micro review #2 Flashcards
is there a toxin associated with B. burdorferi?
no
what are Stx-1 and Stx-2 encoded by?
bacteriophages
H pylori spread: mechanism for host damage:
spread: fecal-oral mechanism for host damage: grows in the mucosa of stomach, releases ureases which converts urea into ammonia—> increases the pH of the stomach, which increases the survival of H pylori It also injects CagA into epithelaial cells which increases inflammation —> erosion of tissue —> peptic ulcers
B. bacilliformis reservoir: vector: diseases:
B. bacilliformis reservoir: ? vector: Lutzomyia verrucarum (sandfly) diseases: carrion’s disease, acute oroya fever, chronic verruga peruana
EHEC spread: mechanism of damage: local impact: systemic impact:
EHEC spread: zoonotic (from GI flora that gets into meat/is used in fertilizer/ gets on vegetables) mechanism of damage: Systemic toxin release EHEC adheres to cells in the colon —> shigatoxins (stx) 1 and 2 which depurinates rRNA, blocking protein synthesis in host cells. Locally: GI inflamation and hemorrage Systemically: endothelial damage, hemolytic uremic syndrome (lysis of RBCs/damage to kidneys)
Tularemia and Francisella tularensis source: spread: 3 manifestations:
source: tick deerfly (which can bite humans directly, or bite rabbits– lawnmower!) spread: local replication (skin) —> drain into a lymph node 3 manifestations: 1. ulceroglandula tularemia (painful ulcer, lymphadenopathy) 2. Typhoidal tularemia (sepsis, hepatosplenomegally) 3. pneumonic tularemia (pneumonia associated with inhalation of org– lawn mowers)
three different tests for Syphilis and when are they used
- Darkfield– over 95% effective for primary syphilis. not used for others 2. Non-Treponemal- good for secondary and latent syphilis, but it wanes over time 3. Treponemal– ok for primary, better for secondary, latent and tertiary, but once positive, always positive!
aschoff bodies, what are they and what disease are they associated with?
aschoff bodies (little foci of inflammatory cells in tissue with rheumatic fever that don’t include bacteria) this is associated with rheumatic fever (S. pyogenes)
Adult foodborne botulism entry: manifestations: prevention:
Adult foodborne botulism entry: toxin ingested manifestations: flacid paralysis prevention:propper canning, proper reheating food (boiling for more than 10 minutes)
anthrax shape: gram stain: spores?
shape: bacillus Gram stain: positive Spores: present and seen as empty vacules withing the bacillis
why aren’t Abx recommended for people with EHEC?
beause damage to the bacteria (caused by Abx) leads to lytic virus and toxin production
pneumonic plague manifestation
fulminant hemorrhagic pneumonia
C. difficile, EHEC, Salmonella, Shigella, C jejuni and Y enterocolitica all cause diarrhea via ________? whereas ETEC and v. cholerae causes what type of diarrhea?
the big group causes diarrhea via tissue damage, whereas ETEC and v cholerae are non-invasive secretory diarrheas
pneumococcal pneumonia who does it affect: spread: manifestations: bacteria description:
pneumococcal pneumonia who does it affect: older adult with risk factors (lung disease, smoking, respiratory virus) spread: droplets from person to person manifestations: acute onset, fever, pleuritic pain, cough, “rust” colored sputum with bacteria description: GPC in pairs
B. quintana reservoir: vector: diseases:
B. quintana reservoir: ? vector: pediculus humanas (body louse) for trench fever diseases: trench fever, bacillary angiomatosis, endocarditis
manifestations of cutaneous anthrax
papule —> eschar —> resolution
where is S pyogenes and s. pneumoniae normally found in the body
pharynx
scarlet fever results from which bacteria? manifestations: etiology:
results from: S. pyogenes etiology: erythrogenic exotoxin
what tests are available to diagnose TB by looking for immune response?
