Medical Microbiology – Flashcards
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| Which bacteria do not have a cell wall? |
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Mycoplasma spp Chlamydiae spp |
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| List 6 ways you can tell a eukaryotic pathogen from prokaryotic |
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1. Prokaryotes lack nucleus 2. Prokaryotes lack membrane-bound organelles (like mitochandria) 3. Prokaryote ribosome = 70S, Eukaryote = 80S 4. Bacteria (with 2 exceptions) have peptidoglycan cell wall 5. Bacteria (with a few exceptions) lack sterol in their cell membranes 6. Prokaryotes = 1 chromosome, eukaryotes >1 (7. Bacteria are much smaller - 1/5 to 1/10 the size) |
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| Periplasmic space |
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| Space between inner cell membrane and cell wall in bacteria |
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| How does the membrane structure of gram + and gram - bacteria differ? |
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Gram + cell membrane thick peptidoglycan cell wall
Gram - cell membrane thin peptidoglycan cell wall outer membrane (permeability barrier, containing porins and LPS) |
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| Mycobacteria spp |
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-waxy cell envelope: anti-phagocytic, helps disease transmission, gram stain doesn't work ; -acid fast stain + M. Leprae - obligate intracellular M. Tuberculosis - facultative intracellular ; |
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| Escherichia coli |
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| gram - rod |
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| Bacillus spp |
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| gram +, has spores |
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| Streptococcus spp |
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mostly aerotolerants pyogenes: ; -group A strep -gram + cocci in chains ; pneumoniae gram + diplococci |
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| Staphylococcus aureus |
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gram + cocci ; |
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Neisseria spp |
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bind human transferrin/lactoferrin and import iron into cell ; gonorrhoeae: gram - diplococci |
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| What structures are unique to gram + bacteria? |
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| lipotechoic acid, which mediates adherence to tissue, and techoic acid |
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LPS |
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lipopolysccharide -present on the outer membrane of some (mainly enteric) gram- bacteria -three parts: -lipid A - endotoxic activity -polysaccharide core -O antigen - provides resistance to bile and complement, very variable among different bacteria |
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| LOS |
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| LPS without O antigen |
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| Spirochetes |
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So thin must use dark field microscopy to see. Can't gram stain, but have gram - structure
Borrelia burgdorferi - Lyme disease Treponema pallidum - syphilis |
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| Salmonella spp. |
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| gram -, facultative intracellular bacteria |
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| Vibrio cholerae |
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| gram -, extracellular bacteria |
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| Chlamydiae spp |
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-obligate intracellular -use host cell energy -lack cell wall -two membranes, like other gram (-)s
Chlamydiae trachomatis: blindness, nongonococcal urethritis pneumoniae Chlamydiae psittacosis: psittacosis (a form of pneumonia) Chlamydiae pneumoniae: pneumonia
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Mycoplasma pneumoniae
1. Characteristics 2. Pathogenesis/Manifestations 3. Diagnosis 4. Treatment
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1. Very small, lacks a cell wall, tiny genome, sterols in membrane, does not grow easily on culture 2. Droplet transmission, colonizes the nasopharynx. Aspiration leads to bronchopneumonia (note mycoplasma cannot enter the alveoli). This results due to mycoplasma being very good at adhesion with a specialized organelle and because it releases peroxidase which damages the epithelial cells. 2 wk incubation period, illness lasts 3 weeks. Mainly occurs in adults, but kids can get it. ATYPICAL pneumonia (dry cough), erythema multiform, anemia 3. Diagnosis Best way is PCR of sputum, since it does not grow well on culture Cold agglutinins - put freshly drawn blood on ice - it will agglutinate due to presence of anti- Mycoplasma antibody. Not sensitive but very specific. 4. Treatment - obviously not with beta lactam. Macrolides, tetracyclins, fluoroquinolones work well. |
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| Parts of the bacterial growth curve |
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lag - slow if any increase, bacteria preparing to proliferate exponentional/log - maximal doubling speed stationary - cells stop growing, number of viable cells decreases while total cells remains constant |
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| spectrum of oxygen requirement in bacteria |
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aerobes - must be in the presence of oxygen to survive - microaerobes - the concentration of this oxygen must be > than that in air facultative anaerobes - grow faster in the presence of oxygen (use respiration), but can survive without it (using fermentation) aerotolerants - use fermentation only, but can survive in the presence of oxygen obligate/strict anaerobes - cannot survive in the presence of oxygen
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| Pseudomonas aeruginosa |
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| aerobe |
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Clostridium spp |
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strict anaerobes gram + spore-forming rods cause gas gangrene (have to remove the infected tissue), anaerobic cellulitis
Clostridium perfringens - most common infection. Releases alpha toxin, a lecithinase that destroys plasma membranes - associated with food poisioning Clostridium septicum - associated with GI tumors Clostridium tetani - spore is found in the soil, infects wounds and travels along the nerve - commonly causes neonatal tetanus by infecting umbilical stump - neurotoxin inhibits release of inhibitory neurotransmitters, causing muscle spasms. - treatment = antitoxin, muscle relaxants, ventilator. Antibiotics don't help because the toxin is what is important ; |
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| Actinomyces spp |
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strict anaerobe gram + rod (non-sporeforming) |
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| Peptococcus and Peptostreptococcus spp |
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strict anaerobes gram + cocci |
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| Bacteroides spp |
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strict anaerobes gram - rods (nonsporeforming) normal flora in colon, vagina, mouth bile-resistant. Bile sensitive species are Porphyromonas and Prevotella not endotoxic Bacteroides fragilis ;- most common anaerobic intra-abdominal and bloodstream infection, although only .5% of gut flora - infection due to rupture of GI tract AND low redox environment - cause peritonitis and abscess formation - treated by abscess drainage and metronidazole |
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| Fusobacterium spp |
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strict anaerobes gram - rods (nonsporeforming) |
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| Ways to get an anaerobic infection (5) |
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1. aspiration of normal mouth flora into lung 2. spillage of gut flora due to wound or tumor 3. bite wound (mouth secretions lower redox potential) 4. Tight cast restricts circulation 5. Antibiotic treatment alters normal flora and alters redox potential, can caus C. diff infection |
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| Characteristics of a non-clostridial, anaerobic infection (5) |
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1. Often polymicrobial (facultative anaerobes lower redox potential) 2. Form abscesses 3. Highly antibiotic resistant 4. low virulence, but can be lethal 5. slow-growing, fastidious, smelly (fermentation) ; |
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| Pseudomonas aeruginosa |
