Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
micro module 5
bacterial diseases
| Question | Answer |
|---|---|
| Respiratory tract: URT consists of what; what microbes live here in URT; LRT consists of what; what lives in LRT | nasal cavity to larynx; contains indigenous flora; trachea to the lungs; should be sterile |
| transmission of respiratory infection: transmission by direct method; transmission by indirect method; | from close personal contact, transfer of secretions, contaminated hands, or inhalation of airborne droplets; from fomites; |
| dissemination of some organisms infecting the respiratory tract: where are microbes colonizing first; where does it move next; after mucus where do they move; after bacteria is in the blooc where can they go to nect | nasalpharyngeal colonization; the mucus epithemium; blood; the CSG and tissues |
| def of bacteremia; does this damage BV | living bacteria in the blood stream; no they are just surviving and living in the blood stream |
| respiratory tract is primary entry point for what | all other infections in the body |
| URT bacterial diseases: Diptheria- acute or chronic; is it contagious; etiologic agent; transmission; | acute; yes; Corynebacterium diptheriae; inhalation of contaminated respiratory droplets; |
| URT bacterial diseases: Diptheria- gram stain; isw there a vaccine; whatare the 2 stages; | positve non-spore forming bacilli; yes; local infection or toxin production; |
| URT bacterial diseases: Diptheria- mild- what happens after organism enters URT; bacteria start to sectrete what; what are the 2 types of exotoxins; | infection occurs b/c organism colonizes in URT and is dividing; exotoxins; A and B; |
| A and B exotoxins: B means what; A means what | organism can bind to host cells (epithelium cells); active- it crosses host cell membrane and enters the cell |
| URT bacterial diseases: Diptheria- what does B exotoxin do; what does A cell do; what does inhibition of protein synthesis do | binds to host cells; it crosses cell membrane and inhibits ribosome function; inhibits protein synthesis and dies; |
| URT bacterial diseases: Diptheria- what happens as cell death accumulates; what does the pseudomembrane look like; the pseudomemebrane can block what; | a pseudomembrane forms in throat; yellows white area in oropharynx cellular debris and enzymes; respiratory blockage |
| URT bacterial diseases: Diptheria- A exotoxin can enter what; CMs of enterence in bloodstream; why can respiratory failure occur | the bloodstream; it can damage endothelial lining of the heart and myelin sheath in nerves; b/c of damage to the myelin sheath around nerves in that area of the body |
| URT bacterial diseases: Diptheria- tx;preventions; can boosters be given; what is toxoid; | abx and antitoxins; DTaP vaccine; yes; the exotoxins that are modified and given in a vaccien so be can produce antibodies against them |
| antitoxin def | antibodies that will coat the toxin and neutralize it so it cannot enter the cells |
| def of DTaP | diptheria toxoid, tetanus, and acellular pertussis vaccine |
| URT bacterial diseases: pertussis- aka; etiologic agent; transmission; is it contagious; who gets it most often; organism starts where and travels to where; | whooping cough; Bardetella pertussis; respiratory droplets; highly infections; children; URT travels to LRT |
| URT bacterial diseases: pertussis- how does bacteria get into the URT; what does organism do once in URT; once colonized in the URT what do the organisms start releasing; what do the cytotoxins do; since the cilia do not move what happens; | droplet inhalation; colonizes in area and reproduces; cytotxins; paralyze ciliated cells into respiratory tract; mucous is stucky and organisms can stay in area |
| URT bacterial diseases: pertussis- what is s/s of paralyzed cilia; why is there a whoop sound; stagnent mucous blocks what; sequela | rapid fire coughing with exhaleation and whoop sound with inhalation; b/c mucous is still present; airway; LRT PNA; |
| URT bacterial diseases: pertussis- Dx; tx; prevention; the vaccine immunity wanes when; is there a high mortality rate | fluerescent antibody test and culture w/ throat swab; ABX;DTaP;in about 5-10 years after vaccine receives and boosters required; yes |
| URT bacterial diseases: pertussis- why is the acellular vaccine safer; peak occurance; | b/c only part of the cell is given and reduces the risk for side effects; september |
| URT bacterial diseases: group A streptococci- etiologic agent; is it painful; aka; gram stain; | streptococcus pyogenes; yes and self limiting; GAS: gram + streptococci |
| what does self limiting mean | immune system can irradicate the infection w/o tx |
| URT bacterial diseases: group A streptococci- pathogenicity is enhanced by what; Dx; what does capsule do; what does M protein do; | capsule, pili, M protein, hemolysins, other toxins;quick antigen tests, cultures, bacitracin; adhere it to cells; allows organism to adhere to cells and destroy them |
| URT bacterial diseases: group A streptococci- what is hemolysis pattern; what does toxin dnase do; what does quick antigen test do; what does bacitracin disk do; | beta hemolysis; destroy the DNA on the cell; it identifies the known infectious organism; show that organism is sensitive to disc |
| URT bacterial diseases: group A streptococci- Tx; why is tx easy; for organisms that are not very resistant what tx should be used; what diseases this causes; | penicillin or erythromycin; little resistance to ABx; use oldest ABX first; strep throat, skin, muscle, blood diseases |