- purified protein derivative (PPD) skin test, IFN-y release assays (IGRA)
path of Yersinia pestis/plague
xenopsylla cheopsis (flea) bites human (or rat does) —-> bacteria spread to lymph node —> MASSIVE inflammation —> either bubonic plague, septicemic plague or pneumonic plague
treatment for diptheria?
antitoxin and antibiotics
localized stage of lyme’s disease timing: site: manifestation: test:
- localized timing:Days site: skin manifestation: erythema migrans test: clinical diagnosis
where is S. aureus normally found in the body?
nose and skin
infant botulism entry: manifestations: prevention:
infant botulism entry: bacterium in the GI manifestations: flacid paralysis – think of the baby slouched on the mother with eyes closed because he can’t keep his eyelids open! prevention: avoid honey < 1yo
tetanus entry: manifestation: prevention:
tetanus entry: bacterium in wound manifestation: rigid paralysis (characteristic “sardonic smile”– bottom lip is curled upward, but top lip is still pulled straight) and autonomic dysfunction (HR is irregular and BP is unregulatable) prevention: vaccination (which includes the toxoid) and wound care
adult wound botulism entry: manifestations: prevention:
entry: bacterium in wound manifestations: flacid paralysis prevention: wound care
treponemal test for syphilis tests for…
the specific Ab against treponemal pallidum
which 4 bacteria cause infectious diarrhea through invasive mechanisms?
- salmonella 2. shigella 3. c. jejuni 4. y. enterocolitica
Bubonic plague mnifestations
fever, massive lymph node (bubo) which can break through the skin, +/- skin lesion at site of infection
Bartonella gram stain: shape: slow or fast growing: pathogenesis (2) diagnosis by:
Bartonella gram stain: positive shape: bacilli slow or fast growing: slow pathogenesis (2): granuloma w/cat scratch disease (occurs in kids), vascular endothelial proliferation —> angiogenesis in bacillary angiomatosis (in people who are immunocompromised) diagnosis by: serology or PCR of tissue. culture is insensitive and slow
Pseudomona aeruginosa: who does it affect: what bacteria does inside the host: bacteria description:
Pseudomona aeruginosa who does it affect: compromised hosts (people w/CF, hospitalized or ventilator pt) bacteria in the host: forms biofilms, aggregates of bacteria in EC matrix bacteria description: non-enteric gram positive bacillus, resistant to Abx and host defenses
ETEC and v cholerae mechanism: fever: leukocytosis: PMN in stool: Blood in stool:
ETEC and v cholerae mechanism: toxins cause ion and water secretion fever: NO leukocytosis: NO PMN in stool: NO Blood in stool: NO
4 mechanisms of tissue damage for S aureus
- alterations in coagulation due to coagulase 2. enzymatic digestion of tissue via hyaluronidase, fibrinolysin, Lipases, DNAase 3. Cytolysins 4. Pyogenic inflammation
how does B. burgdorferi cause damage?
it spreads and recruits damaging immune/inflammatory response
Diptheria description of the organism from a culture: manifestations: how is the damage caused:
organism: irregular club shaped organism– scattered like a torn down picket fence manifestations: fever, malaise, gray membrane, cardiac and neurological manifestations damage: the organism stays in one place, but the A-B toxin spreads, causes ADP ribosylation of EF-2 and blocks protein synthesis
3 bartonella infections
- B hensalae 2. B quintana 3. B bacilliformis
C difficile: mechanism of tissue damage: fever? leukocytosis? PMN in stool? Blood in stool?
C difficile: mechanism of tissue damage: local toxin causes cell death (cytotoxic) fever: yes leukocytosis: yes PMN in stool: yes Blood in stool: yes
3 Infections that affect the soles of hands and feet
- secondary syphilis– scaly rash 2. RMSF 3. TSS—> desquamation of the hands and feet
list the 4 skin and soft tissue infections caused by S. pyogenes
- impetigo 2. erysipelas 3. cellulitis 4. necrotizing fasciitis
describe the immune response to MTB (mycobacterium tb) in someone who has reactivation
- initially MTB proliferates unchecked within phagosomes of macrophages (the immune system has to ramp up to stop it) 2. the TH1 response makes macrophages competent to kill TB (via IFN-y), leading to latency and granuloma formation the failure of the TH1 response leads to reactivation TB
How do you distinguish between Enterococcus and Group D strep given that they’re both GPC, catalase negative, and gamma hemolytic?
bile esculin and high salt test: Enteroccocus has positive growth on both, Group D. Strep can grow on bile esculin, but not in high salt
B burgdorferi is associated with which disease?
