading to Clostridium difficle infection
|
Ampicillin and clindamycin
|
|
|
How is infection with Clostridium difficile treated
|
-mild for will clear upon discontinuation of antibiotic Tx
-severe diseas may reuire vancomycin |
|
|
What is the oxygen relationship of Bacteroides fragilis
|
obligate anaerobe
|
|
|
What is the gram stain of Bacteroides fragilis
|
gram negative, irregularly shaped bacillus
|
|
|
How are infections with Bacteroides fragilis usually initiated
|
-fecal contaminatino of intrabdominal space due to ruptured appenxid or intestinal surgery
-usually mixed infection with E. coli -also found in intra-abdominal abscesses |
|
|
What feature of Bacteroides fragilis makes it more virulent than other species
|
prominent capsule
|
|
|
Describe Bacteriodes fragilis nutritional requirements
|
-uses a wide range of polysaccharides via DNA inversion system (also gives variable surface antigenicity)
-Phase switching system invovles multiple operons for polysaccharide synthesis and transport |
|
|
Describe the associated of Bacteroides fragilis with disease in children and lambs
|
-may cause enterotoxigenic disease but koch's postulates have not ben fulfilled
-production of exotoxin on cultured cells |
|
|
What staining/microscopy methods are used to visualize Borrelia
|
-structurally gram negative but poor stain
-visualize with Giemsa or Wright Stain -bright field micrscopy |
|
|
Describe the incidence of Borrelia species in clinical specimens
|
-B. recurrentis in blood
-B. burgdorferi is rarely visualized in clinical specimens |
|
|
Describe Borrelia growth in the labororatory
|
-grows slowly
-reqiures complex media -microaerophilic conditions -30C optimal growth |
|
|
describe Borrelia motility
|
motilie by way of periplasmic flagella, move in helical wave
|
|
|
What two species of Borrelia cause relasping fever?
Compare them in terms of "demnicity", vector, severity, and vector |
B. recurrentis is epidemic,louse borne, severe (40% mortality), huamans are only reservoir
B. hermsii is endemic, tick borne, less severe, many animals rerservoirs |
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|
Describe the progression and sxs of relasping fever
|
-bacteremia 1 week after insect bite, fever, headaches persist for 3-7 days
-number of bacteria decrease over the week along with sxs -another period of bacteremia follows -several cycles can occur |
|
|
What contributes to the cyclical nature of relapsing fever
|
-increase in anti-borrelia antibodies causes decrease in bacteremia
-relapse comes from antigenic varation in Variable Major Protein (VMP) |
|
|
What causes lyme disease
|
Borrelia Burgdorferi (identified 1981, Dr. W. Burgdorfer)
|
|
|
How is Borrelia Burgdorferi/ Lyme disease transmitted
|
Bites from hard shelled ticks
-Ixodes scapularis, (specifically the immature nymph and young adult) is the major transmitting tick species in WI, feeds on white footed mouse and white tail deer |
|
|
What life stage of Ixodes scapularis is responsible for transmitting Lyme disease
|
immature nymph and young adult
|
|
|
What type of microscopy and staining are used to visualize Borrelia Burgdorferi
|
-bright field microscopy
-Wright or Giemsa stain -rarley seen in clinical specimens |
|
|
Describe the genetic structures and the proteins they encode that lead to variation in Borrelia Burgdorferi
|
-linear chromosome and plasmids
-major outer mebrane proteins (Osps) encoded by unusual linear plasmids -high rate of recombination leading to antigenic variation -no relapse, Osps varation has no impact on pathogenesis |
|
|
Describe the membrane of Borrelia Burgdorferi
|
-Similar to other gram negatives but...