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gram - treat with ciprofloxacin |
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| What is the etiology of sinusitis |
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Usually viral (rhinovirus). May be bacterial - which would cause a high fever and tenderness around the sinuses: ; Bacterial: Streptococcus pneumoniae Haemophilus influenzae |
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| Haemophilus influenzae |
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gram - cause of URI and pneumonia |
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Moraxella Catarrhalis 1. Gram stain 2. Causes which diseases? |
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1. Gram - 2. acute bronchitis |
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| What are the common etiologies of rhinitis? |
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1. rhinovirus 2. coronavirus 3. respiratory syncitial virus (RSV) |
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Acute bronchitis ; 1. symptoms 2. etiology |
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1. symptoms - productive cough, maybe accompanied by wheeze ; 2. Usually viral: -influenzae virus -rhinovirus -adenovirus Can be bacterial, esp on top of chronic: Streptococcus pneumoniae (GPC) Haemophilus influenzae (GN) Moraxella catarrhalis (GN) |
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Pharyngitis/tonsilitis ; etiology |
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usually viral (rhinovirus, coronavirus) the main bacterial cause is Streptococcus pyogenes (GAS) |
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Influenza ; 1. Etiology 2. Presentation 3. Diagnosis |
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1. Etiology - influenza virus A or B 2. sudden onset of chills, sever muscle aches, fever, and cough 3. PCR |
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Community Acquired Pneumonia ; 1. Manifestation 2. Etiology |
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1. Manifestation: fever, cough (often productive), CXR white, sharp pain on inspiration 2.;40% ;Streptococcus pneumoniae ;;; 20%; Haemophilus influenzae ;;; 25% Atypical: Mycoplasma pneumoniae ;;;;;;;;;;;;;;;;;;;;;;; Chlamydophila pneumoniae ;;;;;;;;;;;;;;;;;;;;;;; Legionella pneumophila ;;; 15% Viral ; ; |
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| Etiology of ventilator associated pneumonia |
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"PEAKS" ; Pseudomonas aeruginosa (GNR) Enterobacter coacae (GNR) Acinetobacter (GNR) Klebsiella pneumoniae (GNR) Straphylococcus aureus (GPC) |
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Cystitis ; 1. Symptoms 2. Etiology |
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= lower urinary tract infection (infection of bladder) ; 1. dysuria, increased frequency of urination 2. Escherichia coli (by far most common) Staphylococcus saprophyticus |
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| etiology of encephalitis |
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mainly viral: Herpes simplex virus vector borne viruses (ex. West Nile) |
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| etiology of meningitis |
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1. Streptococcus pneumoniae (GPC) Neisseria meningitidis (GNC) Enteroviruses Listeria monocytogenes (GPR) |
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| Etiology of Diarrhea |
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Bacteria: Salmonella spp. (GNR) Shigella spp. (GNR) Campylobacter spp. (GNR Escherichia coli (GNR) Clostridium difficile - in hospitalized patients Protozoa Giardia lamblia Cryptosporidium Viruses Rotavirus Norovirus |
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| Etiologies of common skin infections |
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| 1. cellulitis Streptococcus pyogenes (GAS) Staphylococcus aureus (NOT S. epidimeridis) 2. abscesses Staphylococcus aureus 3. chronic ulcers in diabetics progress from Strep/Staph to gram neg. to drug resistant gram - (Pseudomonas) 4. dermatitis Candida albicans dermatophytes (tinea, ex.) |
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| FOR EACH immunodeficiency, give a. the reasons it might occur, b. the OIs that tend to occur 1. opsonization, RES 2. B cell deficiency 3. T cell deficiency 4. granulocyte abnormalities |
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| 1. a. complement deficiency (SLE), liver cirrhosis, splenectomy, SCD b. encapsulated pathogens: S. pneumoniae H. influenzae (GNR) N. meningitidis (GNC) 2. a. multiple myeloma, CVID b. IgA def. - Giardia lamblia. IgG - encapsulated pathogens: S. pneumoniae (GPC), H. influenzae (GNR), Neisseria meningitidis (GNC) 3. a. HIV, immunosuppresants such as cyclosporine, azathioprine, glucococorticoids, anti-TNF, anti-lymphocyte Abs b. toxoplasmosis, Candida, PCP, CMV, mycobacteria 4. a. neutropenia (chemo), CGD b. Remember "spa" for the catalase + infections PSeudomonas Aeruginosa ASPergillus StaPhylococcus Aureus |
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| What are the major food-borne pathogens and what is special about them? |
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| Norovirus - most common, onset 1-2 days Staphylococcus aureus (GPC) - intoxication, heat stable enterotoxin. Causes vomiting. Clostridium botulinum (GPR) - intoxication with neurotoxin that can take at least a day to take effect, causes paralysis. Rare. Clostridium perfringens (GPR) - in vivo produced enterotoxin, onset 12 hrs. Causes diarrhea and cramps. EHEC (GNR) - produces shiga toxin which causes diarrhea, but also enters into the circulation and causes kidney failure non-typhoid Salmonella (GNR) - causes inflammation. Onset 12-48 hrs) Shigella (GNR) - causes inflammation. Onset 12-72 hrs. Causes dysentery Campylobacter jejuni - causes inflammation. Onset 3-5 days Hepatitis A virus - onset 10-45 days. Invades systemically, causing the hepatitis. |
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| Name the major water-borne pathogens |
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| Vibrio cholerae Various gram (-) rods (Shigella, E. Coli) Giardia lamblia (1-4 wk onset, chronic diarrhea) Cryptosporidium (5-10 day onset) Entamoeba histolytica (2-4 wk onset) HAV Norovirus Rotavirus Enterovirus |
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| List 5 ways pathogens adapt to survive in the GI tract |
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| 1. Novel pili help them find spots despite normal flora 2. Seek shelter in mucus 3. Adherence 4. O antigen provides bile resistance 5. Ingestion of a large number at a time 6. Production of urease to increase pH |
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| Campylobacter jejuni 1. characteristics 2. source 3. how does it cause infection4. treatment/aftermath |
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| 1. gram (-) microaerophilic oxidase + curved (seagull-shaped) rod, grows best at 42 degrees 2. zoonotic reservoir (chickens), also fecal-oral, handling pets 3. Invades lower SI/upper colon, main virulence factor is LPS endotoxin, causing diarrhea, fever 4. self-resolves after 5 days, so just provide fluids. Sequelae may include Guillain-Barre syndrome (molecular mimicry) |
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| Giardia spp. 1. life cycle 2. source/transmission 3. manifestation 4. Diagnosis and treatment |
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| 1. cysts are in feces: highly infectious, resistant to chlorination. 2. Source = zoonotic reservoir. Water-borne, so occurs in campers/hikers or when treatment plant breaks 3. Often asymptomatic. Acute form occurs about 1-3 wks after infection and self-resolves 1-4 weeks later. Chronic form is also possible, as are relapses. People with IgA deficiency are especially susceptible. Sudden-onset of explosive, greasy, foul-smelling diarrhea 4. Dx: cysts in stools, Treatment: Metronidazole |
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| Cryptosporidium parvum 1. Life cycle 2. Source/transmission 3. Manifestations 4. Diagnosis/Treatment |
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| 1. Complex. Know that oocysts are infectious and in the feces, and that trophozoites are in the intestine 2. Like Giardia, zoonotic reservoir, waterborne pathogen. fecal/oral possible 3. Invades enterocytes, causing diarrhea about 1 week after ingestion. Or can be asymptomatic. Usually self-resolves after a week or two EXCEPT in immunocompromised people, who may develop serious disease and die. 4. Dx: oocysts can be detected by modified acid-fast stain Tx: none, but recent approval of nitrazoxanide |
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| Rotavirus 1. Characteristics 2. Source/transmission 3. Manifestations/Epidemiology 4. Diagnosis, prevention, treatment |