Lymes disease
which bacteria(s) cause infectious diarrhea via the following mechanisms: secretory diarrhea because of toxins (2): tissue damage from systemic toxins (1): tissue damage from local toxins (1): tissue damage from invasive pathogens (4):
which bacteria(s) cause infectious diarrhea via the following mechanisms: secretory diarrhea because of toxins (2): ETEC and V. cholerae tissue damage from systemic toxins (1): EHEC/STEC tissue damage from local toxins (1): C diff tissue damage from invasive pathogens (4): shigella, salmonella, C. jejuni, Y enterocolitica
Tuberculosis how is it spread? what are the two pathways it can take and symptoms of each
tuberculosis spread: airborn from person to person 1) if you have a strong immune response, then the TB will be asymptomatic, and the MTB will persist in a latent phase. If you are ever immunocompromised there can be reactivation of TB leading to fever, night sweats, weight loss, cavitation and cough and extrapulmonary problems 2) if you hae a weak immune response, you can get progressive primary TB which is confined the the lungs and looks like typical lobar pneumonia 2) If you have a weak immune response, the it will progress to primary TB and
Rocky Mountain Spotted Fever (RMSF) vector: pathogen: mode of infection: damage:
Rocky Mountain Spotted Fever (RMSF) vector: Dermacentor tick pathogen: R. rickettsii mode of infection: R. rickettsii infects vascular endothelial cells and then spread directly to new cells via their actin polymerization (like Lysteria monocytogenes) damage: inflammation and endothelial damage —-> increased permeability and coagulation —> thrombosis, hemorrhage and edema —> organ damage/shock which can be legal
how do you distinguish between GPC in chains that are catalase negative and alpha hemolytic (s. pneumoniae vs viridans strep
Optochin susceptibility: S. pneumoniae is sensitive, and viridans are resistant
mechanism of anthrax toxin
the anthrax toxin hasone B and two A groups 1. B binds to cell 2. A portion leaves 3. the b portion multimerizes 4. the A portions (edema factor or lethal factor) binds 5. the multimer toxin is endocytosed 6. Edema factor leads to more cAMP, causing H20 efflux/edema, lethal factor inhibits MAPK kinase which leads to cell death
source/spread of plague and yersinia pestis
xenopsylla cheopsis (a flea) that can bite humans directly or spread it to rat that then bite humans
Salmonella: source/transmission: two pathways in the host:
source/transmission: zoonotic (especially chickens)- served in food, sometimes people (S. typhi and paratyphi) fecal-oral transmission pathways: 1) bacteria enters GI system, gets pulled into the GI mucosa via the M cells and causes inflammation and diarrhea, but stays there 2) bacteria gets into the lymph, then the blood causing prolonged dissemination and enteric fever (S typhi and S. paratyphi)
manifestations of GI anthrax
upper tract: ulceration, edema Lower tract: necrosis, hemorrhage and death (lethal)
where is coagulative staph usually found in the body?
skin
what is the most common strain of EHEC in the US? how can you detect it?
E Coli- 0157:H7 grow it on a maconkey sorbitol plate– it doesn’t ferment so it stains lighter pink
which two bacteria can travel directly from cell to cell using actin polymerization?
L. monocytogenes and R. ricketsii
Legionella pneumophila spread: where does bacteria live in the host: how do you diagnose it: manifestation:
Legionella pneumophila spread: via inhalation (from Air conditioners because of contaminated water)– humans are an accidental host! where does bacteria live in the host: intracellularly- inside phagasomes how do you diagnose it: test for a polysaccaride antigen in the urine (sero group 1) manifestation: atypical pneumonia, non-productive cough, fever, dyspnea– Legionnaire’s disease
mechinism for salmonella invasion:
- Type 3 secretion system injects effector proteins Sop E and SptP —> cytoskeleton rearrangements/membrane ruffling —> engulfment and uptake of bacteria
what are the 4 outcomes of S pharyngitis?
- recovery within 3-5 days 2. scarlet fever 3. suppurative (pus forming) sequelae: otitis media, sinusitis, abcesses, etc 4. nonsuppurative sequelae (rheumatic fever, acute glomerulonephritis)
Verruga Peruana (peruvian wart)
manifestation of bartonella bacilliformis, and lg foci of neovascularization
GPC, catalase + and coagulase + ? GPC, catalase + and coag -?
GPC, catalase + and coagulase +: s. aureus GPC, catalase + and coag -: S. saprophyticus and S. epidermidis
Patterns of typical pneumonia onset: sputum gram: CXR: age: response to B-lactam: common pathogens (4):
Patterns of typical pneumonia onset: acute often severe sputum gram: is visible CXR: lobar (single lobe consolidate) age: > 50 years old response to B-lactam: often common pathogens: S. pneumoniae (most common), S. aureus (usually following influenzae), H. influenzae, K. pneumonia
which two salmonella cause enteric fever upon prolonged dissemination?