-no LPS in outer membrane -large number of lipoproteins, Osps -have endo periplasmic flagella (EF) Little bo BEP lost her sheep but pick up vlsE, Osps, EF |
|
|
Describe the rle of vlsE in B. burgdorferi
|
-encoded on liner plasmid
-also encodes 16 partial gene copies -portions of partial copies moved in and out of expressed region to make unique recombinants -antigenic variation of vlsE allows B. burgdorferi to evade host immune response |
|
|
How many stages are there of Lyme disease
|
3
|
|
|
Describe the first stage of Lyme disease
|
-erthema migrans 3-30 days post infection
-fever, headache, malaise, chills, muscle pain, stiff neck |
|
|
Describe the second stage of Lyme disease
|
-only occurs in 10-20% of induviduals
-secondary lesions, arthritis, Bell's palsy, neurological and cardiac symptoms |
|
|
Describe the third stage of Lyme disease
|
-Neurological symptoms and arthritis (resolves in 60%, 10% have severe destructive)
-bacteria not recovered -sxs likley due to over reactive immune response |
|
|
How is Lyme disease diagnosed
|
-easy when EM and Hx of tick bite
-not usually revoered in blood or tissue -use sxs, hx, and serology -Anti IgG Borrelia Abs more reliable than anti-IgM |
|
|
Where is Lyme Disease endemic
|
Midwest- Wisconsin, Northwest MN, Northeast IL, Northwest Indiana, LP of MI
New England, Small area in northern CA |
|
|
Besides the endmeic areas of the US, where is Lyme disease found
|
Mid lattitudes of Europe and Asia (France, UK, middle Russia)
|
|
|
What is the proper way to remove a tick
|
use tweezers, graps near mouth parts and pull out with steady, upward motion
do NOT use kerosine, matches, or petroleium jelly to remoe -disinfect are with soap and water, rubbing alcohol, H2O2 -record date of bite and be aware of possible sxs |
|
|
Describe the failed Lyme disease vaccine
|
-Contained OspA an outer surface lipoprotein, immunodominant, only found in Borrelia infected ticks yet still effective at preventing infection
-Claims that vaccine caused arthritis, pulled from market |
|
|
What causes syphilis
|
Treponema pallidum
|
|
|
What are the two ways to get syphilis
|
-STD
-in utero mother to fetus |
|
|
Describe the gram stain, morphology and motility of Treponema pallidum
|
-gram negative in priciple but does not stain well
-thin long helical structure -periplasmic flagella |
|
|
How is Treponema pallidum grown in the lab
|
-very hard to grow in lab, will not grow in tissue culture or complex media, animal models only produce limited aspects of the diesase
|
|
|
How may stages of syphilis are there
|
three
|
|
|
Describe Primary syphilis
|
Chancre
-lesion at the site of infection where Treponema is replicating -painless, neutrophil and macrophage infiltration -other aspects caused by host immne response |
|
|
Describe secondary syphilis
|
Disseminated stage
-2-12 weeks after primary -organism spread througout body -general body rash -lesions as local sites of replication |
|
|
Describe tertiary syphilis
|
-can occur years after secondary
-chronic gastric inflammatory disease -granulomatous lesions in bones, brain, heart, skin -neuosyphilis= chronic inflamation of CNS, paralysis, dementia and sensory loss |
|
|
Describe congenital syphilis
|
-transplacental transmission from mother to fetus
-can result in deformed or stillborn fetus -if live child is delivered, it can enter a secondary stage which can progress to tertiary |
|
|
Describe Syphilis sexual transmission
|
-humans are the only rerservoir
-any contact with primary or secondary lesions can cause infection -but bacterium is very sensitive to low temperatures and drying so infection via inanimate object is impossible |
|
|
How is Syphilis diagnosed
|
-clinical presentaiton
-dark field microscopy on material from lesion, look for helical organism -immunofluroescence with anti treponemal antibodies -no biochemical or antibiotic tests (can't be grown up in lab) -Nontreponemal and treponemal tests |
|
|
What are the non treponemal tests used to diagnose syphilis
|
-Test for antibodies to cardiolipin, a compound released from damaged cells in response to Treponema=> aggregation
VDRL-use Pt sera to cause cardiolipin to flocculate |
|
|
What are the drawbacks associated with non treponemal diagnostic tests
|
-subjective to positive/negative problem
-many false positives leading to large clinical and social complications |
|
|
Describe the treponemal tests used to Dx syphilis
|
-FAT-ABS (fluorescent treponemal antibody absoprtion), measure the prescence of specific anti-Treponema pallidum antibodies in serum
Immunoblotting- T pallidium antigens separated by electrophoresis, use Pt serum and measure reactivity |
|
|
Describe the Tuskegee experiment
|
-399 AA men given Syphilis from 1932-1972, no Tx
-experimental treatment with heavy metals, then penicillin in 1947 -Story reported in 1972, huge public outcry resulting in new lawss about human experimentation and informed consent |
|
|
What causes gonorrhea
|
Neisseria gonorrhoeae
|
|
|
Where do Neisseria replicate
|
although both N. gonorrhoeae and N. meningitidis invade cells, the replicate extracellulary
|
|
|
Are all Neisseria pathogenic?
