Smith Micro Exam 4 (2011) – Flashcards
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| Syphilis -Etiology, Description |
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| Treponema pallidum GRAM NONREACTIVE – Lipid coating doesn’t stain well -Might be considered G- Spirochete Hypotroph: Obligate parasite (something alive to grow it in) [bunnies in labs] ID50 = 57 |
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| Syphilis -Transmission |
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| -STD/STI – Humans are the only natural host -Lesions: (Rash) Dental hygienist spread through hands 20 diff patients w/o gloves -Fomites: Dies within minutes in environment, Unlikely to transmit -STORCH: Go through placenta and infect child -Hard to transmit by blood -Light abrasion (rubbing, not even a cut): Genital area |
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| Syphilis -Incubation |
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| 2-3 weeks |
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| Syphilis -Morbidity -Mortality |
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| 40,000 reported Unreported = 80% more People don't know b/c are healthy carriers so they don't report it and also spread it 100 syphilis deaths -If you get 1, you can get all of them, 1 leads to an increase of others b/c break down immune system |
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| Syphilis -Symptoms |
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| Primary Phase Primary Latent Phase Secondary Phase Latent Phase -Early Latent -Late latent Tertiary Phase -Destroy tissues -Cardiovascular -Neurosyphilis |
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| Primary phase |
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| Chancre (lesion) develops at point of abrasion/transmission [genital, eyes, lips] Hard nodule develops and breaks open into a shallow ulcer w/organisms spilling out Lasts 4-5 weeks, transmitting all the time -Indolent: No pain -Males scratch: E. coli, Staph in chancre causes it to burn -Females: Chancre is in vaginal area = Healthy carrier b/c can’t see and there are no symptoms |
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| Primary latent phase |
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| Latent = hidden, Blood sample would have antibodies in it “Teflon pathogen” = Antibodies not produced due to lipid coating 0-6 months: The longer this phase is, the more antibodies produced, More body wins against it |
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| Secondary phase |
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| Flu-like syndrome, Indolent Rash (prominent, all over body, spreads disease), Lymphadenopathy (swollen lymph nodes) Lasts weeks to months after PLP depending on who has it Might miss this stage or mistake it for some other issue -As long as you have the rash, you are infectious |
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| Latent phase |
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| Hidden most of the time Early latent: First 2-4 years having it -Could have outbreaks of secondary phase Late latent phase: After 4 years having it -Can only transfer mother ? Fetus -Usually in US antibiotic treatment ends disease before it gets to this stage -25% Cases = Completely cured, No organism, No symptoms, No antibodies -25% Cases = Remain in Late Latent phase indefinitely (as long as not take antibiotics) Can’t isolate organism, but can detect by DNA (hypersensitivity) Slow destruction of tissues -50% Cases = Progress to tertiary stage, Rapid destruction of tissues |
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| Tertiary phase |
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| Lesions Gumma: Granulomatous, Indolent, Hypersensitivity (can only detect in DNA) -Destroys tissues, Locally destructive (hole in nose tissue) -Cardiovascular: Damages heart, Aorta enlarged, Aneurysms (bubbles/weak areas in vessels that can burst) -Neurosyphilis: Nervous system, Go blind, Deaf, Dementia |
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| Chancre |
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| Syphilis lesion at site of abrasion |
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| Neonatal Syphilis |
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| “Congenital syphilis” Prenatal syphilis |
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| Indolent: |
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| No pain |
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| Neonatal Syphilis: Transmission: |
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| Mother ? Fetus through placenta in 5th month of pregnancy -50% chance w/o antibiotics -2% with treatment |
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| Neonatal Syphilis Incidence |
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| 500,000 (50% of cases where organism passes through placenta) = Neonatal syphilis, survive -60% born with latent cases – Positive for antibodies -40% have -early lesions (rash within few weeks of birth) or -late lesions (gummas of tertiary syphilis develop 2-3 years later) 250,000 (25% cases) = Stillborn, Die in utero b/c infection is so bad 250,000 (25%) = Babies miscarried (heavy infection, early birth, die) |
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| Neonatal syphilis Symptoms |
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| Stigmata: Hutchinson’s Triad -Hutchinson’s incisors = Teeth have notch in them -Interstitial keratitis = Eye cornea scarred, Lead to vision loss/blindness -8th nerve deafness = Beethoven may have had this (bananananana) |
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| Diagnosis of syphilis |
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| -Microscopic examination: Dark field microscope (or fluorescent) Scrape fluid from chancre or rash to see spirochetes swimming around -X-ray: Detect gummas -Serological Test for Syphilis: Looking for antibodies, Kit has antigen to test |