- S typhi, 2. S. paratyphi
Persistent stage of lyme’s disease timing: site: manifestation: test:
- persistent timing: months site: joints manifestation: assymetric red, swelling, pain in joints (particularly knees) test:ELISA/western blot for ab agst org plus WBC count. No gram stain because the organism is so tiny
3 types of plague
bubonic, septicemic or pneumonic
where are S. saprophyticus and enterococcus normally found?
in the gi tract
If you are treated for Syphilis and cured, which diagnostic test would become negative? which would stay positive?
non-treponemal would become negative, but treponemal stays positive
H pylori infections can cause what infections after just a few weeks/months, and will cause what after years (4)
weeks/month: chronic superficial gastritis (just at the mucosal layer) after years: 1. peptic ulcer disease 2. chronic superficial gastritis 3. gastric lymphoma 4. chronic atrophic gastritis (loos of normal mucosa and shrinkage of tissue) —> gastric adenocarcinoma
The difference between botulism toxins and tetanus toxins
Botulism: toxins prevents acetylcholine release from motor neurons —> reduced muscle contraction tetanus toxin prevents gamma-aminobutyric acid (GABA) release from regulatory (inhibitory) neurons —> less inhibition of motor neurons —> increased muscle contraction
how do you distinguish btwn S. epidermidis and s. saprphyticus given that they’re both GPC. catalase + and coagulase -?
Novobiocin plate: S. saprophyticus will grow on it but epidermidis won’t.
acute rheumatic fever (ARF) caused by what bacteria: manifestations: etiology: prevented with Abx:
bacteria: S pyrogenes manifestation: polyarthritis, pancarditis that leads to valve damage, chorea (unusal mvmts), erythema marginatum (red rash ring that moves all over the body, possibly an auto immune response to M proteins) etiology: auto immune? M protein association, aschoff bodies (little foci of inflammatory cells in tissue with rheumatic fever that don’t include bacteria) prevented with Abx: YES
what allows S aureus to escape from host response and how does it work?
surface Protein A– it binds to the Fc portion of an IgG and allows S. aureus to escape specific Ab
3 stages of Lymes disease timing: site: manifestation: test:
- localized timing:Days site: skin manifestation: erythema migrans test: clinical diagnosis 2. disseminated timing: wks site: skin, CNS, heart manifestation: multiple, asynchronous erythema migrans, meningitis, cranial neuritis (paralysis of 1/2 the face), arrythmia (heart block) test: ELISA/western blot for ab agst org plus WBC count. No gram stain because the organism is so tiny 3. persistent timing: months site: joints manifestation: assymetric red, swelling, pain in joints (particularly knees) test:ELISA/western blot for ab agst org plus WBC count. No gram stain because the organism is so tiny
describe the structure/function of clostridium neurotoxins
A-B toxins A portion = “active”- proteases that cleave neuronal molecules needed for synaptic vescicle fusion and neurotransmitter release B portion: “binding”- binds to the cell in order for the toxin to get in
list the 5 skin and soft tissue infections caused by S. aureus:
- impetigo 2. bulous impetigo and SSSS 3. folliculitis 4. carbuncles and furuncles 5. cellulitis
what are the diseases and causes of bacterial upper respiratory tract infections (2)
- pharyngitis caused by S. pyogenes 2. diptheria caused by C. diptheria
what must your body make to protect you against the anthrax toxin?
an antibody against the B portion of the toxin
for each of the Skin and soft tissue Infections say if they’re caused by S. aureus, S. pyogenes or both, and if there are any other bacteria that cause the same infection: Impetigo Bullous Impetigo and SSSS Folliculitis Carbuncle and Furuncle Erysipelas Cellulitis Necrotizing Fascitis
Impetigo: both, plus other Strep Bullous Impetigo and SSSS: S. aureus Folliculitis: S. aureus Carbuncle and Furuncle: S. aureus Erysipelas: S pyogenes and other Strep Cellulitis: both, plus other strep, GNR and more Necrotizing Fascitis: S. pyogenes, plus other staph, other strep, anaerobes and other
Treatment of TB
multiple drugs (3-6) for 6-18 months– long course because TB is sooooo slow growing *therapy is guided by susceptibility tess and local resistance patterns, and multiple drugs are used to prevent the emergence of resistance
salmonella, shigella, c. jejuni, and y. enterocolitica– mechanism of tissue damage: fever: leukocytosis: PMN in stool: Blood in stool:
mechanism of tissue damage: invasive fever: yes leukocytosis: yes PMN in stool: yes Blood in stool: often
bacterial cause and physical manifestations of Pneumonic tularemia
Caused by francisella tularenis pneumonic tularemia: pneumonia associated with inhalation of org– lawn mowers
2 laboratory tests to detect EHEC. Which is best for E. coli 0157:H7? Which detects all sertypes of EHEC?