|
no, some commensal strains like N. cinerea, N. lactamica
|
|
|
Describe the gram stain of Neisseria
|
gram negative diploccooi, kidney shpaed with flat faces towards each other
|
|
|
Describe Neisseria motility
|
-no flagella
-motile via twitching motility on solid substrates mediate by type IV pilli |
|
|
What is unique about Neisseria endotoxin
|
-no repeating O antigen, it has LOS instead of LPS
|
|
|
Do Neisseria have capsules
|
Neisseria meningitidis does
|
|
|
Describe Neissiera transformation
|
naturally competent using type IV pili, results in significant exchange of genetic material between strains
|
|
|
How is Neisseria grown in the lab
|
-grown readily overnight on complex media
-chocolate agar -Thayer-Martin agar selects for Neisseria -must be incubated 5% CO2 |
|
|
Describe Neisseria meningitidis pathogenesis
|
-colonize nasopharynx, can spread to blood and meninges
-systemic infection leads to significant vascular damage due to immune response associated with large amounts of LOS which is shed from surface in outer memebrane blebs -rapidly fatal if not treated, still 20% die |
|
|
What is the source of Nesseria meningitidis
|
strict human pathogen
|
|
|
How is Nesseria meningitidis treated
|
-anticapsular antibodies help with complement fixation and opsonization
-penicillin |
|
|
Describe the N. meningitidis vaccine
What strains are included? What strain is not included and why? |
-5 capsular types
-Tetravalent vaccine including types A, C, Y, W135 -No vaccine for type B because the capsule is componste of polysialic acid, an antigen that is found in humans, a bummer because type B causes 45% of infections |
|
|
Describe N. meningitidis epidemics
|
-kill 50,000 anually
-many in sub-saharan africa (meningitis belt) -might be associated with the Hajj |
|
|
How is Neisseria gonorrhoeae transmitted
|
sexual contact or childbirth
|
|
|
What are the reservoirs of N. gonorrhoeae
|
stric human pathogen
|
|
|
What disease can N. gonorrhoeae cause in newborns
|
opthalmia neonatorium leading to blidness
|
|
|
Describe the complications of gonorrhea in women
|
-PID leading to infertility, ectopic pregnancy, chronic pelvic pain
-50-80% of women are asymptomatic |
|
|
How is gonorrhea treated
|
-antibioitics but problems with resistance
-33% of US isolates resistant to penicillin, tetracycline or both -2% resistant to ciprofloxacin which use to be drug of choice -primary treatment now is ceftriaxone, a third generation cephalosporin |
|
|
Describe N. gonorrhoeae surface molecule variation
|
-extenisve phage and antigenic variation, able to evade host immune response
-alters binding specificities which allows it to bind different tissues or spread to different hosts -protective immunity is not developed |
|
|
define antigenic variation
|
alteration of the primary sequence of a protein or the chemical composition of a CHO that results in antigenic differences recognized by the host
|
|
|
define phase varation
|
the prescence or abscence of either a single or multiple virulence or antigenic determinants.