| URT bacterial diseases: group A streptococci- sequelae; scarlet fever is causes by what; who gets scarlet fever; | scarlet fever rheumatic fever and glomerulonephritis; erythrogenic exotoxin producing strain; very young; |
| URT bacterial diseases: group A streptococci- scarlet fever- how does erythrogenic exotoxin cause a rash; | it damages capillary wall and causes inflamation with increased capillary permeability at top layer of skin causing rash |
| URT bacterial diseases: group A streptococci- what causes rheumatic fever and glomerulonephritis; in rheumatic fever Abs cross react with what; in glomerulonephritis whatis damaged; | inflammatory response to specific M proteins; with heart tissue causing inflammation; nephrons usually short term but some go into kidney failure |
| URT bacterial diseases: group A streptococci- how long does someone have glomerular nephritis; what sequelae is long term | 4-6 weeks; rheumatic fever |
| LRT bacterial diseases: PNA- def; what are some lung defenses; etiologic agents; | impairement of lung defense mechanisms can lead to PNA; cough reflex, mucocilliary clearance, macrophage phagocytosis, inflammatory response; viruses, bacteria, fungi, and chemicals |
| LRT bacterial diseases: PNA- what happens to alveoli and respiratory membranes; is there increased or decreased perfusion ratio; decreased ventilation/perfusion ratio leads to what; alveoli made of what type of cell; what surrounded epithelial cells; | they will fill with fluid; decreased; hypoxema and hypercapnia; squamous epithelial cells; basement membrane |
| LRT bacterial diseases: PNA- where does fluid accumulate; basement membrane aka; def of lobar pna; def of double pna; def of broncho- pna; what is most common pna | the basement membrane; respiratory membrane; entire lobe; R and L lung; patches of infection in resp. passageways; broncho-pna |
| def of hypoxemia | decreased oxygen in the blood |
| def of hypercapnea | increased Co2 in blood |
| LRT bacterial diseases: PNA- what has more damage bacteria or viral pna; why is viral pna less severe; | bacteria; b/c there is less tissue damage; |
| LRT bacterial diseases: PNA- how many deaths per year; complications; | 40,000s/ year; absesses, bacteremia, pleural effusions, pneumothorax, respiratory failure, |
| compare/ contrast viral and bacterial PNA-def viral; def bacterial | mild, self limiting pna, less tissue damage, can develop secondary bacterial pna; acute, severe pna due to increased tissue damamge |
| compare/ contrast viral and bacterial PNA- mode of transmission - - viral ; bacterial | droplet inhalation; droplet inhalation |
| compare/ contrast viral and bacterial PNA - who is at high risk: viral; bacteria | young, elderly, immunocomprimised; young, eldery and immunocomprimised; |
| compare/ contrast viral and bacterial PNA: CMs - - viral; bacterial; | low grade fever, non productive cough, chest pain, chills, fatigue, SOB and decreases sputum; high grade fever, productive cough, chest pain, chills, fatique, SOB, and increased sputum |
| def exogenous; def of endogenous | inhaling the organisms from outside of body to inside of body (pna); movign organism from URT to LRT (pna) |
| compare/ contrast viral and bacterial PNA- sputum- viral; bacterial | decreased sputum, no baceria, lymphocytes; increased sputum that is yellow and rust colored due to blood and tissue damage, bacteria, neutraphils and macrophages; |
| compare/ contrast viral and bacterial PNA - tx: viral; bacterial | supportive, antiviral meds in some cases; supportive, abx |
| def atypical pna | presenting as viral ppna (may be caused by both virus or bacteria) |
| pna: what are supportive tx | fluid oxygen, nebulizers |
| compare/ contrast viral and bacterial PNA- ex. of etiologic agents: viral, bacteria | infuenza virus, RSV, others; streptococcys pneumoniae, E. coli, klebsiella pneumoniae, pseudomonas aeruginosa, mycoplasma pneumoniae, |
| pna: what bacterial agent presents as and atypical pna | mycoplasma pneumoniae |
| LRT bacterial diseases: pneumococcal pna- most common agent of what; etiological agent; how many serotypes are there; gram stain; what is the hemolytic pattern; does it have a capsule; is it optochin sensitive | bacterial pna; streptococcus pneumoniae; >90; gram + diplococci, alpha; yes; optochin sensitive |
| LRT bacterial diseases: pneumococcal pna- who is predisposed to this pna; this is a potential sources for what other infection; | malnutrition, smoking, viral infections, and immunosuppressive tx; bacterial meningitis; |
| LRT bacterial diseases: pneumococcal pna- tx for nonresistant strains; tx for resistant strains; prevention; | simple abx tc; susceptibility testing needed to know what agents will destroy it; vaccination for elderly and young, prevents 23 serotypes |
| LRT bacterial diseases: pna haemophilus influenzae- gram stain; who is at risk; | gram neg. bacillus; elderly and immunocompromised |
| LRT bacterial diseases: pna staphylococcus aureus- gram stain; who is at risk | grma + cocci; common nosocomial pna |
| LRT bacterial diseases: pna klebsiella pneumoniae- grma stain; who is at risk | gram neg. baccillus; increased in alcoholics or those with impaired pulmonary function and nosocomial pna |
| LRT bacterial diseases: atypical bacterial pna- what is onset like; CMS; def myalgia | gradually onset and slow; fever, dry cough, decreased sputum, Ha, myalgia, patch involment of lungs, less tissue damage usually; muscle pain |
| LRT bacterial diseases: legionnaires' disease: aka; mortality rate; etiologic agent; diseases itc can causes; what disease is most virulent; what disease is milder | legionellosis; 15-20%; legionella pneumonphila; legionnaires disease and pontiac fever; legionnaires; pontiac |