- sorbitol-MAC (maconkey agar): detects E. Coli 0157:H7, the most common serotype, because it doesn’t ferment sorbitol and so it is light pink 2. immunoassays for Stx 1/2 will detect ALL serotypes and is more sensitive than S-MAC
what are the diseases and causes of bacterial lower respiratory tract infections (2)
- pneumonia (S. pneumoniae, L. pneumophilia, primary M. tuburculosis 2. Tuberculosis (extrapulmonary) caused by M. tuberculosis
Bacillary andiomatosis caused by: reservoir: vector manifestations:
caused by: Bartonella hensalae and B. quintana reservoir: Bartonella hensalae is cats, but B quintana is unknown vector: no vector for Bartonella hensalae but B quintana is spread by Pediculus humanus manifestations: little red lesions that are neurovascular foci
diagnostic tests of TB are divided into what two general categories?
- detection of the bacteria (active disease using acid-fast stain, culture or PCR) 2. detection of the immune response (latent or active disease using PPD or IFN-y resease assays (IGRA)
Ehrlichiosis and anaplasma Bacteria: Vector: where does it live: Disease: manifestations
Ehrlichiosis Bacteria: Ehrlichia chaffeensis Vector: Amblyomma americanum tick lives: obligate intracellular bacteria in cells of hematopoietic system Disease: monocytic ehrlichiosis manifestations (same as anaplasma) THROMBOCYTOPENIA AND LEUKOPENIA Fever, headache myalgias Anaplasma Bacteria: Anaplasma phagotyophilium Vector: ixodes ticks lives: obligate intracellular bacteria in cells of hematopoietic system Disease: granulocytic anaplasmosis manifestations: (same as ehrlichiosis) THROMBOCYTOPENIA AND LEUKOPENIA Fever, headache myalgias
Poststreptococcal acute glomerulonephritiscaused by what bacteria: manifestations: etiology: prevented with Abx:
caused by: S pyogenes manifestations: edema, high BP, rusty urine etiology: immune complex deposition preventable with Abx: NO
similarities/Difference between EHEC and V cholerae
similarities: cause secretory diarrhea, spread via fecal-oral route (usually in contaminated water/food) EHEC: enterotoxic diarrhea that is the most common cause of traveler’s diarrhea, it’s mild and self-limited V. cholerae: mild to severe and is life threatening, more voluminous, often associated with hypotension and a cholera outbreak, and can be spread from shellfish
which GPCs are catalase positive?
all staph (the hospital staff (standing in a cluster) loves their cat!)
what tests are available to diagnose TB by looking for the actual bacteria?
- acid fast stain 2. culture (but very slow growing!) 3. molecular test (PCR)
legionnaire’s disease cause manifestation
cause: L pneumophilia, usually from inhalation from Air conditioner manifestation: non-productive cough, fever, dyspnea
B anthracis causes damage via:
local damage from toxins +/- bacterial spread
where is plague an issue
the 4 corner region(utah, colorad, new mexico, arizona
bacterial cause and physical manifestations of Typhoidal tularemia
Caused by francisella tularenis Typhoidal tularemia: sepsis, hepatosplenomegally
Prevention of TB
- infection control 2. vaccination with BCG, a live attenuated strain that isn’t that effective
septicemic plague manifestation
fever/sepsis w/out Bubo (hg lymph node)
which bacterial infectios cause of diarrhea RARELY CAUSES FEVER? Which never causes fever?
Rare: EHEC which = STEC Never: ETEC
Patterns of atypical pneumonia onset: sputum gram: CXR: age: response to B-lactam: common pathogens (4):
Patterns of atypical pneumonia onset: mild-severe sputum gram: usually not visible/scant CXR: bilateral patchy infiltrate age: children and adults response to B-lactam: NO common pathogens (4): L. pneumophilia, M. pneumoniae, C. pneumoniae, respiratory viruses
how does ehrlichiosis look on a blood smear?
like a little inclusion that looks like a mullberry inside of a WBC
two A portions of the anthrax toxin
- edema factor (increases cAMP —> H20 efflux) 2. lethal factor (inhibits MAPK kinase —> cells death)
How does S. pyogenes escape host defense?
surface M protein is antiphagocytic and exists in multiple serotypes
GPCs that cluster, GPCs that are in chains
cluster: Staph aureus, saprophyticus and epidermitis chains: strep and enterococci
vector
an arthropod that transmits an infection
where is S. agalactiae normally found in the body?
vagina and GI tract
nontreponemal test for syphilis tests for…
nonspecific antibodies that react to cardiolipin using VDRL (Venereal Disease Research Laboratory) test and Rapid Plasma Reagin (RPR) test.