|
|
|
T/F it is possible to undergo phase variation without antigenic variation
|
true
|
|
|
T/F Meningococcemia can occur without meningitis
|
true, 25% mortality even when treated
|
|
|
List the variable components of the gonococcal cell surface and their relative reates of shifting
|
-Pili vary at fequency of 1/10-1/00
-LOS , vary at 1/10,000 -Opacity proteins, vary at 1/10,000 |
|
|
Describe pili antigenic variation in Neisseria
How is the genetic information affected? |
-series of transcriptionally silent pilin gene copies (pilS1, pilS2, pilS3, etc)
-One is expressed (pilE) -homologous recombination occurs between the silent and expressed genes -Net result is a change in coding sequence, the old sequence is permanently lost and the new copy is an antigenic variant of the pilus |
|
|
Describe Neisseria pili phae switching
|
-recombination in pilE can insert a translational stop codon
-transcriptionally active gene but truncated non funcitonal protein -results in bald/ non piliated cell |
|
|
Neisseria is naturally competent. How can it release DNA in the environment for others to uptake
|
-active secretion with type 4 secretion system
-autolysis |
|
|
What is the relationship between Nessiera pili and virulene
|
-non-piliated variants are virtually never isolated from infections except from women during menses
-In certain circumstances during pathogenesis the bald state may help reduce opsonization by the host anti-pilin antibodies |
|
|
Describe the phase varation of opa in Nesseria gonorrhoeae and opc in N. meningitidis
|
-occurs by slipped strand misparing during DNA replication
-contain multiple copies of CTCTT in the portion of the gene encoding the N terminal region -9 copies -repeat or loss results in frame shift and insertion of stop codon |
|
|
What proteins/ Neisseria species undergo slip strand misparing resulting in phase varation
|
N. gonorrhoeae- opa
N. meningitidis- opc |
|
|
Why are repeat infections with gonoroheae so common
|
-antigenic variaton, no protective immunity
-scotish man-whore James Doswell gets gono 17 times in 30 years |
|
|
T/F gonococcus has protein exotoxins
|
false
|
|
|
List 4 virulence derminantes of Neisseria gonorrhoeae and breifly describe what they do
|
1. Pillin-initial binding to epithelial cell
2. Opa- (outer membrane protein) intimate attachement, invasion of cost cell, microcolony formation 3. LOS- microcolony formation, inflammatory response 4. IgA protease- evade host immune response by cleving IgA remember "Gonorrhoeae Produces Outstanding Leisons In people" |
|
|
Describe what happens to the fallopian tube cells when the host is infected with gonorrhoeae
|
-death of cilliated fallopain tube cells because of release of LOS and peptidoglycan dervied cytotoxin
|
|
|
Desribe the gonococcal genetic island
|
-encodes a type IV secretion system
-genes with homology to TFSS and DNA processing proteins -present in gonococcal strains but not meningitids |
|
|
Describe the gram stain and unique membrane of Clamydia Rickettsia
|
-small gram negative like cell envelope
-atyipcal outer envelope -ridig outer membrane strengthened by disulfide corss linked cysteine rich membrane proteins -lack biochemically detectable complete peptidoglycan but may of the genes are expressed and Chlamydia is sensitive to d-cyclosterine suggesting D-alanine D-alanie ligase activity |
|
|
What is the relationship of Chlamydia and Rickettsia to their host/ how are they grown in the lab
|
obligate intracellular parasites, must be cultivated on host cells and cannot be grown on media
-Chlamydia requires host ATP, Rickettsia does not |
|
|
What is the motility of Chlamydia and Rickettsia? Do they form spores?
|
non motile, no spores
|
|
|
Are Chlamydia or Rickettsia normal flora
|
no, they are strict pathogens
|
|
|
Describe the life cycle of Chlamydia
|
Elementary body attched to cell and is ingested, phagosome fusion leads to reorganisation into reticulate body, multiplication of RB then condenstation into elementary body. Mature inclusion then extrusion and release of infectious elementary bodies
|
|