| LRT bacterial diseases: legionnaires' disease: transmission; ex of aerosols; is it spread person to person; can outbreaks occur; cms | aerosols; water collection systems, filters, hot tubs; no; yes; atypical pna and CNS in some |
| LRT bacterial diseases: legionnaires' disease: what does it do to cells; who gets CNA involvement; does it have a high death rate; it enters cells and does what | it enters cells; ppl who are immunocomprimised ; yes; destroys them |
| LRT bacterial diseases: chlamydial pna- etiologic agent; is bacterium small or large; what type of parasite; | all chlamydia sp; small; obligate intracellular parasite; |
| LRT bacterial diseases: chlamydial pna- chlamydia psittaci- causes what in parrots; humans acqure what; how do we get infection; what type of pna;outcome | psittacosis; zoonotic lung infection; inhalation contaminated dust and bird feces; atypical; good |
| LRT bacterial diseases: chlamydial pna- C. pneumoniae- causes what; is it common; what type of pna; how is it transmitted; who is at risk | chlamydial pna; yes; atypical; human to human; young adults b/c of social behavior |
| LRT bacterial diseases: chlamydial pna- tx; tetracycline treats what bacterial ;dx; what is serological testing | tetracycline for a few weeks; used for intracellular parasite bacteria; serological ID; ID the antigens |
| LRT bacterial diseases: Mycoplasma pneumoniae- what type of pna does it cause; it is the smallest what; how is it acquired; aka; what is unique about the structure; what can happen with out a cell wall | primary atypical; bacteria; in the community; walking pna; no cell wall; it is pleomorphic (many shapes); |
| LRT bacterial diseases: Mycoplasma pneumoniae- how Dx; s/s; what are immunofleorescnets; when disease s/s most prodominent; | s/s b/c culture takes a few weeks and immunofleurescents; dry cough, low grade fever, little sputum production; looking for antigens and antibodies; later in disease |
| LRT bacterial diseases: Mycoplasma pneumoniae- how is it passed from humans to human; can others get disease; nost common in who; can it be gram stained; why most common in teens | droplets; no; children and teens; no; b/c it is a common bacteria |
| LRT bacterial diseases: Mycoplasma pneumoniae- do we have lifelong immunity; what type of pna; what season is it most common; tx; what happens if you do not finish tx; | no; atypical (presents as a viral pna; year round; erythromycin and tretrocycline; the pt can be reinfected and infect others |
| LRT: Tuberculosis: what does extra pulmonary TB mean; kills how many per year; how many are infected annually; transmission; where is organism inhaled into; | many systems throughout the body are infected ; 2 mill; 2 bill; airborne droplets; alveoli |
| LRT: Tuberculosis: usually what type of exposure is needed for one to develop disease; etiologic agent; how long is generation time; what does the generation time mean; slow or fact grower; | repeated re-exposure to develop; mycobacterium tuberculosis; 16-20 hours; the organism doubles every 16-20 hours; slow grower long incubation period; |
| LRT: Tuberculosis: what stain is done on organism; why is acid fast stain done; shape of organism; is this acid fast positive or negative; Dx; what does TB skin test show; | acid fast; b/c there is a high mycolic acid content in the cell wall and this allows the organism to resist acid alcohol decolorazation; bacilli; positive; chest x-ray, sputum cultures, TB skin test, cat scan, biopsy; that person has only been exposed; |
| LRT: Tuberculosis: how long does a culture take; what is a faster way to identify; what are genetic probes; how long does it take to get genetic ID; | 6-8 weeks; through genetic probes; the genetic genome of organism;4-6 hours |
| LRT: Tuberculosis: primary stage of disease- what has to be done for one to get organism; what cell in body phagocytizes bacteria once in lungs; what does bacteria do once in macrophage; | inhalation of bacilli laden airborne droplets into lungs; macrophage; it divides in it; |
| LRT: Tuberculosis: primary stage of disease- the dividing in the macrophage causes what s/s; the acute inflammation is simmilar to what disease; what happens to the infected macrophages | acute inflammation; PNA; they fuse together and form a large cell |
| LRT: Tuberculosis: primary stage of disease- what is the large cell of macrophages called; phagocytic cells in the body release what around the tubercle; what happens as the tubercle hardens and as enzymes are released; why does the tubercle become large; | tubercle; enzymes; the center breaks down; b/c the body is trying to heal the inflamed tissue and scar tissue forms |
| LRT: Tuberculosis: primary stage of disease- what happens as the tubercles break apart; who is at risk for disease spreading to other parts of the body; def of tubercle; | the bacilli is released and can cause more tubercles in the lungs; immunocomprimised; macrophages, lymphocytes, bacilli, fibrous tissue, calcium; |
| LRT: Tuberculosis: primary stage of disease- what is the appearance when the tubercle center breaks down; when does organism spread in lungs; def extrapulmonay Tb; extrapulmonary TB aka; | it is caseous or cheesy in appearance; when center breaks down; it is spread throughout the body; miliary TB; |
| LRT: Tuberculosis: miliary stage of disease- where can the bacteria spread to; what happens if immune system cannot contain infection in the lungs; | liver, kidney, meninges and bone; systemic infection |
| LRT: Tuberculosis: how long is intitial tx; how long is second phase of tx; what are the 4 drugs used; multidrug resistant TB strains needs what tx; ex of XDR stain; | 2-4 months; 4-7 months; isoniazid, rifampin, pyrazinamide, ethambutol; more modified; this is drug resistant strain |