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| 1. dsRNA virus (reovirus family) with icosahedral capsid and no envelope (resistant to acid) 2. source = human reservoir. transmission = fecal/oral 3. most common cause of infectious diarrhea in children <2, symptoms are worse in children. Vomiting followed by diarrhea, appearing within 48 hrs and self-resolving. 4. Diagnosis is by EM or serologic testing, prevention is by an oral vaccine which is recommended for infants now, and there is no treatment except fluids. |
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| Hepatitis A Virus 1. Characteristics 2. Source/Transmission 3. Course of disease 4. Diagnosis, Prevention, Treatment |
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| 1. HAV = picornavirus, singlestrand+ RNA, no envelope, only known serotype 2. Transmission = oral/fecal (human reservoir), through contaminated food or water 3. Course of disease more than 50% are asymptomatic, others will develop flu-like symptoms 2-4 weeks after ingestion. the body can make neutralizing antibodies at this point against HAV; if it does then the infection stops here if the body fails to do this, then HAV will spread into the blood and infect the liver, leading to hepatitis and jaundice this will last 2 months, and then go away. NOT a chronic condition like Hep B and C. very few people will die from it because they develop fulminant hepatitis infection confers permanent immunity 4. Diagnosis - only by presence of IgM antibodies against HAV Prevention - HAV vaccine post-exposure or to high risk folks such as travelers Treatment - no anti-virals available. May give passive immunity post-exposure |
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| Characteristics of Treponema pallidum |
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| spirochete, must see by dark field microscopy. gram (-) structure microaerophilic corkscrew movement slowly replicating (doubling time >30 hrs) |
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| Course of syphilis |
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| Primary: Chancre occurs within 3 weeks of infection, self-resolves. Maybe some lymphadenopathy Secondary: Within 3-6 weeks the bacteria has disseminated to liver, brain, skin. You have a rash (on palms and soles), fever, malaise, condyloma lata, hair loss. RARELY neurosyphilis Latent: Secondary syphilis resolves, and you can have latent syphilis for 3 to 30 years Tertieary: gummas - large granulomatous lesions, can be anywhere neurosyphilis |
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| Syphilis diagnosis and treatment |
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| Dx: can be by microscopy from skin scrapings Usually done by serology Non-treponemal: VDRL, RPR tests for Ab to cell membrane lipids and lecithin. The levels of these can be used to track how therapy is going Treponemal: Antibodies to the bacteria itself - are positive for life and therefore can't be used to track Algorithm: ELISA for treponemal Ag, then if + RPR. If RPR- do treponemal Ab. Tx: Penicillin - highly effective |
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| Hantavirus 1. Characteristics 2. Reservoir/Transmission 3. Manifestations 4. Diagnosis/Treatment |
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| 1. Bunyavirus family, segmented (3) (-) strand RNA with RNA pol, spherical, enveloped 2. Reservoir in deer mice (and other rodent species) - virus is in saliva, urine and feces, aerosolized and inhaled. 3. Often asymptomatic. Hemorrhagic Fever = fever, malaise, chills, GI problems, myalgia. Can be accompanied by renal distress. Hantavirus Pulmonary Syndrome can arise: build up of fluid in lungs leads to respiratory failure. Mainly a T Cell infiltrate without marked necrosis. Mortality is ~52%. 4. Diagnosis by PCR of lung tissue, serology. No treatment available except fluids, dialysis for kidney failure |
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| Rabies virus 1. Characteristics 2. Reservoir/Transmission 3. Pathenogenesis/Manifestations 4. Diagnosis/Treatment |
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| 1. Rhabdovirus family, single (-) strand with RNA pol, helical capsid, enveloped. Large bullet shaped virus 2. Reservoir = many mammalian hosts. Transmitted through a bite or a scratch 3. Virus replicates in muscle cells, then enters peripheral neurons through AchR. Travels to CNS, other organs (e.g. saliva). Incubation period of 12 months. Causes lethargy, confusion, paresis, increased salivation, behavioral changes. 4. Diagnosis by symptoms, history of animal contact. Immunofluorescence of suspected animal's brain tissue. No anti-viral treatment available, fatal. High-risk people given HDC vaccine. Post-exposure: HRIG injected around wound to neutralize, HDCV given in other arm. |
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| Rickettsiae spp. 1. Characteristics 2. Reservoir/Transmission 3. Pathenogenesis/Manifestations 4. Diagnosis/Treatment |
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| 1. Small, obligate intracellular bacteria with gram (-) structure (but too small to stain) 2. Reservoir is ticks with transovarian transmission to offspring. Transmission to humans through tick bites 3. Rickettsiae virulence factors include filopodia and toxins. Invade many cells, but particularly capillary endothelial cells, leading to lysis and capillary destruction, which in turn causes the spots. Manifestations occur within 2-12 days. Generalized symptoms: severe headache, malaise, fever, GI problems, abdominal pain, myalgia, meningitis, respiratory and renal problems, conjunctivitis. Note 10% do not have the spots. 4. Dx by history and manifestation. Can do culture on specimens, or Weil-Felix test = Ab against Proteus vulgaris antigen (cheaper). Treatment is tetracycline, which is successful if given early enough. |
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| Borrelia Burgdorferi 1. Characteristics 2. Reservoir/Transmission/Location 3. Pathenogenesis/Course of Disease 4. Diagnosis and Treatment |
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| 1. Spirochete 2. Ticks. Tick bite must be 48 hrs. Coastal areas of southern NE and New York, Midwest (Wisconsin, Minnesota, Michigan), Coastal woodlands of Calif and Oregon 3. Osps = surface lipoproteins: tropism and tissue attachment Invades skin and widely disseminates, getting into the blood and the CSF. 3 stages: a early: bulls-eye rash (erythema migrans) - absent in 50% general symptoms b early disseminated: 10% have cranial neuropathy, meningitis. Some have iritis, retinitis c late: oligoarthritis in large joints (60%), which continues post-Lyme disease ECM lesions lead from fatigue to dementia Chronic Lyme/Post-Lyme disease: resembles fibromyalgia and chronic fatigue, not caused by the infection. 4. Diagnosis: by tissue culture from ECM. Serology - problem is you need to treat before you can see the Abs. ELISA followed by WB (similar to HIV test). Treatment: Early - amoxicillin or doxycycline. Late - IV ceftriaxone |
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| What is the risk of transmission in needlestick injury for the following diseases: 1. HIV 2. HCV 3. HBV |
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| 1. HIV = .3% 2. HCV = 3% 3. HBV = 30% |
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| For HAV thru HDV give the route of transmission and whether it causes chronic hepatitis and leads to liver cancer |
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| HAV. Transmission = fecal-oral. No chronic disease/HCC HBV. Transmission = parenteral, sexual, and perinatal. Chronic disease + HCC HCV. Transmission = parenteral. Chronic disease + HCC HDV. Transmission = parenteral. Chronic disease + HCC |
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| What prophylaxis is available for HAV thru HDV |
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| HAV - HAIG + vaccine HBV = HBIG + vaccine HCV = none HDV = HBV vaccine |
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| Hepatitis B virus 1. Family 2. Structure/contents 3. Genome |
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| 1. Family - Hepadnaviridiae 2. consists of an envelope with the embedded protein HBsAg, an icosachedral core made up of the protein HBcAg, a DNA molecule that has one incomplete strand, and a DNA polymerase with RT activity 3. HBV encodes 4 genes: HBsAg, HBcAg, Pol, and X (a transcription regulator) |
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| Hepatitis B 1. Pathogenesis 2. Manifestations 3. Diagnosis 4. Treatment |
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| 1. "S" ORF protein attaches to hepatocytes -> invasion. Multiplies without killing the hepatocyte. Makes the cell produce excess HBsAg as a decoy. Damage as a result of CTL response (inflammation). Oncogenesis possible if integrates into DNA. "X" ORF thought to play a role. 2. Within 1-6 months, 3 possibilities: Asymptomatic, Acute (RUQ pain, jaundice, malaise), fulminant. After this, 90-98% of adults will clear the infection. 2-10% of adults and 90% of newborns will develop a chronic persistent infection that may be asymptomatic, or may develope into chronic hepatitis, cirrhosis, and hepatocellular carcinoma (any of these can develop from the asymptomatic stage) 3. elevated LFTs. Serology: HBV DNA, HBsAg are always present during infection. HBeAg is present during acute infection - if it is present in chronic infection it indicates increased virulence. Anti-HBsAG is the antibody conferring protective immunity. It, along with Anti-HBcAg and Anti-HBeAg will appear if the person has ever been infected. Anti-HBsAg only will show up if the person was vaccinated. 4. Prevention: Vaccine Acute Treatment: HBIG Chronic Treatment: Interferon, lamivudine (an RTI) |
