Midterm 2 Flashcards
Pseudomonas pathogen type
Opportunistic, leading cause of HAI
Who Pseudomonas affects most
Fibrosis patients, CFTR mutation, MDR PA with salty mucin
Pseudomonas reservoir
Soil, water, plants
Pseudomonas transmission
Healthcare workers/equipment, burn and surgery wounds
Pseudomonas diseases
Fibrosis patients, burns and wounds, skin, eye and ear, HAI
Pseudomonas binding pathogenesis
Pili opportunistic binding (flu expose URT/upper respiratory tract receptors), LPS bind to chloride channels in LRT/lower respiratory tract
Pseudomonas dissemination pathogenesis
Elastase degrades complement and elastin lung protein, ExoS ADPR G proteins to disrupt PMN, ExoA ADPR EF2 like DT, NA cleaves sialic acid, phospholipase degrades surfactants
CF test
Sweat test, high sweat because salt balance is off
Pseudomonas resistance
Intrinsic barrier to antibiotics by forming biofilm
Special pseudomonas protocol
No fruits or veggies to hospital patients
Pertussis past
One of the most frequent diseases prior to vaccination
Pertussis reservoir
Human aerosols
Pertussis transmission
Air droplets
Pertussis diseases
Infants (whooping cough), Adults mild cough, Complications (secondary bacterial pneumonia)
Pertussis catarrhal stage
Colonization first 2 weeks, very contagious, runny nose, fever, cough, bug recovered from culture, antibiotics help
Pertussis toxemic stage
2-8 weeks, whooping cough, bug is gone, symptoms due to toxin PT, antibiotics don’t help
Pertussis convalescent stage
Gradual recovery (months), susceptible to secondary infection
Pertussis pathogenesis
Inhalation, attachment to ciliated cells, paralyze ciliated cells, toxins inflame RT and stop clearing of mucus
Pertussis adhesins
PT A1B5, and FHA (filamentous hemagglutinin) binds ciliated cells like PT
Pertussis toxins
PT ADPR Gi to increase cAMP (reduce phagocyte killing), introduce own ACase to increase cAMP, tracheal cytotoxin damages ciliated cells, lethal toxin necrosis
PT mechanism
Normally Gs activates ACase, all deactivated by Gi, when Gi is ADPR then the system isn’t inhibited
Pertussis testing/detection
Culture 1st 2 weeks, PCR 1st 4 weeks, serology Ab test 2+ weeks
Pertussis prevention
DTaP vaccine uses PT & FHA, Tdap booster every 10 years, Tdap booster every pregnancy
Anthrax
Large cells with infectious spores (bioterror)
Anthrax reservoir
Soil
Anthrax transmission
Spores from animals/products (NOT human-human)
Cutaneous anthrax information
Most common, spores enter wound, germination, lesion develops with edema (rarely highly fatal septicemia)
GI anthrax information
Very rare, ingest spores from contaminated meat, invade mucosa and lymphatic system, high death rate
Inhalation anthrax information
Infection 1wk-2mo of inhalation, germination in Macs, bacteria in bloodstream, septic shock and high death rate
Anthrax capsule
Anti phagocytic (PGDG) poly gamma d glutamic acid resistant capsule
Anthrax toxin
2A1B, protective antigen binds up to 3 A portions, lethal toxin causes lethal effects w cell lysis and cytokine storm, and edema factor causes edema in cutaneous anthrax w/ own ACase
Anthrax treatment
60 days, ensure all spores germinated, antibiotics good if early, antitoxin to PA (protective antigen)
Anthrax bioterror
Release anthrax spores into the environment or infect livestock and transmit with infected carcasses
Anthrax Pasteur vaccine
Inject live strain into livestock and 5 doses of IM shots with boosters for military of PA
TB general information
Gram + like, acid fast +, white plague, only in humans
TB reservoir
Only humans
TB transmission
Highly contagious droplets/aerosols
LTBI information
Not infectious and no symptoms, skin test positive but nothing else
TB disease information
Highly infectious, skin test +, X-ray +, sputum +, cough fever, weight loss
TB predisposing factor
HIV knocks out CD4+ T cells, TB takes advantage
Primary TB pathogenesis
Inhale droplets into lung aveoli, invade Macs, body CD4+ T cell response, formation of tubercule (usually LTBI)
Primary TB disease information
5% of total cases, usually pulmonary, occasionally EPTB, and even more rarely military TB with cancer like tubercule formation
Secondary TB information
5-10% of LTBI cases, tubercules break down and infectious again, rarely EPTB
TB virulence factors
Resistant and waxy cell wall, has mycolic acid fatty acid chains, cord factor sticking cells together, Wax D. Also LAM (lipoarabinomannan) cell wall glycolypid which modifies phagosome
