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87 Cards in this Set

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Staph aureus
• G+, aerobic, cooci,
• Lives in the nostrils
• Can be opportunistic
• Normally lives on the skin or the mucous membranes, oropharynx,GI, urogenital tract
• Shedding common
• Major cause of infection of surgical wounds
• Resistant to dessication
• High heat, antiseptic and disinfectants sensitive
• Transmission directly or fomites
what are some of the extracellular proteins and enz and their function w/s. aureus
• Coagulase=bind thrombin and help clot
• Staphkinase/fibrolysin= inhibits clotting
• Lipases and penicillinase=drug resistance
• Catalse+= allows invasion
• Hylurodinase and nucleases=allow colonization andinvasion
how does one differentiate b/t staph and strptococci
staph is catalase + nd strep is not
what are some of the virulence factors in staph aureus
• Surface proteins that allow colonization, fibrinogen, fibronectin and collagen binding , these allow it to bind to the host
• Capsule, IG binding protein A, glycoacalys, peptidoglycan= slime layer and the capsule allow it to escape phagocytosis
• Toxin=like panton valentine leukicidin toxin that is responsible for causing necrotizing pneumonia, and toxic shock toxin, i.e. that causes toxic shock syndrome
what are the major diseases caused by staph aureus
• It can cause both community and nosocomial pneumonia
• It causes three types of pneumonia, community acquired, nosocomial, and hematogenous pneumonia
• It also called epmpyema
what are the characteristics of different pneumonias that caused by s.aureus
Community = usually after influenza, acute and often accompanied by empyema
Nosocomial= very young, aged, these people already have underlying respiratory disease, there are patchy infiltrates and abcesses
Hematogenous= common in patients with bacterimia or endocaditis
what is empyema
rare comlicaton associated with community acquired pneumonia caused by staph, it present with friction rub upon auscultation due to pus in pleural space, usually requires that pus be removed by inserting a tube
what is the diagnosis of nosocomial pneumonia caused by s. aureeus
• Test for clumping factor like coagulase, hemolysins, and thermostable deoxyribonucleosidase
• Latex agglutination
how are community and nosocomial s.aureus treated
• Penicillin or amox for methicillin sensitive this is community
• Vancomycin for methicillin resistant this nosocimial
community or nosocomial is methicillin resistant
nosocomial
how is spread of staphy. aureus controlled
• Isolated patient and staff that are infected, MRSA
• Patients are treated to eradicate carriage of MRSA
pseudomonas aeruginosa
• G –, bacilli, non fermentative, aerobic
• Ubiquitous
• Mainly infects ventilation equipment, people that aspire from those tubes can get pneumonia
• Can cause bacterimia
• Colonizes in respiratory and GI tract of hospital patients
• More than 50% produce pytocyanin
what is the exracellular enz with pseudomonas aeruginosa
oxidase +
what is the pathogenesis pseudomonas aeruginosa
• Normally a pathogen can be opportunistic
• Invasive and toxigenic
• Bacterial attachment and colonization
• Bloodstream dissemination and systemic diseases, it is important in people with chronic respiratory diseases like CF
• Most commonly found on the ventilation equipment
what are the virulence factors of pseudomonas aeruginosa
• Pigments= this makes blue (polycyanin), polyverdin (green) and polychelin (greenish yellow) pigments that are that are virulent
• Exotoxins
• Exoenzymes
• Proteases and hemolysins
clinical symptoms seen with pseudomonas aeruginosa
• Lower respiratory infections=second most common cause of nosocomial pneumonia, can be fatal or fulminant
• Necrotizing bronchopneumonia