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| Hepatitis D 1. Characteristics 2. Manifestations 3. Diagnosis/Prevention/Treatment |
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| 1. Deficient virus - RNA virus with core comprised of delta antigen, with HBV envelope containing HBsAg. Must be a co-infection or superinfection of an HBV patient. 2. More severe version of HBV, increased risk of chronic hepatitis and cancer 3. Serology: Anti-Delta Ag 4. Prevention - protection from HB vaccine, treated with interferon 2 alpha |
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| Hepatitis C 1. Characteristics 2. Manifestations 3. Diagnosis/Prevention/Treatment |
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| 1. Single + strand RNA virus of flavivirus family. Error-prone RNA pol means lots of errors, evasion of immunity 2. Similar to HBV with a sub-clinical acute phase but a much higher risk of contracting chronic infection, and a much higher risk of developing cirrhosis and cancer 3. Diagnosis by serology - anti-HCV Ab or RT-PCR. No vaccine or IG therapy possible because of rapid mutations. Treatment is interferon and ribavirin. |
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| Epstein-Barr Virus 1. Family2. Course of disease 3. Diagnosis |
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| 1. Herpesvirus 2. Spread by saliva, infects epithelial cells and spreads to B cells (naive and memory). CTL response to B cells responsible for IM. Asymptomatic in children. In adolescents, you have extreme pharyngitis, lymphadenopathy, fatigue. Also can get a beta-lactam rash and there is a significant risk of splenic rupture in traums to the area. The CTL kills almost all the infected B cells except a few memory B cells, where the virus remains latent. Chronic infection, where the T cells fail to kill it, or it comes back from the memory cells is associated with many human cancers - Burkitt's lymphoma, etc. PTLD is a significant risk for people who are in latency or who are receiving an EBV+ organ: the immunosuppressant drugs reduce the T cells, allowing the memory B cells to expand and this can lead to cancer. Diagnosis: Acute is by monospot - an agglutination test with antibodies to sheep, cow RBCs. "Heterophile antibodies" To detect a past infection you use specific anti-EBV antibodies If PTLD is suspected, you do PCR to detect the viral load, or do a biopsy and look at the tissue in question. |
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| What infections commonly occur in cystic fibrosis? |
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| Pseudomonas aeruginosa |
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| What are the most common inhalation-associated pathogens in the following situations 1. CNS injury 2. T cell deficiency 3. IgG deficiency |
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| 1. aspiration pneumonia, abscesses. Caused by anaerobic streptococci, fusobacteria 2. PCP, CMV 3. infection by encapsulated microbes, e.g. pneumococcus |
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| What common inhalation-acquired pathogens are generally NOT aspirated (i.e. - they come from an exogenous source and cause a LTI) |
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| Legionella Histoplasma Tuberculosis Anthrax F. Tularensis |
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| Adenovirus 1. Structure 2. What accounts for the different serotypes3. Why are the serotypes significant4. What factors would lead you to suspect adenovirus in the diagnosis5. Transmission6. Pathogenesis (including virulence factors) 7. What manifestation tends to appear in the summer? Which manifestation is associated with nosocomial infections8. What are the options for diagnosis and pros and cons 9. Treatment? Prevention? Vaccine? |
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| 1. dsDNA virus, non-enveloped 2. Fiber protein (a surface protein) variation determines serotype 3. Different fiber proteins are specific for different cellular receptors, and so different serotypes are associated with different disease 4. epidemic outbreak + patient immunocompromised 5. host-restricted. Droplets -> URI infection, aspiration -> LRI. GI secretions/stool. Rarely waterborne 6. Invades epithelial cells and lymphoid tissue (ex. tonsils). Early genes (E1A and E1B) inhibit host mRNA transport to the cytoplasm and translation, leading to viral mRNA accumulation. Early genes also block apoptotic signals, interferon signals, and inhibit MHCI expression. The disease remains latent in immunocompromised hosts and is shed for a long time 7. summer - pharyngocunjunctival fever. nosocomial - epidemic keratoconjunctivitis 8. Culture (shell vial method)- expensive, can't do for GI serotypes. Serum Ab (many false positives because they last a long while). Ag detection - false (-) because you need a lot of antigen. PCR - on specimen or serum. 9. Treatment - none. Prevention = isolate infected people and get their contacts. Vaccine - military one was effective and discontinued, now being reinvestigated. |
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| What are coccobacilli |
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| Technically rods, but are short and wide so are somewhere in between rods and cocci |
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| Haemophilus influenza 1. Characteristics 2. Virulence factors 3. Diagnosis |
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| 1. gram (-) coccobacilli, pleomorphic 2. LOS, IgA protease, CAPSULE promoting invasion/bacteremia, can get iron from lactoferrin and heme, adhesins 3. toddlers + lack of immunization = H. flu gram stain of CSF, ear fluid, sputum culture: grows on chocolate agar, not on blood |
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| Characteristics of the Enterobacteriaceae How you tell them apart Members and what diseases they cause |
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| Gram (-) rods, facultative anaerobes, can use glucose as sole carbon source, can be isolated on MacConkey agar, oxidase (-). Tell them apart with triple sugar iron medium. E. coli uses lactose, while Salmonella and Shigella do not. Salmonella produces H2S gas. E. coli - diarrhea, dysentery, UTI Salmonella - diarrhea, typhoid (enteric fever) Shigella - dysentery, diarrhea, Yersinia - dysentery, plague, lymphadenitis in immunocompromised people, many members of this family can cause UTIs, bacteremias (E. Coli, Proteus, Klebsiells (which can also cause pneumonia), Enterobacter, Citrobacter, Serratia) |
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| What do the following serotypes of E. Coli correspond to O148:H28 O26:H11 O157:H7 O4:H5 K1 |
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| O148:H28 = ETEC O157:H7 = EHEC O26:H11 = EPEC O5:H4 = UTI K1 = meningitis |
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| Describe the toxins made by various E. Coli strains |
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| Endotoxin (LPS): common to all E. Coli Hemolysin (Hly): a surface toxin, causes kidney damage in pyelonephritis Heat-Stable Toxin (STa): A small polypeptide, causes diarrhea. Heat-Labile Toxin (LT): A large protein, causes diarrhea Shiga Toxin (Stx): A large protein, blocks ribosomal activity, affects kidney cells |
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| Describe the different strains of E. Coli that cause GI illness |
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| 1. ETEC (O148:H28) - attaches to cells with unique CFA pili (colonizes novel sites) - produce STa or LT - responsible for diarrhea in infants and traveler's diarrhea in adults, causes food poisoning 2. EPEC (O26: H11) - attaches to epithelial cell with bundle-forming pilus. Using a T3SS, secretes factors into the cell that promote pedestal formation; also secretes TIR into the cell. It then produces intimin on its surface, causing it to adhere tightly to the surface. - no enterotoxin; causes attachment and effacement (A/E) lesions - infant diarrhea in developing countries 3. EAEC - forms a biofilm on top of the epithelial cells, gets trapped there by mucus production - may secrete a toxin: EAST - mild disease, responsible for traveler's diarrhea, infant diarrhea in U.S., common in HIV+. No blood or leukocytes in stool, low fever. 4. EIEC - no unique pili, just afimbrial adhesions - gets endocytosed, breaks out of endosome, replicates intracellularly, spreads laterally to neighboring cells (similar to Shigella) - stool has blood, leukocytes 5. EHEC (O157:H7, but can be other serotypes) - the same as EPEC, but produces Shiga toxin - Shiga toxin will cause hemmorhagic colitis (leading to a bloody stool) and it can also cause hemolytic uremic syndrome (HUS), = acute kidney failure, in about 5-10% of those infected, most often in children - associated classically with eating undercooked meat, petting zoos e |