TB diagnosis
Acid fast test heat/acidify bacteria (need many bugs/doesnt separate other myobacteria), NaOH sputum culture (slow generation time), PPD TST (skin test with boiled protein extract look for hard raised bump), TB blood test (most accurate, IGRA [interferon gamma release assay])
TB treatment
For LTBI INH for 9 months, for disease INH + RIF (RNA Pol Inhibitor) + EMB + PZA for 9 months, all targeting cell wall synthesis, XDR and MDR TB can form if not full course
TB vaccine
BCG live attenuated vaccine with M. bovis, scar formation administered in some countries to protect kids
Cholera general information
Curved rod, gram -, flagella, causes “blue death”, hella diarrhea and rapidly fatal
Cholera reservoir
Water/humans/shellfish
Cholera transmission
Fecal/oral, NOT direct, poop water
Cholera severity
10% severe, generally cleared after a week
Cholera pathogenesis
Ingested and adheres to small intestine, produces cholera toxin (CT) and acts on mucosal cells causing huge diarrhea and dehydration/circulatory collapse
Cholera symptoms
Typically very fast (<1 day), extreme thirst, cramps and blue skin, liquid stool and shock, rice water stool
Cholera adherence
Tcp (toxin coregulated pilus) binds to small intestinal mucosa, NA, CT
Cholera toxin
5B1A, ADPR Gs, binds to mucosal surfaces
Cholera toxin mechanism
ADPR Gs to not allow Gi to inhibit the production of ACase, raise cAMP, phosphorylation of chloride ion channel, chloride/K+ leaves and so does water
Cholera treatment
Rehydration, necessary to have glucose included for uptake
Cholera vaccine
VAXCHORA live attenuated vaccine with deleted A portion, given to travelers
C. diff general information
Gram +, forms spores, causes watery diarrhea and colitis, very resistant to most things other then bleach
C. diff risk factors
Long term antibiotics (colon microbiome depletion)
C. diff reservoir
Spores in air, soil, water, human and animal intestine
C. diff transmission
Fecal-oral, spore ingestion, contaminated surfaces
C. diff diseases
Pseudomembranous colitis, toxic megacolon, colon rupture
C. diff pathogenesis
Ingested spores, germination and colonization of colon, produce TcdA and TcdB, diarrhea and ulceration, sepsis and death
TcdA and TcdB mechanisms
Largest known toxins, UDP glycosylate G proteins, block Rho GTPase activity, different B portions recognize different epithelial cell surfaces, result in disruption of tight junctions and increase inflammatory response
C. diff testing
ELISA Ab test for A and B in feces, NAAT for toxin gene in stool (PCR)
C. diff treatment
Antibiotics, oral vancomycin, FMT (fecal microbiome transplant)
C. diff prevention
Contact precaution (wash hands), bleach contaminated surfaces, avoid unnecessary antibiotics
Kleb. pneumoniae information
Gram -, principally extracellular, carbapenem resistant
Kleb. pneumoniae risk factors
Ventilators, catheters, IV, long term antibiotics
Kleb. pneumoniae reservoir
human intestine and oropharynx
Kleb. pneumoniae transmission
Person to person, NOT air, usually medical device/contaminated hands
Kleb. pneumoniae diseases
Pneumonia, UTI, sepsis
Kleb. pneumoniae pneumonia pathogenesis
Colonize oropharynx, inhalation and biofilm growth in lung, pneumonia and lung scarring, bacteremia and sepsis
Kleb. pneumoniae virulence (HV strains)
Hypercapsule (77 types), pili biofilm formation, LPS block C1 binding and inflammatory response, siderophore iron scavenging proteins
Kleb. pneumoniae diagnosis
Respiratory panel PCR
Kleb. pneumoniae treatment
Bug is carbapenem resistant due to outer membrane alterations and efflux pump up-regulation and (ESBL) extended spectra beta lactate enzymes which break down penicillins
Salmonella general info
Gram -, motile rod with flagella, food poisoning and typhoid fever, many variants
(NTS) Non-typhoidal salmonella information
Largest food borne bacterial disease cause
NTS reservoir
Human and animal intestinal tract
NTS transmission
Contaminated food and water
NTS disease
Food poisoning
NTS symptoms
12-72h after infection diarrhea, cramping, fever for up to 1 week and asymptomatic carrier for up to 3 months
NTS pathogenesis
Ingestion, invade enterocytes, replicate in macrophage
NTS virulence
Pef (plasmid encoded fimbriae) adhesin which bind to microvilli, Salmonella pathogenicity islands (T3SS) invade cells, SPI-1 mucosal invasion and SPI-2 systemic survival produces SpvB toxin which ADPR actin to dusrupt cytoskeleton