| LRT: Tuberculosis: prphylactic tx is used for whom; what is drug used for prophylactic tx; preventions; how effective is the vaccine; is skin test positive with vaccine | others that come into contact with somone with active disease; rifampin; positive skin test used to help screen for exposure, vaccine; only 50% effective; yes |
| dissemination of some organisms infecting the respiratory tract: list where organism infects first to last; | nasopgaryngeal conolization, invasion of mucus/epithelium, bacteremia, CSF and tissues; |
| does bacteremia mean there is a disease | no, it just means there is an infection of the blood, body can still irraticate organism |
| bacterial meningitis: etiological agents; how does one get disease | neisseria meningitis, haemophilus influenzae (type B), streptococcus pneumoniae; URI disseminations to bacteremia and then to meningitis |
| bacterial meningitis: what etiologic agent is indigineous flora; what etiologic agent is most commone; what % of pple carry neisseria meningitis; what etiologic agent is declineing; | neisseria meningitis; neisseria meningitis; 20%; haemophilus infuenzae |
| commpare and contrast viral and bacterial meningitis: what one is most common; what one has less tissue damage; what one is serious; what one is fatal; what one has a higher fever | viral; viral; both; bacterial; bacterial |
| commpare and contrast viral and bacterial meningitis: viral- how long does it last; spread by what; what is etiologic agent; CMS; tx | 7-10 days; contaminated respiratory secretions; multiple viruses (ex intestines); fever, HA< stiff neck, light sensitivity, N/V; supportive, possibly antiviral meds; |
| commpare and contrast viral and bacterial meningitis: bacterial- how long does it last; spread by what; what is etiologic agent; CMS; tx | acute onset ; contaminated respiratory secretions; 3 primary ones; similar to viral plus confusion, sleepiness, bruises under skin; antimicrobials and supportive; |
| exogenous def | outside body |
| indigenous | inside body |
| bacterial meningitis: symptoms are variable for what age; classic CMs; s/s of stiff neck; s/s of neurologic deficits; s/s <2 yo | <2 yo; high fever, HA, stiff neck, sensitivity to bright lights, N/V, neurologic deficits; difficulty turing head touching chin to neck; seizures, confusion; irratibility, inactivty, loss of appetite |
| Septicemia: from bacteremia depending on toxins released this can cause what; what is difference from bacteremia; septicemia causes what; | septicemia; there are s/s and infection with growth and spreading of bacterial cells in blood ; organ failure, meningitis; |
| Septicemia: CMs; why can septic shock occur; | spiking fever (cyclic variation up and down), chills, rapid breathing, rapid heart rate; b/c as body is fighting infection increase of release of cytokines cause this |
| Septicemia: increase release of cytokines is aka; | cytokine storm; |
| septic shock- gram - bacterial septicemia: when bacteria die what is there an increase of in circulation; macrophage release an increase of what in response to lipid A; the increased release of cytokines causes what; | lipid A released from bacterial cell wall as it dies; cytokines; circulatory and respiratory collapse, ischemia hypoxia and death |
| bacterial meningitis: meningococcal meningitis- etiologic agent; trasmission; where is there an increased risk; is this common or rare; gram stain; shape; why at risk in crowds; | neisseria meningitis; respiratory droplets; crowds, classrooms, camps, dorms, military; rare; negative; diplococci; b/c there are carriers in population (20%) |
| bacterial meningitis: meningococcal meningitis-URT infection is first and this has what s/s; the URT infection leads to what; after sepsis the bacteria bind to the meninges causing what; | influenza s/s; sepsis; meningitis; |
| bacterial meningitis: meningococcal meningitis- s/s; what is cause of rash; petechiae means person has had disease for how long; what syndrome can occur in young children | classic plus skin rash; petechiase caused by capillary hemorrhaging; late in disease and this is not a good sign; waterhouse-friderichsen syndrome; |
| meningococcal meningitis- waterhouse friderichsen syndrome- def; common in whom; cms ok decreased aldosterone; | adrenal gland lesions develop due to release of bacterial endotoxin into the blood; inflants/young children; hypovolemia, orthostatic hypotension, tachycardia, hyponatremia, hyperkalemia, death in 10-12 hours due to shock; cortisol, aldosterone, epinephri |
| meningococcal meningitis- waterhouse friderichsen syndrome- aldosterone does what to body; | effects the kidneys and if high ammount is being released then sodium is released and hypotension occurs; |
| bacterial meningitis: meningococcal meningitis- high mortality rate when; what can persist in survivors; dx; tx; who should be vaccinated; what does petechiae look like; | if not treated; neurophathies, hearing loss and seizures; culture ID serological antigen testing for quick results; penicillin, 3rd generation cephalosporins; college students, military recruits, those in large crowds; red, blue/black spots due to capilla |
| bacterial meningitis: haemophilus meningitis- etiolotic agent; gram stain; does it have a capsule; shape; transmission; what age is at risk; | maemophilus influenzae type B; negative; yes; baccili; resp. droplets human to human; <5 yo; |
| bacterial meningitis: haemophilus meningitis- an URT infection can lead to this how; why does an older pt not get it; rapid or slow onset; | disseminates in bacteriemia and then meningococcemia; we have been exposed; rapid; |