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| In uropathogenic E. Coli, what allows them to cause pyelonephritis |
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| P-pili or Pap-Pili - binds to the P blood group antigen, also known as Forssman's antigen, on kidney epithelial cells |
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| What does the K1 strain of E. Coli cause and how |
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| Causes meningitis - K1 antigen is associated with a capsule that helps it evade phagocytosis and complement, leading to invasion. Responsible mainly for neonatal meningitis (second leading cause). |
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| When do you not use antibiotics in treating E. Coli? |
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| In the case of HUS, and in the case of most of the GI infections like ETEC. |
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| Helicobacter pylori 1. Describe it 2. Name the virulence factors 3. Normal disease progression 4. Diagnosis 5. Treatment |
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| 1. similar to Campylobacter jejuni, is a curved gram (-) rod that is motile. 2. Urease = allows it to survive in stomach acid by locally raising the pH Motility = It has a flagella that propels it through the mucus layer in the stomach VacA - secreted, damages epithelial cells CagA - secreted via a T4SS directly into stomach epithelial cells, causes inflammation 3. At first, causes mild NVD symptoms. Then cases chronic gastritis (mild stomach inflammation). In more than 1%, causes an ulcer (mainly due to the toxin activity). All duodenal ulcers and most gastric ulcers have this as the cause. 4. Diagnosis is commonly done by breath test 5. Treatment is antibiotic + ppi (excample Clarithromycin + omeprazole) |
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| Clostridium difficile 1. Characteristics 2. Pathogenesis (virulence factors) 3. Progression of disease 4. Diagnosis 5. Treatment |
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| Enterococcus faecalis/faecium 1. Characteristics 2. What diseases does it cause and how3. Prevention/Treatment? |
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| 1. Gram (+) cocci, facultative anaerobe, frequently in chains 2. It is normal gut flora that can infect the skin of sick patients -> contact transmission by transient hand infection, etc. The major diseases it causes are vascular-line related bacteremia, endocarditis, and catheter-related UTI. 3. Prevention = swab patients rectum for VRE - if they have it then they get isolated/contact precautions Treatment. Many strains of E. faecium are vancomycin resistant, also ampicillin resistant. Against VRE you have linezolid, tigecycline, daptomycin. |
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| Klebsiella 1. Characteristics 2. What diseases does it cause and how does it cause them3. Treatment |
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| 1. GNR, facultative anaerobe 2. Like Enterococcus, normal gut flora that colonizes the skin of sick people -> person to person transmission. Causes bloodstream infection through vascular line, catheter-related URI, and pneumonia. 3. ESBL strains are resistant to all beta lactams except carbapenems. |
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| Airborne precautions - what are you protecting against - what diseases do you use this in - what are the precautions |
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| protection against fomites you use it in TB, measles, chicken pox N95 dusk mask, negative pressure room |
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| Droplet precautions - what diseases do you use this in - what are you protecting against - what are the precautions |
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| mumps, rubella, influenza, meningococcus droplets from sneezes surgical mask, private room |
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| Contact precautions -what diseases do you use this in - what are the precautions |
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| - a lot: MRSA, VRE, C. diff, enteritis, hepatitis A, RSV, lice and scabies - gown and gloves required, private room, patient-dedicated stethoscopes and thermometers |
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| Name some pathogens that invade the epithelium but do not go deeper. Resp - Skin - Urogenital - GI - Why is this the case? |
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| Resp - rhinovirus, influenza Skin - HPV Urogenital - Chlamydia trachomatis, HPV GI - rotavirus, Shigella Could be because it gets too hot past the epithelium, or the pathogen has specific adhesins for epithelial cells only |
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| Name some example organisms that invade through the epithelium and then just keep going Skin GI tract Respiratory Urogenital |
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| Skin - Stapholococcus aureus GI - Salmonella typhi, Poliovirus Resp - Measles, VZV, Mycobacteria Tuberculosis Urogenital - HSV, Treponema pallidum |
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Complete the following table
Yersinia spp Shigella spp Salmonella spp
Genes Mode of Entry Cells/Tissues invaded Site of replication |
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| Genes: Yersinia - 3, the main one is invasin Shigella - 30, all of which are on plasmids Salmonella - 30, all of which are chromosomal Mode of entry Yersinia - invasin binds to beta-1 integrin on epithelial cells, resulting in changes in the host cell through signal transduction. This causes the host cell membrane to adhere to the bacterium at multiple points, leading to the host cell "zippering it up" Shigella - Temperature triggers expression of Ipa, which is released from the bacterium and forms a complex on the host cell surface, causing massive actin polymerization and ruffling - this results in macropinocytosis Salmonella - same as above except the released protein is Sip Cells/Tissues invaded Yersinia - M Cells of colon and ileum only, then spreads through lymph, ending at mesenteric lymph nodes. Resists phagocytosis with Yops Shigella - M cells only, does not breach epithelium, mainly infects colon Salmonella - M cells or enterocyes - some species breach epithelium, mainly infects ileum Site of replication Yersinia - extracellular Shigella - Cytoplasm Salmonella - Endosome |
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| List of example pathogens that disseminate via the blood |
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| Extracellular: Strep pneumoniae Hepatitis B Trypanasoma spp In RBCs: malaria In leukocytes: Listeria monocytogenes In leukocytes: Measles |
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| Shigella 1. Pathogenesis 2. Diagnosis 3. Prevention and treatment 4. Which are the most virulent? |
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| 1. Using a Mxi-Spa translocon needle, it secretes Ipa (T3SS), which assembles on the surface of M cells in the colon and causes membrane ruffling, leading to uptake by macropinocytosis. It is transcytosed and picked up by a macrophage which it kills. It either enters another macrophage, or it enters the basal surface of a colonocyte. Once in the colonocyte it can spread from cell to cell using the IcsA (gives it motility via cells actin) or IcsB (forms a projection onto the next cell). The macrophages will recruit polys to the site, resulting in inflammation, fecal leukocytes. Inflammation and hemmorhagic colitis also caused by Shiga toxin, released by some strains (mainly S. dysenteriae) 2. Diagnosis is by fecal leukocytes + culture (MacConkey agar, grows yellow because lactose -) 3. Prevention by good hygiene, a vaccine is in the works. Treatment can be by antiobiotics, but make sure not to use anti-motility agents 4. S. sonnei is mild, S. flexneri and S. dysenteriae are bad |
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| Name 3 organisms that have prevalent beta-lactamase activity-against which drugs? |
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| 35% of H. flu and 100% of M. catarrhalis have beta lactamase activity against amoxicillin. It is also extremely common in Staphylococcus aureus |
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| In what species are ESBLs commonly found? |
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| Klebsiella, E. Coli, and other GNR |
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| Which organisms mount resistance to beta lactams by altering their PBP? |
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| Staph aureus (MRSA), E. faecium, S. pneumoniae |
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| How does Pseudomonas aeruginosa mount resistance to quinolones? |