|
List 3 Chamydial species, thier subtypes, and the disease they cause
|
1. C psittaci, many subtypes, causes Psittacosis
2. C. pneumoniae, one subtype, cause acute respiratory infeciton 3. C. trachomatis -subtypes ABC cause trachoma -subypes DEFHIJK oculogenital problems and infant pneumonia -subtypes L1,L2, L3 cause lymphogranuloma venerum |
|
|
Describe the clincal spectrum of C. trachomatis infections
|
-Servoars A, B, Ba, and C cause trachoma
-B, Ba, and D to K cause oculogenital disease and infant pneuomnia -L1, L2, and L3 cause lymphogranuloma venereum |
|
|
What does Clamydia psittaci primarily infect and what disease does it cause
|
-birds
-rare infection in humans usualy those associated with infected animals -disease is psittacosis usually manifesting as acute pneumonia |
|
|
What diseases result from Chlamydia pneomniae infection
|
-respiratory illness (pharyngitis to pneumonia)
-high prevalance -may be associated with coronary atherosclerosis and adult onset asthma |
|
|
How is Chlamydia trachomatis classified
|
classified based on serovars which are based on antigenic differences in major outer membrane proteins (MOMP)
|
|
|
Describe trachoma
What causes it? Where is it endeimc What are the results |
-Cuase by Chlamdia trachomatis serovars A, B, Ba, and C
-endemic in Asia, Africa, areas of poor hygene, not in US -inflammatory damage to the conjuctiva elicited by repated or persistant ocular infections, blindness can result from mechanicla scraching of the cornea by disfigured eyelids |
|
|
Describe Chlamydia trachomatis spread by sexual
Which servars cause infection What is the prevalance in the US |
-attaches to and invades epithelial cells
-does not require breaks in skin or membranes -infection caused by D,E,F, H, I,J,K -15% of sexually active US women, 10% of sexually active men |
|
|
Describe the sxs of Chlamydia trachoma servars D-K infection
|
-less purulent than N. gonorrhoea, more asymptomatic causes
-mild purulent inflammation resulting from infection and destruction of columanr epithelial cells or cervix, uterus, fallopain tubes, urethra, rectum, nasopharynx, conjuctiva -long term disease is immune mediated, chronic inflammation leads to scarring and fibrosis of local tissue |
|
|
Describe the reproductive complications of Chlamydia trachoma in women
|
scarring of the fallopian tube causes a blockage and prevents fertilization, can lead to infertlity and etopic pregnancy
|
|
|
What type of secretion system does Chlamydia trachoma have
|
type III
|
|
|
Describe lymphogranuloma venereum
|
-STD caused by Chlamydia trachoma serovars L1, L2, L3
-almost non existant in US but significant problem in Africa and South America -infeciton of genital tract followed by dissemination to regional lymph nodes |
|
|
Describe Rickeettsia
-host relationship -gram stain/ cell wall -staining |
-obligate intracellular parasite, replicates freely in host cytoplasm
-gram negative cell wall with LPS and detectable peptidoglycan (unlike Chlamydia) -gram stain poorly, use Giemsa or wright |
|
|
What diease does Rickettsia rickettsii cause. Describe the location of the diesae
|
-Rocky Mountain spotted fever
-prevalant in rockies and applacains -not in Midwest |
|
|
How is Rocky Mountain Spotted fever spread
|
-transmitted by wood and dog ticks
-evidence that wild rodents are a reservoir for ticks (and thus humans) |
|
|
Describe the sxs of Rocky Mountain Spotted Fever
|
-1 wk post bite fever, headache, chills, pain ,nausea, rash
-characteristic spotted reash ~6 days post sxs onset, ~10% never develop rash -~20% die due to MOF -preferential infection of endothelial cells =>blood vessel leakage -long term seuelae includes paralysis of lower extremeties, gangrene=> amputation, movment and language disorders |
|
|
How is Rocky Mountain spotted fever diagnosed
|
-not grown in lab routinely but can be in TC cells
-difficult to locate and stain in biopsy -Dx by clinical presentation and Rickettsial antibodies (immunoflor for IgM or IgG in blood) -increase Abs by end of first week |
|
|
What causes Louse borne (epidemic) typhus?