| bacterial meningitis: haemophilus meningitis- CMs; what s/s is not common for this type; what airway s/s does it cause; what is s/s in ears; | classic ones of bacterial Meningitis; petechiae; epiglottitis; otitis media |
| bacterial meningitis: haemophilus meningitis- dx; Tx; prevention | thebacteria is in CSF, serological ID, cultures; 3rd generation cephalosporins; vaccine (in DTaP |
| why are 3rd generation cephalosporins used | they are small enough to cross the blood brain barrier |
| bacterial meningitis: Pneumoccoccal meningitis- etiolotic agent; gram stain; shape; transmission; who is at high risk | streptococcus pneumoniae; gram -; diplococci; contaminated respiratory secretions; <2 yo, elderly and immunocomprimised; |
| bacterial meningitis: haemophilus meningitis- diseases this bacteria can cause; tx; prevention; | bacterial pna, otitis media, septicemia, meningitis; penicillin, quinolones; vaccine |
| bacterial meningitis by age group: newborns; greater than one month; why does newborn get these ones; | streptococcus agalactiae (grp. B strep), E. Coli, listeria moncytogenes; streptococcus pneumoniae; Neisseria meningitidis, others, haemophilus; b/c they can be picked up from vaginal flora from mom; |
| food intoxication def; why is the organism not the problem; do toxins cause a quick or slow onset; | a disease caused by bacterial toxins being ingested the organism is not the problem b/c it is the toxins that they secrete that causes s/s; quick |
| staphylococcal food poisoning: staphylococcus aureus- number 1 what;caused by what; how long is incubation; this toxin can withstand how much heat; | food poisening in US; enterotoxin ingestion (exotoxin in the food); 1-6 hours; 100 degrees C for 30 minutes; |
| staphylococcal food poisoning: staphylococcus aureus- how is it distributed to food; what does enterotoxin mean; after incubation what are s/s; how long do s/s last; | from cough and sneeze, b/c the organism is found in our nares; it is found in the intestines; abdominal cramping, N/V, diarrhea; 8 hours; |
| staphylococcal food poisoning: staphylococcus aureus- prevention; is there any change in food, any change in odor; Tx; | protect food from contamination by organism; no; no tx for healthy adults, required infants and elderly may require supportive tx (fuilds and electrolytes) |
| food borne botulism: etiologic agent; oxygen requirements; does it form spores; gram stain; shape; infection caused by what; | clostridium botulinum; anaerobic; yes; postive; bacilli; neurotoxin ingestion not the organism |
| food borne botulism: this neurotoxin is significant how; what destroys it; | it is the most potent neurotoxin; it is inactivated by boiling the food products; |
| food borne botulism: improper canning can cause what; when do s/s occur; the neortoxin does what to somatic motor neurons; decrease of ACh causes what | the organism germinates and neurotoxin is secreted; 18-36 hours after ingestion; prevents acetylocholine from being secreted; flaccid paralysis |
| food borne botulism: CMs; tx; what is early on s/s; will our immune system help us; | skeletal muscle weakness, blurred or double vision, swallowing difficulties, faccid paralysis, respiratory arrest; antitoxin and respiratory support; weakness, double vision, swallowing difficulties; no; |
| other types of botulism: wound- is this comon; transmission; once in wound what is produced; neurotoxins go where; once in blood what is s/s; how long until s/s and noted; | no; how does it enter body; enters an anarobic wound with necrotic tissue; neurotoxin production; blood; flaccid paralysis; week |
| other types of botulism: infant- is this common; how do they get infected; what may they ingest; the organism enters that intestines and then does what; | yes; they ingest clostridial spores; fresh honey, soil; germinates and secretes that neurotoxin; |
| other types of botulism: infant- when are s/s; once toxins enter the blood stream what happens; the muscle paralysis in babies is aka; tx; do they require an antitoxin; | with in 1-2 days; muscle paralysis; floppy baby syndrome; hospitalize and supportive therapy; no; |
| clostridiual food poisoning: etiologic agent; agent also causes what other disease; #2 what; infection caused by what; gram stain; shape; oxygen requirements | clostridium perfrigens; gas gangrene; food poisening agent; the enterotoxin not microbe itself; gram +; bacilli; anaerobe |
| clostridiual food poisoning: what has to be ingested; when are s/s noticed; s/s after 8-24 hours; when is recovery; | the toxin to get food poisening; with in 8-24 hours; abdom. cramping, diarrhea; about 24 hours; |
| clostridiual food poisoning: tx; what food usually is contaminated; common in what setting;s why common in buffets; | none needed body recovers on its own; meat, poultry and beans; buffets; b/c food is not maintained at proper temp; |
| food borne and water borne: does it have a longer or shorter incubation time that intoxications; what must happen before s/s appearl | longer; bacteria must multiply |
| food borne and water borne: typhoid fever: aka; etiologic agent; who is the host; gram stain; shape; why is it important that it is acid resistant; | enteric fever; salmonella typhi; humans; negative; bacilli; it can survive our gastric juices |
| food borne and water borne: typhoid fever: how does it enter s. intestines; how does food and water get contaminated; once in intestines where does it travel; | from contaminated food and water; faulty sewage and water systems also uncooked shellfish, raw fruit and veggies; blood; |