• Bacterimia=dissemination from other sites, shock may develop, could cause bacterimic pneumonia, w/c can cause chills, fever, purulent sputum and productive cough
• Bilateral bronchopneumonia consisting of nodular infiltrates, cavitation w/ or w/out pleural effusion
• Lobar pneumonia uncommon
who is @ a higher risk with pseudomonas aeruginosa infection
• Immunocompromsied, CF, COPD patients
pseudomonas aeruginosa treatment
• 2 drug combo therapy= antipseudomonal beta-lactam and aminglycoside
BURKHOLDERIA SPP, how many subsets are there
• G -, bacillus, aerobic
• Mainly infects moist environment
• Used be considered pseudomonas
• 3 forms, pseudomallei, mallei, cepacia, galdioli
linicalwhat is the c disease B. pseudomallei
-causes MELIODOSIS, seen in the tropical climate, spreads via contaminated water and soil, can cause mild bronchitis- pneumonia
-normal sputum hall mark
mainly people with HIV and CF are effected by the blood borne type, this can lead to toxic shock
what is the clinical disease with mallei
-caused glanders
-picked by domestic animals, “possible bioterrorism weapon” , symptoms depend on the route of infection, can be pus forming cutaneous infection, pulmonary infections could be pneumonia and pulmonary abscess, blood stream infections can be fatal w/in 7 days
what is the clinical disease with B. cepacious
no disease, usually causes colonization
what is the disease B. gladioli
can cause respiratory infection in people with CF, chronic granulomatous disease, UTI in catherized patients, can colonize fluids in the hospital
how are diagnosis for pseudomallei and mallei made
• Pseudomallei=blood, sputum, urine, skin lesions
• Mallei=localized infections in the lobes of the lungs
what is the prevention
none, theres is not vaccine
what is the key with all burkholderia spp and bloof stream infections
lethal if the infection is in the blood stream
what is actinomyces israelii
• G+, anaerobic bacilli
• Fungus like, crooked filamntous branches
• Unable to invade health tissue
• Lives in mouth and intestinal tract
• Catalse +
• Pathogenic only when trauma is induced
• Can lead to actinomycosis
actinomyces israelii clinical symptoms
• Thoracic actinomycosis
• Fever
• Cough
• Purulent sputum
• Destroys lungs tissue and possible invasion of ribs
actinomyces israelii
• Look for specimen in pus, sputum, and look for sulfur granules in tissue specimens
• Cultur in brain-heart infusion agar
actinomyces israelii
• Must last many months, clinamycin and E-mycin
• Surgical exicision
nocardia spp
• Member of mycob and actinomyceae
• Weakly acid fast
• G+, rods, aerobic,
• Looks like actinomyces but temember that this acid fast
• Catalse, urease
nocardia spp virulence factors
• PG cell wall along with mesopiaminopimelic acid
• Urease
• Facultative intracellular in MAC
nocardia spp diagnosis
• Difficult, slow growt
• Mainly by gram stain, and acid wall stain
• Definitive=by isolating the organism from the sputum
• Wih acid fast test if you see branches it is Nocardia
nocardia spp s n s
• Nocardiosis, Pulmonary granulomas, abscesses, CNS abscesses as sequelae
nocardia spp treatment
• Surgical
• antimetabolites
Enterbactereriacae:
• G-, part of normal flora
• Soil, water, and vegetation
• Susceptible to drying
• Largest medically important family
• Mainly associated with intestinal infections
• Can be highly pathogenic
• Biostrips and enterotubes are used to ID them
what are the virulence factors of enterobacteria
• Endotoxin- lipid A component of LPS since it’s G-
• Capsule
• Ag variation
• Type 3 secretion system= it’s a syringe like mechanism, inject the secretion in the cell by piercing the membrane, so can’t be detected by the host’s immune response
• Sequestering of growth factors=Fe chelating, grabs the host’s Fe supply
what is unique about proteus
it is from enterobacter family
• Associated w/pneumonia in elderly and those with underlying disease
• Motile
• Non-lactose fermenting