What is the primary reservoir |
Rickettsia prowazeki
huamans are primary reservoir problem in WWI |
|
|
What causes murine (endemic typhus)
|
Rickettsia typhi
slower onset and less mortality than epidemic typhus |
|
|
Describe the actin motility displayed by Rickettsia
Who does it? How does it work? |
only R. ricketsii and R. typhi not R. prowazekii
induction of actin polymerization similar to Listeria and Shigella -facilitates cell to cell spread |
|
|
List the 4 mycobacteria that are animal pathogens
|
avium
bovis marinum avium sp paratuberculosis |
|
|
List the four species of mycobacteria that are human pathogens
|
avium (AIDS opportunist)
leprae tuberculosis bovis |
|
|
Describe the mycobacterial cell wall
|
-mycolic acids
-lipoarabinomanna -peptidoglycan -PIM |
|
|
Describe the unique morphology of mycobacteria
|
acid fast stain reveals characteristic roping or serpentine cords
|
|
|
Describe the prevalance of Mycobacterium tuberculosis worldwide
|
-1/3 to 1/2 of popluation infected
-2 million deahts per year |
|
|
describe mycobacterium lab culture
|
-slow growth, can take up to a month for colony (implications for Dx and Tx)
-cultured in vitro under BSL-3 -animal studies |
|
|
Describe Mtb as an intracelluar pathogen
|
-prevents phagosome maturation, fusion with lysosome
-granuloma formation |
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T/F Mtb has toxins
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false, sxs are cause by host response to bacteria
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List some important virluence factors of Mtb
How does it prevent maturation in the phagosome? How does it survive in the phagosome? |
used to prevent maturation in the phagosome:
-cell wall components like lipoarabinomanin (LAM) -secreted proteins (ESX-1 system, PknG kinase) (EScapte The PaKaGing) surviveing in the phagosome: -iron aquisition (mycobactins, exochelin) for survival in phagosome |
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List and desribe the three stages of Mtb pathogenesist
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1. Infection: Mtb activley replicationg, sxs of respiratory illness
2. Latent/ chronic: Mtb are low in number, no sxs, not contagious 3. Reactvation: MTb increase in number, host immune response causes sxss |
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What are the sxs assocaited with active Mtb
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coughing, tiredness, fever, chest pain, coughing blood (Hemoptysis), weight loss
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How is Mtb Dx'ed
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skin test, lung x-ray, culturing, sputum, blood test
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Describe the use and implications of the BCG vaccine
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-Bacillus Calmette-Gurein
-live attenuated M. bovis - Not used in US -Cannot be given to AIDS pts |
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Describe the Mtb skin test
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-measures hypersensitivity to Mtb protein derivaties
-inject PPD intradermally and look for induration and erythema post 3 days -Positive test may indicate infection, false positive if infection with different mycobacteria or vaccinated -false negtaive with AIDS |
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Describe the first line of Tx for Mtb
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Isoniazed-inhibits mycolic acid synthesis
Ethanmbutol-arabinogalactan synthesis Pyranzinamide-fatty acid synthesis -Rifampicin-inhibits RNA polymerase All 4 drugs iven for 2 months then INH and RMP for 4 months, never induvidually Remember "Is Every Penis Raging? Maybe All Fornication is Ronchy" |
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Describe the seond line of Tx of Mtb
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-ciprofloxacin (fluorounone, DNA gyrae)
-Moxiflocaxin (fluoroquinoe) -Amikasin (amnoglycoside, protein synthesis) |
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What are the definitions of MDR and XDR MTb
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MDR- resistant to at least isoniazix and rifampicin
XDR- resistant to isoniazie, rifampicin, a fluoroauinone, and at least one other second line drug |
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What is the Dogma of Mtb
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-humans are main reservoir, 1/3 to 1/2 or world is infected
-Majority of infected do not develop disease -those that develop disease are the induviduals who can transmit the infection to the non infected, active TB is more common in imunocomp adults |
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What causes leprosy (Hansen's disase)
How is it spread |
caused by Mycobacterium leprae, spread person to person
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What is the animal reservoir of Mycobacteirum leprae?
Where is the disease endemic |
nine banded armadillo
endemic in SC and SW US |
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Can M. leprae be grown in the lab
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not neither free living or in culture
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What are the two forms of leprosy
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Tuberculoid (paucibacillary)
Lepromatous (multibacillary) |
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Compare the immune response of the two forms of leprosy
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tuberculoid/paucibacillary= strong celluar weak humoral
lepromatous/multibacillary= strong antibody low cellular |
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Compare the number of of bacteria in the two forms of leprosy
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paucibacillary=few bacteria
multibacillary= high numbers |
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Compare the sxs of the two forms of leprosy
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paucibacillary= nerve thickening, defined plaques
multibacillary= patchy plaques, extensive tissue destruction |
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Describe the disease caused my M. paratuberculosis and its importance to humans
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-causes chronic wasting in cattle (Johne's disease/ garden hose disease)
-Association with Crohn's disease but Koch's postulates have not been demonstrated, possible contamination in meat/milk? |
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Which of the bacteria that we studied have LOS instead of LPS
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Campylobacter, Neisseria, Haemophilus
Lost Cat Needs Home |
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Which of the bacteria that we studied have humans as the primary reservior
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Neisseria
Treponema Mycobacteria Chlamydia Haemophilius Bordetella pertussis Borrelia recurrentis Never Try Rubbing My Cheesy Husband Before Bed romping |