| food borne and water borne: typhoid fever: transmitted by what five Fs; Cms; rose spots are s/s of what; is a large dose needed to becoem infected | flies, food, fingers, feces, fomites; intestinal ulcers, bloody stools, fever, malaise, delirium, abdomen covered with rose spots; hemorrhaging; yes |
| food borne and water borne: typhoid fever: what % of victems becoem carriers; can other strains cause this; can is destroy intestinal tract; rose spots are what; | 5%; yes; yes; cappillary hemmorhaging in the abdomen; |
| food borne and water borne: typhoid fever: typhoid mary- what did she do; what is she responsible for; | she traveled alot and she was a cook; thousands of deaths; |
| food borne and water borne: Salmonellosis - etiologic agent; gram stain; shape; oxygen requirements; what can be contaminated; | salmonella typhi, S. enteritidis and others; negative; bacilli; facultative anaerobe; poulty, egges, fruits, veggies, uncooked eggs and reptiles; |
| food borne and water borne: Salmonellosis - for eggs where can it be; when contaminated food is ingested how long before s/s; CMs; how long does it last; what can it cause in serious cases | on shell and inside the egg; 6-48 hr; abdominal cramping, N, watery diarrhea; fever, ulceration, dehydration; 1-4 days; sepsis |
| food borne and water borne: Salmonellosis - tx; why are ABX not given; who can recover on their own | supportive tx; they can induce carriers and are only used in serious disease; healthy immunity |
| food borne and water borne: shigellosis- aka; etiologic agent; gram stain shape; who is the reservoir; spread by what; do you need a large or small amount of organism to be infected | bacillary dysentery; shigella dysenteriae, S. sonnei; negative; bacilli; humans; the five Fs; large |
| food borne and water borne: shigellosis- what can increase the spread of it; Dx; how long is incubation; oxygen requiremetns; | improper hand washing; fecal specimens; 1-4 days; facultative anearobe; |
| food borne and water borne: shigellosis- is small or large dose required; can it survive gastric acids; what toxins does the organism release; the toxins destroy what; shiga toxins can cause what | small; yes; shiga toxins; the intestinal wall; dysentary |
| food borne and water borne: shigellosis- s/s of dysentary; how long does one have s/s; can body reocover on its own; why is there bloody diarrhea; | mucoid and bloody diarrhea, fever, abd. pain, dehydration, electrolyte imbalance; 2-7 days; yes- self limiting; bc/ of ulcers; |
| food borne and water borne: shigellosis- where is it most common; | preschoolers and nursing homes; ABX and supportive therapy |
| food borne and water borne: cholera- etiologic agent; gram stain; shape; is it motile; what is contaminated; | vibrio cholerae; negative; bacilli; yes; fecal contamination of water sources, raw oysters; |
| food borne and water borne: cholera- what happens after ingestion of water or food that is contaminated; once intestinal colonization occurs what is released; why is a large dose needed; | intestinal colonization occurs; enterotoxin is released; in order to survive that gastric juices |
| food borne and water borne: cholera- CMs; when is there a high mortalilty rate ; why does rice water stools occur; Tx | large fluid loss with rice water stools; untreated due to dehydration and electrolyte imbalances; the enterotoxin eats at the intestinal wall and the "rice" is little slivers of wall; electrolytes and glucose |
| diarrhea due to E. coli- many __ that cause diarrhea; | strains; |
| diarrhea due to E. coli- infantile diarrhea- caused how; what do the enterotoxin due that are released; tx | since they have not been exposed to strain they pick up a strain; cause dehydration/electrolyte imbalance; ABX and fluid and electrolyte imbalance |
| diarrhea due to E. coli- travelers diarrhea- aka; what other organisms can cause this diarrhea; what s/s do the enterotoxins cause; | montezuma's revenge; giardia, salmonella, shigella; water loss and possible electrolyte imbalance; |
| diarrhea due to E. coli- strains 0157:H7: shed by whom; the feces contaminates what; what s/s does the enterotoxins cause; the genetic change is what; whp is at risk for fluid loss | cattle, sheep, deer, elk; the food by soil or direct contamination; bloody diarrhea and hemorrhagic colitis; they picked up shigga toxins so it is similar to shigella; very old and young |
| diarrhea due to E. coli- strains 0157:H7: what syndrome happens in kidneys; this syndrome causes what; s/s of kidney failure; who is it fatal in; | hemolytic uremic syndrome; kidney failure; seizures, coma, heart and liver damage, colon perforations; elderly and <5 yo |
| Peptic Ulcers: def; etiologic agent; is it motile; gram stain; shape; originally peptic ulcers were caused by what | mucous membrane lesions, esophagus, stomack or duodenum; helicobacter pylori; yes; gram neg.,; curved bacillus; stress; |
| Peptic Ulcers: why is it microaerophilic; why is it able to survive in the stomach; | b/c it lives between the mucous and epithelial lining; b/c it is resistant to gastric acid; |
| Peptic Ulcers: how does it get in stomach; do we know all the sources; what does it do once it enters the stomach; what is body response to colonization; | it is ingested; no; it colonizes and multiplies in the gastric mucosa; inflamatory response |
| Peptic Ulcers: what leads to the destruction of the lining; dx; what does breath test drink; what is purpose of urea and carbon 13; Tx; after tx what is cure rate; | the constant inflammatory response from our enzymes cause ulcer; breath test; urea and carbon 13; the organism breaks down urea and carbon 13 is expelled as Co2; omeprazole, antibiotics, bismuth for about 2 weeks; 94% |