• Lysine-
• H2S+
• Urease+
E-COLI:
• Lysine+
• Citrate-
• Indole, acetate, lactose+
• Treating E-coli with antibacterials can put the patient at severe risk or death because when you kill this bacteria, it will release toxins and that can cause many problems
SERRATIA MARCESENS:
• DNASE
• LIPASE
• GEALTINASE
• Resistant to many antibacterials due to the R-factor via plasmids
KELBSIELLA PNEUMONIAE:
• G-, facultative anaerobe, bacilli
• Non flagellated
• Large polysaccharide capsule
• Bet lactamase +
• Lives in respiratory and enteric tracts
• Aspired or inhaled, via respiratory droplets
what are some of the risk factors of klensiella
• Homeless, diabetics, immunocompromised
• Hospitalized patients
what are some of the clinical signs of klebsiella
• Can cause both community (for homeless, diabetics, and immunocompromised) and nosocomial pneumonia (hospitalized patients on ventilators)
-Nosocomial= necrotizing destruction of the alveolar spaces and cavity formation, currant jelly sputum aka muccoid, blood tinged bacterimia, high fatality rate
how is klebsiella diagnosed
• Gram stain
• Must differentiate this from other members of Enterbactericae via biochemical tests
• Must do drug sescpetibility tests since this is B-lactamase producer
what is prevention strategy for klebsiella
• No vaccine
• Can be treated with multiple antibacterials since it does have resistance to many antibiotics
what are the major causes of atypical pneumonia
MYCOPLASMA SPP., CHALYMYDIA SPP., AND LEGIONELLA
MYCOPLASMA PNEUMONIAE:
• Cell wall less, must differentiate form mycobacterium w/c is ACID FASt
• Rod
• Cholesterol like molecule in plasma
• Doubling time 6hrs
• Requires that growth media must contain serum
• Membrane proteins, glucolipids and lipoglycans are the major Ag determinants
what is an absolute growth requirement for MYCOPLASMA PNEUMONIAE:
serum to be added to the Agar
MYCOPLASMA PNEUMONIAE virulence factors
• P1 antigen= allows adhesion to the host’s respiratory epithelia
• Cytotoxicity is due to host’sresponse
MYCOPLASMA PNEUMONIAE transmission
• Person – person, by contact w/respiratory secretions
what population are at risk for MYCOPLASMA PNEUMONIAE infections
• Mainly in military or college students
• Also leading cause of problems in school children
MYCOPLASMA PNEUMONIAE:clincal S n S
• URT infections like pharyngitis, otitis, atypical pneumonia
• Lingering symptoms of malaise, cough, cold longer than 7 days, so this make it different frominfluenza
• Scattered rhonci= rattling sound when breathing
• Localized rales
• Wheezing = this is not characteristic of bacterial infection
• Sequelae= scute chest syndrome, persistent cough during convalescence
how do you differentiate MYCOPLASMA PNEUMONIAE symptoms this from influenza
lingering infection that last longer than 7 days
MYCOPLASMA PNEUMONIAE diagnosis
• Main test is cold agglutination with convalescent and acute sera to measure the antibody titer of IgM
- culture looks like fried egg colonies or mullberry
is mycoplasma pneumoniae associated with anyother syndromes
yes, it is calleed the Raynaud's symptom
when is it raynaud's symptom and when is it associated with mycoplasm
it you just have bronchspasm, then it is just raynaud's
CHLAMYDIA SPECIES:
• G-, obligate intracellular parasite, inert on the outside
• Avoids death via prevention of formation of phagolysosome
• LPS, genus specific
• Called energy parasite b/c it relies on the host’s ATP
• Growth in culture requires cells
• It will only grow inside a cell
• Infectious stage is extracellular and called elementary body,it is a tough spore like formation, it fuses with a cell and becomes a reticular body , it is metabolically inert until it gets in to a cell
• Reticular body is not the infectious stage, it is replicative, R= replicative, reticular, it marks the intracellular replicative stage of Chlamydia spp, this is metabolically active and has lots of ribosomes