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| Combination of 2 mechanisms: 1. Downregulation of OprD porin, by which quinolones enter the cell 2. Increased efflux pump |
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| Which drugs is E. Coli commonly resistant to? |
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| It has beta-lactamase, ESBL is mounting. Also commonly resistant to TMP/SMZ |
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| Describe resistance in Enterococci spp |
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| Naturally resistant to many antibiotics. All we have is ampicillin and vancomycin - resistance to these is mounting |
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| How does HA-MRSA differ from CA-MRSA? |
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| It has different genes: MecA which encodes its altered PBP, Panton-Valentine Leukocidin which is a cytotoxin. Importantly, while HA-MRSA is only susceptible to vancomycin, CA-MRSA has broader susceptibility, including clindamycin |
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| Mechanism of resistance in S. pneumoniae? |
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| Altered PBP |
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| What type of resistance is commonly seen in group A strep and how does it work? |
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| Macrolide resistance: 3 mechanisms. 1. Altered target - methylation of the ribosome. Phenotype is called MLSi or MLSc, caused by erm(A) and erm (B) genes. 2. Altered target - ribosomal mutations 3. Increased efflux pumps. MefA is the gene responsible |
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| Define the following terms: Transformation Transduction Conjugation |
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| Transformation - picking up of naked DNA Transduction - picking up DNA from a virus (bacteriophage) Conjugation - two bacteria contact one another and plasmid is transferred |
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| Describe the process of transformation |
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| - only occurs between bacteria of similar species - cell lyses and the DNA floats away - a single strand is picked up by a surface DNA receptor and endocytosed - it goes to the nucleus and recombines homologously with chromosome |
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| Deescribe the process of transduction |
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| A bacteriophage infecting a cell accidentally puts a piece of bacterial DNA in its capsid instead of its own, then it infects another bacteria. That piece of DNA does homologous recombination with the host genome. - phages are usually host-restricted (i.e. happens between similar/same species) - host must have phage receptor |
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| What do all plasmids contain? |
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| - an origin of replication - Cop - a gene determining copy number (larger plasmids tend to make fewer copies) - a protein that initiates replication known as "rep" gene. Aside from this gene, relies on the host machinery for replication |
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| What does comes compatible mean in regard to plasmids? |
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| Two plasmids are compatible if they can reside together in the same cell |
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| What does it mean to say that a plasmid is conjugative? What genes does a conjugative plasmid have? Are R plasmids typically conjugative? |
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| Conjugative = it encodes genes to initiate conjugation (formation of sex pilus). These are encoded by the Tra genes. R plasmids are generally conjugative. |
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| What does oriT refer to? Describe the process of conjugation |
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| - the site where the plasmid is nicked during conjugation. A sex pilus is formed, the plasmid is nicked, and one strand is transferred across. Then replication in both bacteria restores the plasmids to dsDNA |
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| Describe integrons |
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| Mobile DNA elements that capture genes and insert in various sites via homologous recombination. Associated with carrying multiple drug-resistant cassettes. |
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| Transposons: Insertion sequences vs. transposons conservative vs. replicative What do they have at their ends? |
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| Insertion sequence: a short piece of DNA that only carries genes necessary for its own movement. Transposon: carries the transposase protein, needed for its movement, along with other unrelated genes, for example antibiotic resistance Conservative = cut and paste. Replicative = copy and paste Inverted repeats |
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| Types of antibiotic therapy and their descriptions, examples of when used if applicable |
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| 1. Prophylaxis: - malaria - immunocompromised, against PCP, CMV, fungal - on burns and wounds - ascites - inducing bacteremia, to prevent endocarditis (controversial as transient bacteremia occurs daily) 2. pre-emptive - means you are looking at lab results, but there are no clinical symptoms. Ex. bone marrow transplant patient who is immunosuppressed, you see CMV PCR titer increasing 3. empiric - means patient is sick, but you don't know the organism - use in CAP, VAP, neutropenic fever. DO NOT use in the following situations: URI, chronic illness, cultured MRSA or VRE or coag negative staph in the blood. The patient must be sick. 4. pathogen-directed - means you know the organism, but not what antibiotic it's susceptible to. Hospitals have charts of what % of isolates of a given organism are susceptible to what 5. susceptibility - directed - you know the organism and its susceptibility - could have been determined by disk-diffusion assay or MIC. Then you choose the antibiotic that is the most effective, is the cheapest, has the least toxicity, and is the narrowest spectrum |
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| Definition of MIC, explain procedure, is low good or bad? |
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| Minimum inhibitory concentration- you put different dilutions of the antibiotic in a test tube with culture broth and observe the minimum concentration at which there is no growth. Low MIC = low concentration needed to inhibit = good. |
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| How can you stain fungi? Does gram staining work? |
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| silver stain, calcofluor stain, periodic acid-Schiff test. Gram-staining does not work |
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| What is in the fungal cell wall? |
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| glucans sometimes chitin |
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| Describe the 3 types of fungi |
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| molds - composed of hyphae, which are long rods of tubular cell(s). Mycelium = mass of branching hyphae yeasts - resemble bacteria when grown on a plate. Unicellular, although can become pseudohyphae if elongated. Reproduce by budding dimorphic - mold-like in the environment, hyphae-like in the body |
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| Amphotericin 1. Mechanism 2. Activity 3. Toxicity |
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| 1. Binds to ergosterol, increasing membrane permeability 2. against practically all fungi 3. Severe nephrotoxicity limits its use |
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| Nystatin 1. MEchanism 2. Uses/Activity |
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| 1. Binds to ergosterol, increasing membrane permeability 2. Topical only |
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| -azoles 1. Mechanism 2. types and uses 3. What can fluconazole NOT be used against |
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| 1. Prevent the production of ergosterol from lanosterol. 2. imidazoles = topical triazoles = for severe fungal infections 3. molds |
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| echinocandins 1. Mechanism 2. Activity/Uses (what is it not good against?) 3. Names of specific drugs |
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| 1. prevent synthesis of 1, 3 beta glucan (cell wall component) 2. Good against candida and aspergillus, NOT against cryptococcus 3. Caspofungin, micafungin, anidulafungin |
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| Flucytosine 1. Mechanism 2. Uses |
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| 1. Inhibits thymitidyl snythetase, which is necessary for fungal DNA synthesis 2. Never used alone because resistance crops up rapidly, generally in combination with amphotericin. Common usage in this way for cryptococcal meningitis |