S. typhi special feature
Found only in humans
S. typhi reservoir
Human intestine/gallbladder and shellfish
S. typhi transmission
Poop contaminated food/water
S. typhi symptoms
Sustained high fever, stuporous state, body aches, flushed appearance, diarreah
S. typhi asymptomatic carriers
Around 5% of affected, carriers for months-years
S. typhi disease
Typhoid fever
Typhoid fever incubation phase
Ingestion, growth in macrophages in MLN (lymph nodes), 1 -3 weeks
Typhoid fever systemic period
Septicemia intestinal ulcers, typhoid toxin LPS shock
Typhoid fever asymptomatic period
Live in gallbladder, shed bugs for years, hard to clear with antibiotics (targeting to gallbladder)
S. typhi virulence
Typhoid toxin A1B2, (hybrid of PT/CDT)
A1-PltA=pertussis-like toxin ADPR unknown target
A2-CdtB (cytolethal distending toxin)=DNAse activity
B-PltB=Binds only to human glycoprotein target
Antiphagocytic Vi (virulence) capsule
S. typhi prevention
Water sanitation
S. typhi treatment
Antibiotics
S. typhi vaccine
Live attenuated oral for travelers, Vi capsule IM shot
Diarrheagenic E. coli information
Gram -, flagellated rod
O antigen = LPS
H antigen = Flagella
K antigen = capsule
Top 6 pathogen for death because of resistance
ETEC (enterotoxigenic E. coli)
Traveler’s diarrhea, human/animal reservoir, noninvasive
ETEC virulence
Noninvasive, small intestine adherence, LT (heat labile toxin) ADPR Gs, ST (heat stable toxin) activates GCase, increase cGMP for water release, no inflammatory response
EAEC (enteroaggregative E. coli)
Persistent watery diarrhea in children, human only reservoirs
EAEC virulence
Noninvasive but clump aggregation, EAST (EA stable toxin) activates GCase like ST, hemolysin like toxin, no inflammatory response
EPEC (enteropathogenic E. coli)
Watery/bloody diarrhea, human reservoir, moderately invasive
EPEC virulence
EAF (EPEC adherence factor), intimin (glue) no microvilli at binding sites, pedestal under bacteria, no diarrheal toxin, disrupt signal transduction
EHEC (enterohemorrhagic E. coli) / STEC
Shiga toxin producing E. coli, livestock reservoir
EHEC virulence
Moderately invasive, intimin, Shiga toxin (A1B5) stops protein synthesis by cleaving 28s RNA, only human receptor
EHEC diseases
HC (hemorrhagic colitis) causes bloody diarrhea and HUS (hemolytic uremic syndrome) causes kidney/organ failure with bloody urine
EIEC (enteroinvasive E. coli)
Dysentery, bloody and mucous diarrhea, human reservoir
EIEC virulence
Very invasive, colon adherence, spread laterally to adjacent cells, no diarrheal toxin, damage due to mucosal destruction
Types of ExPEC (extraintestinal pathogenic E. coli)
UPEC (urpopathogenic E. coli), NMEC (neonatal meningitis E. coli), SEPEC (sepsis associated E.coli)
Cause of UTIs
90% of the time, UPEC
UTI/UPEC reservoir
Colon and vaginal colinzation
UTI/UPEC transmission
From colon or vagina or sex, most common in women due to anatomy
Community acquired UTI/UPEC pathogenesis
Ascending infection, urethra (urine discharge), bladder (cystitis), ureters (tubes), kidneys (pyelonephritis and sepsis)
HAI UTI/UPEC pathogenesis
Ascending infection due to catheter restricting fast flow and rarely hematogenous UTI from blood infection
UPEC adhesion
Pap pili (pyelonephritis associated pili) for uroepithelial cell adhesion and mountain climbing, type 1 pili bind to bladder cells and promote invasion, Tamm-Horsfall protein/uromodulin (THP) most abundant urine protein to clear type 1 pili by binding, S fimbriae (sfa) bind intestinal epithelial cells
Other UPEC virulence
Hemolysin (HlyA) pore forming toxin causes damage in pyelonephritis and promotes invasion, LPS fatty acid bind O antigen core, mediates bladder colonization, resistance to hydrophobic antibiotics and toxins, siderophores, and K1 sialic acid capsule
UPEC prevention
Wipe front to back, pee after sex, cranberry juice prevent type 1 pili binding
UPEC treatment
Antibiotics, but disrupt normal colon/vagina flora, and spermicides inhibit lactobacillus
NMEC disease
Leading cause of infant meningitis
NMEC reservoir
Human GI/vagina
NMEC transmission
Like GBS, prenatal due to trauma or procedure, early onset due to exposure during delivery, and late onset due to caregivers or invasive devices
NMEC virulence
S fimbriae adhesion to EC components, IbeABC allows crossing of blood brain barrier, siderophores, and K1 sialic acid capsule
NMEC treatment
Antibiotics (no vaccine)