• Once the reticular body gets out it becomes elementary, and becomes pathogenic
• Mainly spread via respiratory secretions and aerosol and direct contact
CHLAMYDIA pneumoniae
spread thru respiratory droplets, and direst contact as an ocular infection, this is not spread sexually, causes atypical pneumonia and bronch/pharung/sinusitis, minor s n s but chest x-rays show massive bilateral infiltrates
CHLAMYDIA psittaci
form infected birds, spread by respiratory secretions, causes atypical pneumonia and bronch/pharung/sinusitis, minor s n s but chest x-rays show massive bilateral infiltrates
CHLAMYDIA tarchmattis
sexually transmitted, genital and ocular infections, trachoma, chronic inflammation of the eye due to hand eye contact, can lead to blindness, most common cause of pneumonia in new born, atypical pneumonia 5-25 weeks after
what is prevention strategy for chlymydia spp
• For C. psittaci, controlling the infection in the birds can help
• For C. trachomatis, safe sex, also it can occur w/recurrent gonorrhea infections
• For C. pneumonia, antibiotic treatment should be prolonged to at least 2-3 weeks
Sequelae= for C. pneumoniae, infections may be associated with atherosclerotic changes, Alzheimmer’s. asthma, and reactive arthritis
whata are the sequelae associated with chlamydia pneuminiae
for C. pneumoniae, infections may be associated with atherosclerotic changes, Alzheimmer’s. asthma, and reactive arthritis
BACILLUS ANTHRACIS
• G+, spore forming rods, aerobic
• Capsule but its not a polysaccharide, it is a poly-d-glutamate
• Non-motile, non-hemolytic
• When treated it must be treated for 60 days b/s it is a spore former and the spores can break up into vegetative cells, the treatment does nothing for the spore but is effective for the vegetative cell
-woorster's disease
BACILLUS ANTHRACIS virulence factors
• Poly-D capsule is anti phagocytic
• Exotoxins like EF(edema factor), LF(lethal factor), and PA(protective Ag), all of these combined are called anthrax factor
• PA= binds to the receptors, LF= has the Zn and MAPKK activity, and EF= adenlyl cyclase activity
• PA+ LF= produce lethal activity
• EF+PA= produce edema
• All three combined will produce edema, necrosis, and is lethal
• EF+LF=these will inhibit the PMN from engulfing and launching a respiratory burst
• Human anthrax receptor binds the PA portion of the toxin
• The toxins get in through different endosomal models depending on the pH, CMG2 toxin likes lower pH i.e acidic conditions as opposed to TEM8 w/c likes pH of 6
BACILLUS ANTHRACIS transmission
• Zoonotic,
• Bioterrorism
• Spores can live for decades
• Person-person spread doesn’t occur
BACILLUS ANTHRACIS clinical symptoms
• Incubates for 2-3 days
• Malaise with mild fever, chest pain
• Massive chest edema
• Widened mediastinum
BACILLUS ANTHRACIS diagnosis
• Gram stain on blood agar form the blood of patient
• Look for widened mediastinum
• Test for motility, look for lysis by gamma phage= w/c is no hemolysis
• It must be differentiated from B.cereus and that’s done by the factors like, thiamin requirement, glutamyl-polypeptide capsule, lysis by gamma phage, and string of pearl test, also remember gamma lysis meas there is no hemolysis and B-cereus has hemolysis
• Test for poly-D glutamly capseule via Mcfayden reaction
BACILLUS ANTHRACIS prevention strategy
• Vaccine for PA portion of the toxin
• Mainly given to the healthcare professionalism, or vets or military person deployed to the endemic regions
FRANCISELLA TULARENSIS
causes tularemia
• G-,
• Thin glycocalyx
• Requires cysteine for growth
• Endotoxin
• Localized in reticuloendothelial cells
FRANCISELLA TULARENSIS transmission and risk factors
• Zoonotic
• Arthropod transmission= deer flies or tick bite
• Handling infected cotton tail rabbits
• Ingesting contaminated food