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| Terbanifine 1. Characteristics 2. Mechanisms 3. Uses |
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| 1. Allylamide 2. Inhibits squalene epioxidase, which inhibits lanosterol and those ergosterol synthesis. 3. Oral or topical use for treatment of superficial fungal infections (i.e. dermatophytes) |
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| Under what conditions only do fungi cause infections in humans? |
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| immunocompromised |
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| Name (and categorize, if applicable) the major fungal pathogens, and if applicable, what disease they cause |
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| Candida spp (yeasts) Cryptococcus neoformans (yeast) Aspergillus spp (molds) Zygomyces spp (molds) Sporotrichosis - sporothryx schenckii (dimorphic) Geographic dimorphics: -Histoplasma capsulatum (Dimorphic) -Coccidioides immitis (Dimorphic) -Blastomyces dermatitidis (Dimorphic) Pneumocystis jiroveci (Yeast) Dermatophytes: - zoophilic: microsporum canis (causes tinea capitis - ringworm) - geophilic - anthrophilic: Trichophyton rubrum (causes tinea pedis and tinea cruris). Various ones case Onychomycosis - nail infections. |
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| Candida spp 1. 1st and 2nd most common infectious species 2. Pathogenesis (normal habitat, etc.) 3. Disease manifestations 4. Treatment |
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| 1. C albicans (most common) and C Galbrata 2. Normal flora of GI tract, mouth, vagina. - kept in check by local flora (AB therapy -> candidiasis) - kept in check by mucus membrane integrity (chemotherapy breaking down membranes and GI surgery -> candidiasis) - kept in check by immune system (corticosteroids and other IS -> candidiasis) 3. A wide spectrum. Superficial infections of mouth (thrush), skin (diaper rash), esophagus, vagina. More seriously, can disseminate, causing blood infection, endocarditis, abscesses in multiple sites. 4. Amphotericin, echinocandins, or azoles |
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| Cryptococcus neoformans 1. Geographic location 2. Where does it live3. How does it get into the host4. Virulence factors 5. Presentation 6. Diagnosis 7. Therapy |
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| 1. Ubiquitous 2. Soil, bird droppings, trees, rotted wood 3. Inhaled 4. Polysaccharide capsule - antiphagocytic, antidetection, source of the cryptococcus antigen. Melanin - protects it against radical oxygen species. It grows best at 37 degrees C. 5. Most common and seriously is cryptococcal meningitis - usually a subacute meningitis (headache, vague neurological complaints, +/- fever). Also can cause pneumonia, cryptococcemia, skin lesions, prostatitis 6. India ink stain of CSF, culture of CSF, or detection of cryptococcus antigen in blood or CSF 7. Amphotericin + flucytozine, followed by fluconazole for maintenance |
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| Aspergillus spp 1. Common organisms causing infection 2. Risk factors 3. Presentation 4. Diagnosis 5. Treatment |
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| 1. A fumagatus, A flavus are common, A niger is rarer 2. Neutropenia, corticosteroids 3. most mild: ABPA (allergic bronchopulmonary aspergillosis) - an allergic reaction to the spores colonizing. Generally the person will have underlying asthma or CF - complains of asthma worsening. IgE and IgG against aspergillus are present, eosinophilia. aspergilloma - a ball of fungus in the lungs, can be asymptomatic or can cause pneumonia-like symptoms, hemoptysis. Can also occur in maxillary and ethmoid sinuses invasive aspergillosis - 90% mortality rate in some populations (transplant recipients). Mainly occurs in the immunocompromised Can also colonize external ear (mainly A niger here) - otomycosis. 4. Difficult. Can be by BAL -> culture, microscopy, detection of galactomannan antigen in BAL, blood. 5. Voriconazole = drug of choice. Also amphotericin, caspofungin, posiconazole, but NOT fluconazole (doesn't work on molds) |
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| Zygomycete 1. How does it get into the body2. What does it cause3. Prognosis? |
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| 1. Inhaled 2. Pneumonia-like symptoms 3. High mortality because it is resistant to antifungals |
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| Sporotrichosis 1. Causative organism. Mold or yeast2. Source of organism and how it gets into the body 3. Symptoms |
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| 1. Sporothryx schenckii (dimorphic) 2. Found in soil, plants that are woody and thorny (think of a rose gardener). Infects the skin 3. Erythema nodulosa. Can spread by lymph and cause inflamed subcutaneous nodles |
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| Histoplasma capsulatum 1. Where2. Source of organism, route of entry 3. Clinical manifestation 4. Diagnosis 5. Treatment |
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| 1. Ohio and Mississippi river valleys 2. Soil, bird droppings. Inhaled 3. ->Histoplasmosis. 90% are asymptomatic or have mild flu-like symptoms. Can progress to chronic pulmonary histoplasmosis or cavitary pulmonary histoplasmosis, and disseminate. 4. Culture, Histoplasma Ag in blood and urine 5. Amphotericin B, Itraconazole |
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| Coccidioides immitis 1. Where and what does it cause (popular term) |
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| SW US. Valley fever |
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| Blastomyces dermatitides 1. Where2. Progression of disease and manifestation |
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| 1. Ohio and Mississippi river valleys (much rarer than histoplasmosis) 2. Inhaled, colonizes lungs, then disseminates. Causes serious lung and skin lesions (plaques, etc.) |
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| Pneumocystis jiroveci 1. Characteristics 2. What disease does it case and describe it. How can it be prevented? |
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| 1. Yeast-like, lacks ergosterol in membrane 2. Pneumocystis pneumonia - subacute pneumonia, unproductive cough, low oxygen saturation). Prevent with bactrim prophylaxis |
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| Dermatophytes 1. Yeast or mold2. Where do they infect3. Diagnosis |
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| 1. Molds 2. Superficial keratin layer 3. Skin scrapings ->culture or microscopy. |
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| List all of the pathogenic parasites and their classification |
answer
| Protozoa: Plasmodium spp Babesia spp Trichomonas vaginalis Toxoplasma gondii Trypanosoma Cryptosporidium parvum Microsporidium spp Giardia lamblia Leishmania Entamoeba hystolytica Acanthamoeba Intestinal roundworms: Ascaris lumbricoides Hookworm (Necator americanus, ancylostoma duodenale) Pinworm (enterobius vermicularis) Whipworm Strongyloides stercoralis Tissue roundworms: Wuchereria bancrofti (-> elephantiasis) Brugia malayi (-> elephantiasis) Onchocerca volvulus (->river blindness) Loa loa spp Mansonella spp Tapeworms (cestodes) Taenia solium Taenia saginata Echinococcus granulosus Flukes (trematodes) Schistosoma spp |
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| Definitive host vs. Intermediate host |
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| Definitive host = where the parasite reproduces sexually Intermediate host = where the parasite reproduces asexually |
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| Entamoeba hystolytica 1. Life cycle 2. Pathogenesis and manifestations 3. Epidemiology 4. Treatment |
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| 1. Trophozoites are in the gut, they can come together to form infectious cysts which are in the feces - they are ingested and then enter the next person's gut, where they mature into trophozoites 2. 90% just cruise through, asymptomic. 10% trophozoites will invade the colonic mucosa, causing bloody diarrhea. They can migrate to the liver through the portal blood causing a liver abscess 3. Rare in the us except MSM and facilities 4. Metronidazole |
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| Acanthamoeba spp. What do you need to know about them? |
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| They swim around in fresh water and infect your eyes if you if you use that water to wash your contacts. ->keratitis (infection of the cornea) |
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| What are the four protozoa that cause diarrhea, and what is notable about each of them? Where do they occur? |
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| 1. Entamoeba hystolytica - mostly abroad, a bit in the U.S. Can cause liver abscesses 2. Giardia lamblia - everywhere. People with IgA deficiency are susceptible. Leads to frothy, smelly diarrhea and abdominal bloating 3. Cryptosporidum parvum - everywhere. Prolonged diarrhea 4. Microsporidium spp. - everywhere. Common in immunocompromised (AIDS) |