TSS manifestation: bacterial cause: mode of damage:
manifestation: high fever, hypotension with sunburn like or maculopapular rash followed by subsequent desquamation of rash on palms and soles of feet bacterial cause: mostly S. aureus, some S. pyogenes mode of damage: Toxic shock syndrome toxin-1 (TSST-1)– superantigen binds constand region of TCR— HUGE T-cell inflammatory response
how do you differentiate between S. pyogenes and non group A Strep, given that are Beta hemolytic (GPC growing in chains)
bacitracin susceptibility test: Strep A= sensitive to bacitracin (doesn’t grow) non-strep A beta hemolytics (like Strep B) = bacitracin resistant (grows)
manifestations of inhalation anthrax (from spores)
respiratory failure, sepsis, death
salmonella (or shigella) on macConkey Agar vs escheria coli on a MacConkey Agar. Why?
Salmonella and shigella are growing but clear because they don’t ferment lactose E coli are growing and turning the plate red because they’re fermenting the lactose in the MacConkey agar which changes the pH
bacterial cause and physical manifestations of ulceroglandular tularemia
Caused by francisella tularenis ulceroglandula tularemia: painful ulcer, lymphadenopathy
which two forms of salmonella have exclusively human hosts?
S. typhi and S paratyphi
RMSF manifestations:
fever, headache and myalgias followed by a characteristic rash 2-6 days later on PALMS AND SOLES. The rash is macules (flat), petechial rash. - there is also damage to the CNS, GI, liver, kidneys, etc
Disseminated stage of Lymes disease: timing: site: manifestation: test:
- disseminated timing: wks site: skin, CNS, heart manifestation: multiple, asynchronous erythema migrans, meningitis, cranial neuritis (paralysis of 1/2 the face), arrythmia (heart block) test: ELISA/western blot for ab agst org plus WBC count. No gram stain because the organism is so tiny
C difficile: spread: mechanism of damage
C difficile spread: fecal oral mechanism of damage: Local toxin leads to collitis abx wipe out normal flora —> overgrowth of C diff —> toxins A and B sereted —> inactivate Rho within host cells —> disrupts the cytoskeleton causing apoptosis and inflammation —> colitis
where does the serotype diversity of EHEC come from?
bacteriophages that move between strains of E. Coli
do type III secretion systems inject exotoxins?
NO!!!!!!!!!!!!!
cat scratch disease caused by: reservoir: manifestations:
caused by: Bartonella hensalae reservoir: cats manifestations: papule on cheek feels fine, not a severe infection!, lymphadenopathy
EHEC/STEC mechanism of tissue damage: fever? leukocytosis? PMN in stool? Blood in stool?
mechanism of tissue damage: systemic toxin leading to cell death fever: rare leukocytosis: yes PMN in stool: yes Blood in stool:yes
B hensalae reservoir: vector: diseases:
B hensalae reservoir: cats vector: none for humans diseases: cat scratch disease, bacillary angiomatosis, endocarditis
3 ways for humans to come into contact with B anthracis and the outcome of each
- inhalation of spores—> inhalation Anthrax (respiratory failure, sepsis, death) 2. ingestion—> GI anthrax (upper tract: ulceration, edema, Lower tract: necrosis, hemorrhage and death—> lethal) 3. skin (from contact with animal products) —> cutaneous anthrax (pupule —> eschar —> resolution)
how do you prevent Diptheria?
a toxoid vaccine, the antibody neutrolizes the toxin preventing host damage. The disease is very rare where the vaccine is used
mechanism of spread of ETEC and V cholerae
fecal oral spread (water or food) —> growth of bacteria and AB toxin production in the GI tract —> AB toxin binds to cells, leads to an increase in cAMP, which increases adenylate cyclase —-> this activates Ion (Cl and bicarb) and H2O efflux out of the cells
mechanism of EHEC adhesion
Type III secretions system injects receptor and effector proteins —> leads to binding and cytoskeleton rearrangements —> causes pedestal formation and tight adherence