-hunters at risk
FRANCISELLA TULARENSIS, signs and symptoms, different type sof disease
• Tularemia
• Two types
• Ulceroglandular= swelling of regional lymph nodes, skin lesions as papules, papules are necrotic at the centers with raised edges, fever chills and sweating and cough
• Pneumonic tularemia= due to already existing respiratory problems or inhalation via aerosols
FRANCISELLA TULARENSIS diagnosis
• Blood specimen
• Handled as biohazard, only in a level 3 lab
• Requires glcose-cysteine-blood agar
• Microagglutination with IgM
• Forshay’s test= + test w/in 7 days
FRANCISELLA TULARENSIS prevention
• Avoid exposure
• Protective clothing and insect repellent
• Timely removal of ticks
• Vaccine live attenutated but only given to high risk
LEGIONAELLA PNEUMOPHILIA: LEGIONARIES’S DISEASE
• G-, coccabacilli,
• Fastidious growth- iron salts and cysteine
• Nonfermetative
• Intracellular parasite that effects the alveolar MAC and monocytes
LEGIONAELLA PNEUMOPHILIA virulence factors
• Capsule
• Endotoxin
• Enzymes, phosphatase
• Lipase and nucleas
• Aquatic habitat, parasites of amoeba
• Survives high temp and high level of Cl-
• 50% are human pathogens
• Cause many nosocomial infections
LEGIONAELLA PNEUMOPHILIA transmission
• Inhalation of aerosols
• No person-person
LEGIONAELLA PNEUMOPHILIA risk factor
• Middle ages or older than 55
• Immunocompromised
• Alcoholics
• Smokers
• COP
• Diabetics
• Transplant patients
LEGIONAELLA PNEUMOPHILIA signs and symptoms
• Legionaire disease= Fever chills, non-productive sputum, cough, myalgia, pneumonia and pleural effusion, somnolence, delirium, confusion
• Pontiac fever= shorter incubation, similar to flu, chills, fever, and myalgia, NO GI TRACT MANIFESTATIONS, NO CNS MANIFESTATIONS, self limiting, no pneumonia, no lung abscess, no renal problems
LEGIONAELLA PNEUMOPHILIA diagnosis
• Silver impregnation stain, DFA test
• Nucleic acid probes
• Culture= growth on buffered charcoal yeast extract
• Id through cell wall fatty acids and DNA homology
• Definitve= diagnosis of pneumonia through CXR and positive lab test
• CDC lab criteria for diagnosis= isolation of LDB from respiratory secretions, lung tissues, pleural fluids, four fold increase in antibody against Legionella pneumophilia serogroup 1 between paired acute and convalescent sera, and demonstration of this via RIA or ELISA
prevention strategies of legionella
• No vaccine
• Hyper chlorination or increased water temp
• copper –silver ionization of water
YERSINIA PESTIS:
cause pneumonic plague
YERSINIA PESTIS:
• causes plague
• first ID from hong kong
• all cases of plague in US have been zoonotic
• mainly in Mexico, Arizona, Utah
YERSINIA PESTIS transmission
• zoonotic urban or sylvanic (wild )
• rats are the most important reservoirs
• rat flea or xenopsylla cheopsis is the most important vector
• or xenopsylla Montana that bite the rat, pick up it’s blood and then bite the human and regyrgitates in to human cell
YERSINIA PESTIS: virulence factor
• capsule
• coagulase
• YOP= yersisnia outer proteins, these are injected into the host cell via injectosome
• type 3 injection systems that allows it to inject it’s its content into the cytoplasm with out + an immune response
YERSINIA PESTIS: risk factor
• flea bite
• contact with the patient or sick animal
• outdoor activities
• researchers or vets
YERSINIA PESTIS clincal disease
• there are 3 different types of plagues
• bubonic= due to the bite, chills, swollen LN, 2-6 days of flea bite, fatal 14%
• septicemic plague= spread through blood, this is ID by the blood culture, 30-50% fatal
• primary pneumonic plague= rare form of the plague, person-person spread via respiratory droplets, fever, malaise, dyspnea, 90% fatal
yersinia pestis diagnosis
• CIN,= cefulosan, irgasan, novobiocin
• Cold enrichment for yersinia
• Bipolar or safety pin type of appearance