| Peptic Ulcers: what is omeprozole; what does the proton pump inhibiter do; | a proton pump inhibiter; it decreases acid in stomach; |
| soilborne and arthropodborne bacterial diseases: tetanus- etiologic agent; is it caused by organism or toxins; reservoir'; does it form spores; gram stain; shape; | clostridium tetani; toxins; soil; yes; positiv;e bacilli; |
| soilborne and arthropodborne bacterial diseases: tetanus- they like to adhere to what fomite; hwere do spores enter body; does the wound have to be anaerobic or aerobic; once spores in anaerobic wound what happens; | rough surfaces (rusty nails); deep puncture wound; anaerobic; spores germinate into vegatative cells; |
| soilborne and arthropodborne bacterial diseases: tetanus- once germination occurs, what toxin does the cell secrete; is tetanospasmin an exo or endotoxin; what does tetanospasmin effect in body; | tetanospasmin; exotoxin; somatic motor neurons; |
| soilborne and arthropodborne bacterial diseases: tetanus- s/s of somatic motor neuron stimulation;what is first s/s; | all muscles will contract (prime mover and antagonistic muscles all move) with uncontrolled skeletal movement; jaw stiffness, difficulty swallowing |
| soilborne and arthropodborne bacterial diseases: tetanus- tx for muscle contractions; tx for toxins; tx for organism; is there a vaccine; how often shoukld you get booster; what are presentation in US; why are hyperbaric chambers used; painful; | muscle relaxants; antitoxins; ABX; yes; every 10 years; weak disease; since it is an anearobe it can get organism out; yes |
| soilborne and arthropodborne bacterial diseases: Gas Gangrene-etiologic agent; this organism can also contaminate what; what does this infect; gram stain; shape; does it have spores; oxygen requirements | clostridium perfringens; food and cause food poisening; wounds; positive; bacilli; yes; strict anaerobe |
| soilborne and arthropodborne bacterial diseases: Gas Gangrene- how is it introduced into the body; after it germinates into tissue what is released from microbe; | injury, surgery into dead necrotic tissue; enzymes and toxins |
| soilborne and arthropodborne bacterial diseases: Gas Gangrene- the release of enzymes and toxins do what; when our cells die what do they release; s/s of release of potassium; how long until host cell death occurs; | destroy cells; potassium, sodium; Ht issues, 12-48 hrs |
| soilborne and arthropodborne bacterial diseases: Gas Gangrene- what does tissue look like initially, as cells die, once cells die; does it spread quicly; s/s; why is gas released; how is it stopped; what can result if we cannot control it; | red, green, black; yes; odor, gas; b/c of metabolic reactions being released; to amputate; death, shock; |
| soilborne and arthropodborne bacterial diseases: Gas Gangrene- tx; why is tissue debridement done; what chamber is used; does it have a high mortality rate; if you press gently on tissue what can be heard | ABX, tissue debridement; cleans wound out, keeps it open for oxygen and provides drainage; hyperbaric chambers; yes; crackles |
| soilborne and arthropodborne bacterial diseases: Bubonic plague- aka; history; is it present today;etiologic agent; | black death; pandemics through hx; yes; Yersinia pestis |
| soilborne and arthropodborne bacterial diseases: Bubonic plague- tx; who is the vector; where in body does bacilli enter; what is the infective stage caleld | ABX; rat fleas; the bloodstream, lymph nodes, lungs; |
| soilborne and arthropodborne bacterial diseases: Bubonic plague- who is at risk;when rats die they jump to what; how does it enter blood stream; the | crowded areas and improper sanitation and rats; humans; from flea bites |
| soilborne and arthropodborne bacterial diseases: Bubonic plague- pneumonic plague- involves what area of the body; is it infective; ones infected nedd to be what; this results in what; name for tissue hemmorrhaging; bubos are located where | respiratory; yes; separeated; tissue hemmorhaing; buboes (redpurplish splotches); lymph nodes |
| soilborne and arthropodborne bacterial diseases: Bubonic plague- what happens if organism enters blood; how fatal is septicemic plague; tx; is tx effective | septicemic plaque; 100% fatal; ABX; yes; |
| contact diseases: Group A strep- etiologic agent; what is tx; is there alot of resistance; gram stain; shape; | streptococcus pyogenes; penicillin G; no; positive; cocci; |
| contact diseases: Group A strep- virulence- what is M protein; function of streptokinase; function of hyaluranidase | 70 types, so we can be exposed to it 70 times, it helps in adherence, anti-phagocytic antigenic; breaks down blood allows oranism to move deelpy; breaks this down between cells and separates tissues and moves deepers; |
| contact diseases: Group A strep- common in infections; throat; skin; others; antibody mediated responses; | strep throat; folliculitis, cellulitis, impetigo, necrotizing fasciitis; scarlet fever, toxic shock syndrome; Ra, glomerulonephritis |
| contact diseases: Group A strep- folliculitis- what does it infect | hair follicile |
| contact diseases: Group A strep- cellulitis- where does it enter; how does it spread; s/s; can it be life threatening; is it contagious; | break in skin; deep infection of the skin cells; swollen, hot to touch; yes; no; |
| contact diseases: Group A strep- imetigo: who gets it; what are vesicles; s/s of vesicles; what happens after they erupt; vesicles are located where; when is it contagious; does it spread; what area is infective | children and infacts; small fluid filled ones; red, tender and then erupt; yellow/brown crust; nose, mouth; when it errupts; yes; the reddened areas |