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| Trichomonas vaginalis 1. Route of transmission 2. Symptoms/Manifestations 3. Diagnosis 4. Treatment |
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| 1. STI 2. Male - asymptomatic. Female - Vaginal irritation, soreness. Frothy discharge with characteristic fish odor 3. Wet mount = pear shaped protozoa with flagella twitching around 4. Metronidazole |
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| Babesia -vector -geography |
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| - ticks - U.S - esp. Northeastern (Martha's Vineyard, Cape Cod, Nantucket Island) |
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| Leishmania spp 1. Vector 2. Geography 3. Manifestations |
answer
| 1. Sandfly 2. Central and South America, Middle East and Africa (Iraq - think veterans) 3. Varies depends on the organism and host immune system. Can cause disfiguring skin ulcers, or can have visceral effects (=Kala azar - hepatosplenomegaly) |
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| Diseases, reservoirs, and vectors of the Trypanosoma spp. |
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| Chagas disease = American trypanosoma. Vector = Kissing bug reduviid. Causes colonic/esophageal dysmotility, cardiac arrhythmia, myocarditis. May cause neuronal damage as sequelae due to autoimmune molecular mimcry Sleeping sickness = African trypanosoma. Vector = Tsetse fly. Reservoir = cattle. Severe meningo-encephalitis. Fatal. |
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| Ascaris lifecycle and treatment |
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| Ascaris. adult worm in gut lays eggs. Contaminated feces are then consumed, the eggs hatch and the larvae enter the bloodstream. There they travel into the lungs and throat, where they are coughed up and swallowed into the gut for the second time, where they mature into an adult. Treated with mebendazole, albendazole, ivermectin |
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| Pinworm symptoms, diagnosis, and treatment |
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| Pinworm (enterobius vermicularis) - perianal itch - perianal scotch tape, test it in the morning for eggs - treat whole family with albendazole, mebendazole, or pyrantel |
question
| Hookworm and strongyloides lifecycle ancylostoma disease course vs. strongyloides disease course. strongyloides treatment. |
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| In soil, eggs and hatch and larvae penetrate the skin. They swim to the gut, where they mature and lay eggs. Ancylostoma = not a human disease (from dog poop). Therefore just causes a rash on the feet that self resolves. Strongyloides = lifelong infection. Waits around for the immune system to be deficient, then causes pneumonia, GI rupture by the worms perforating membranes. Treatment is with ivermectin. |
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| Filariasis 1. Causative organisms and their lifecycle 2. Clinical manifestations 3. Organisms and what they cause |
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| 1. Wuchereria bancrofti, Brugia malayi, Onchocerca volvulus, Loa loa spp, Mansonella spp. Larvae are transmitted through insect bite, they mature into adult worms in the lymphatics, causing elephantiasis and blindness if it occurs in the eye. The organisms are tissue nematodes. EB and BM cause elephantiasis. OV = river blindness |
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| Schistosoma spp. 1. Lifecycle 2. Manifestations 3. Diagnosis 4. Treatment |
answer
| 1. Adult worms in the veins of the GI tract and bladder lay eggs, which are passed out by urine or feces. These get into fresh water, where they infect a snail (intermediate host). In the snail they turn into cerceriae, which then penetrate the skin of humans. They turn into larvae which swim to the liver and lungs, mature into worms, and then swim into the veins of the bladder and GI tract. 2. acute schistosomiasis = Kataya fever. chronic schistosomiasis -> liver cirrhosis, bladder cancer. 3. Diagnosis is by detecting the eggs in feces and urine. Also see eosinophilia 4. Treatment = praziquantel |
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| T. solium lifecycle |
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| Adult tapeworms in gut lay eggs, that humans can ingest, or more commonly are ingested by animals. In the pigs GI tract the eggs hatch to become oncospheres and then create cysts all over the body. The cysts are then ingested when you eat undercooked pork - the larvae then invade your GI tract and do the same hting as well as maturing into worms. Cysts all over body = cysticercosis. Neurocysticercosis = seizures. |
question
| What is the beef tapeworm called |
answer
| Taenia saginata |
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| Echinoccocus granulosus 1. What disease does it cause 2. Lifecycle 3. Treatment |
answer
| Hiyatid fever 2. Dogs are the definitive hosts, eggs can be ingested by sheep and humans. Invades and causes cysticercosis 3. Albendazole |
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| Lice -Genus and species of different spots infected - treatment |
answer
| Pediculosis capitus Pediculosis corporis -permethrin, ivermectin, malathion |
question
| Scabies 1. Causative organism 2. Pathogenesis 3. Where4. Treatment |
answer
| 1. Sarcoptes scabei 2. Feces cause the itching 3. Webbing of hands. 5% immunocompromised = Norwegian scabies. 4. Permethrin cream or PO ivermectin. |
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| Thayer-Martin media |
answer
| Grows Neisseria spp exclusively |
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| Neisseria meningitidis 1. Characteristics 2. How can you tell it apart from N. Gonorrhoeae3. Virulence Factors 4. Pathogenesis 5. Presentation 6. Diagnosis, Prevention, Treatment 7. Why hasn't vaccine reduced the incidence in infants? |
answer
| 1. Gram (-) diplococci, oxidase (+), grow on Thayer-Martin media, non-motile 2. It has a capsule and turns maltose into acid - N. Gonorrhoeae does neither 3. Capsule - anti-phagocytic, anti-complement. Comes in different serotypes - A,B,C,W135. Pili, Outer membrane proteins - aid in adhesion, have some antigenic variation. IgA protease, transferrin, LOS 4. Colonizes nasopharynx (many carriers). Invades into blood, spreads to skin and brain. Destroys capillaries in skin, causing purpura, infects brain meninges. Also can cause arthritis and osteomyelitis 5. High fever, headache, nuchal rigidity, purpura. 6. Gram stain of CSF fluid. If it's diplicocci gram (-) you can be sure it's N. meningitidis. Prevention - give antibiotics to contacts, immunize college students, children, those who are susceptible (complement deficiency, asplenics). Treatment - a wide range of antibiotics work - penicillins, fluoroquinolones, cephalosporins. Latest vaccine = Menactra. 7. Organisms with the B capsule - the body won't make antibodies against them because they look like the sialic acid residues on neuronal cells. This B capsule accounts for 80% of neonatal infections (also some younger kids, college students). |
question
| Streptococcus pyogenes 1. Characteristics 2. How do you differentiate S. pyogenes from S. agalactiae3. Reservoir and spread4. Bacteremia5. Virulence Factors 6. Disease Manifestations 7. Diagnosis 8. Treatment 9. Prevention |
answer
| 1. Gram (+) cocci in chains, catalase (-), non motile, non spore forming 2. PYR test, susceptibility to bacitracin (pyogenes is) 3. Human reservoir - spread through fomites 4. Yes, it can occur. Less likely in pharyngitis because there is more competitive local flora to inhibit it. 5. M protein - lots of variation. A protein that sticks out through the cell wall. Binds to Factor H -> molecular mimcry. W/ LTA, adheres to the fibronectin around epithelium. Causes rheumatic fever and poststreptococcal glomerulonephritis (PSGN). Lipotechoic acid (LPA) -> adhesion to fibronectin. Hyaluronic capsule -> anti-phagocytic, looks like ECM (momecular mimicry). C5a peptidase. Streptolysin O and Sterptolysin S = hemolysins. Destroy RBCs mainly, also WBCs and tissue. Streptokinase A = dissolves blood clots that the body tries to make to wall it off. Streptodornase = DNAse. Hyaluronidase - digests ECM. Erythrogenic toxins -> get into blood and cause toxic shock syndrome by activating T Cells 6. Suppurative = pharyngitis with abscesses, cellulitis, abscesses, pyoderma, necrotizing fasciitis. Toxogenic - erythrogenic toxin gets into blood stream, causing scarlet fever. Non-suppurative = Rheumatic fever, PSGN (hematuria, edema, HTN, self resolves) 7. gram stain pus from wound, culture throat swab (too many other streps to gram stain) 8. Penicillin, other antibiotics 9. No vaccine, penicillin prophylaxis if rheumatoid fever. |
question
| Streptococci classification scheme |
answer
| Beta (complete) Group A: pyogenes Group B: agalactiae Alpha (partial) Pneumoniae Viridans Gamma (Non) Enterococcus Viridans |
question
| What is fabulation? |
answer