| contact diseases: Group A strep- necrotizing fasciitis- how does it enter body; what happens once enters; how does it spread; s/s; tx; | small cut and enters a specific strain; it spreads through fascia; by way of the fascia; inflamed skin, blisters, necrosis of tissues, death within 1-4 days; surgical removal of fascia and iv ABX; |
| contact diseases: Group A strep- toxic shock syndrome- what is infection due to; why does fever go up; where can it infect; is it local or systemic; | the pyrogenic toxin; because of the pyrogenic toxins, it causes the fever to go up; skin and wound; both; |
| contact diseases: Group A strep- toxic shock syndrome- s/s; hypotension leads to what; tx; is there only one or multiple toxins involded; | high fever, red rash, vomiting, watery diarrhea, desquamation of palms and soles, confusion and hypotension; organ failure; clean infected area and abx; multiple |
| contact diseases: Group B strep- etiologic agent; B is for what; what percent of healthy women have this as vaginal and rectal indigenous flora; | streptococcus agalactiae; baby; 15-40$; |
| contact diseases: Group B strep- when are pregnant women checked for it in pregnancy; if carrier while preggo what is tx; | 35-37 week; IV abx during belivery; |
| contact diseases: Group B strep- vaginal delivery of child can lead to what infections in newborns; | neonatal meningitis, pna, and sepsis |
| contact diseases: staphylococcus aureus- what are some of its virulence factors; gram stain; shape; one of the toxins is an exfoliatin what syndrome does this cause; | coagulase, hemolysin, leukocidins; positive; staphylococci; scalded skin; |
| contact diseases: staphylococcus aureus- scalded skin syndrome-who gets scalded skin syndrome; what does it damage; s/s ; is healing rapid or slow; mortality rate; why is it called this | neonates and children; the epidermis; red moist and exposed bright red cells; rapid; low ; child looks bright red |
| contact diseases: staphylococcus aureus- how can it cause food poisening | through and enterotoxin |
| contact diseases: staphylococcus aureus- Toxic shock syndrome- is it more or les potent than the streptococcal toxin; deadly ; s/s | more; yes; same as other tss |
| contact diseases: staphylococcus aureus- other diseases; | PNA, meningitis, osteomyelitis, acute bacterial endocarditis, septic arthritic, septicemia, UTI, skin infection (impetigo, cellulitis) |
| contact diseases: staphylococcus aureus-why is it difficult to handle | b/c it secretes so many exotoxins |
| contact diseases: staphylococcus wpidermidis- where is it normal flora on body; causes what kind of infections; how can it enter body; disease that is causes; subacute bacterial endocarditis can damage what | skin; nosocomial; IV lines, and wounds; subacute bacterial endo carditis; heart valves |
| contact diseases: bacillus antrhacis- how is one infected; what is inhaled; what else can spores contaminate; what is ingested | by handling infected animals or soil; spores; wounds; spores; |
| contact diseases: bacillus antrhacis- when is disease present; when is skin infection s/s present; shape; grma stain; what is most common; o2 requirements | 7 days; 1-2 days; bacillus; positve; cutaneous; aerobe |
| contact diseases: bacillus antrhacis- cutaneous anthrax- fatality rate; what necrodes on body; who at risk; as the tissue is destroyed what is s/s; can it disseminate from legion | 20%; local tissue necrosis; farmers, soil handlers, vets; black legion; yes |
| contact diseases: bacillus antrhacis- pulmonary anthrax0 what is inhaled into the lungs; once in lungs what is produced; s/s of toxin production; who could use this for harm; is it usualy fatal; when does it need to be treated | spores; toxins and infection; respiratory distress; terrorist; yes; immediately or death |
| contact diseases: bacillus antrhacis- GI anthrax- is it common or rare; what is ingested; once spores are ingested what happens; | rare; spores; tissue death; |
| listeria monocytogenes: where is it found; gram stain; shape; who is at high risk; two ways it is transmitted; | soil and water; positive; bacilli; pregnant women it can harm fetus, immunocomprimised; ingestion and vaginal transfer during birth; |
| listeria monocytogenes: what can it contaminate; can it live in fridge; what foods can be contaminated; can normal ppl handle it fine; | food; yes; raw milk and cheese that are nonpasteurized and veggies; yes |
| listeria monocytogenes: dieases that it can cause; what does pasteurization do; | neonatal meningitis, meningitis in the immunocomprimised, septicemia and other; destroy it |
| E. coli- where else was this discussed; gram stain; shape; transmission; diseases; what can make it attach to urethra | diarrhea and foodtransmission; negative; bacilli; fecal/oral, ascending urtethra, catheter colonization; newborn meningitis, UTIs, nosocomial pna and sepsis, diarrhea; the fimbrea |
| C .diff- does it have spores; oxygen requirements; gram stain; shape; def; where does it reside in low numbers; | yes; anaerobic; gram positive; bacilli; endogenous disease of the intestinal tract following excessive ABX use; colon; |
| C .diff- cause; since other bacteria is wiped out what can happen; | loss of many intestinal bacterial species; it can overgrow |
| C .diff- once overgrown what is it called; s/s of pseudo colitis; the membranes cause what | pseudomembranous colitis; yellow membraneous lesions covering the intestinal lining; diarrhea and watery stools |
| C .diff- tx; | stop use of offending abx and allow colonizaton of colon |
Created by:
jmkettel
Popular Biology sets