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| Diagnosis of syphilis Serological tests |
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| Screening Test: “Nontreponemal” (not growing out organism b/c would require rabbits) -Rapid Plasma Reagin (RPR): Tube test -VDRL (vineral disease research laboratory test): Slide test Take sample of blood + Cardiolipin (from membrane of mitochnodria, syphilis affects mitochondria causing them to release cardiolipin) Reagins/Wasserman/Immunoglobulins (IgG, IgM): Antibodies produced to clean up cardiolipin from disease -Test detects antibodies produced b/c syphilis or other causing antibodies against cardiolipin to be produced 16-18% false positives – Other diseases/vaccines 10% false negatives – (This test is cheap) Specific Test: Have to grow out Treponema pallidum (antigen) -Take blood sample + organism -Flourescent Treponemal Antibody Absorption test: Reiter strain used -Hemagglutination Treponema Test for Syphilis: Nikol strain used Almost no false positives b/c more sensitive so # false negatives is down |
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| Treatment of Syphilis |
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| Benzathine Penicillin G (not resistant yet) -1 dose for less than a year -More than 1 for over a year EPT (Expedited partner Treatment): Partner will re-transmit disease back to cured Index (first) patient -Give Index patient medication for partner as well, so they both get cured |
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| Gonorrhea – “The Drip” Etiology: |
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| Neisseria gonorrhoeae GRAM – Diplococci Capneic incubation: Microaerophilic ?O2 ?CO2 -Enriched media: Chocolate agar (blood with nutrients) -Thayer Martin Selective Agar (isolation in clinical lab), -Inhibit w/ Vancomycin (G+) Colistin (Polymyxin B, G- rods) Nystatin (yeast) so organism may grow out |
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| Gonorrhea Transmission: |
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| STD -Opthalmia neonatorum: Get in baby eyes from birthing canals -Fomites: Dies within hour, Unlikely |
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| Gonorrhea Morbidity: |
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| 350,000 each year reported (most unreported, probably millions) |
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| Gonorrhea Symptoms - Male |
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| [Common for all types of urethritis/urethra irritation from STD to E. coli] Males: 10-20% asymptomatic (healthy carriers) – Shedding disease but don’t have symptoms -Purulent urethral discharge: Pus (neutrophils loaded w/ organism as WBCs phagocytize it) out uthethra -Dysuria: Painful urination, G- neissera dies and releases endotoxin irritating the urethra -Frequency of urination: When irritated, want to pee more often -Convalescent carrier: Recovering from symptoms you once had, Still shedding organism in recovery -Complications: Urethral stricture – Narrowing due to scar tissue buildup -Get gonorrhea over and over, Mutates, No resistance builds Sterility: Epididymus inflamed and damaged (where sperm multiplies) Chronic prostatitis: Prostate gland inflamed |
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| Gonorrhea Symptoms - Female |
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| Females: -Purulent urethral discharge -Dysuria (endotoxin pain) -Frequency of urination -Invade cervix: Cervicitis – UTI (could also be caused by E. coli from thong) -PID (Pelvic Inflammatory Disease): Uterus (endometritus) – Hysterectomy needed Fallopian tubes (salpingitis) - Sterility: Scar tissue buildup 750,000 cases PID reported, 75,000 (10%) turn sterile -Some caused by chlamydia trachomatis, E. coli |
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| Other Forms: Gonorrhea |
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| : Anal gonorrhea – Rectum Pharyngeal gonorrhea – Pharynx Gonococcal arthritis: 16-50 years old -Septic arthritis: Organism involved [Aseptic = No organism involved, Pain from overwork, knee] |
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| Gonorrhea Diagnosis: |
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| Microscopically: Check for GRAM – Intracellular Diplococci -Check the pus dripping out during acute phase -Males = 99% accurate -Females = 50% accurate b/c many organisms growing Cultural: Thayer Martin Selective Agar – Antibiotics make only gonorrhea grow out (-Nothing actually inhibited, they just grow slower says Mr. Smith) -Males = 60% -Females = 40% Biochemical Tests: Oxidase Positive (like pseudomonas and others) -Carbohydrates Antigen-Antibody Reactions: -Serology: Not effective b/c Neisseria gonorrheae keeps mutating PCR: DNA from urine sample where organism is |
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| Gonorrhea Treatment: |
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| PPNG – Penicillinase Producing – DOC = Ceftriaxone (works against your syphilis too) (+Chalmydia trachomatis) = Ceftriaxone does NOT work ? Post gonococcal utethritis Doxycycline or Azithromycin to go along with -Azithromycin no longer effective against syphilis |
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| Gonorrhea Prevention: |
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| Opthalmia neonatorum DOC = Erythromycin -Adults = Education, Trace contacts to make EPT possible Test all females = Most likely to be healthy carriers (2/3 – ? asymptomatic) (67%-75%) Test everyone positive for 1 STD to test for all STDs |
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| Meningitis Etiology: |
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| Neisseria meningitidis Epidemic (contagious), Spread by droplet infection, 1% 99% healthy carriers Will develop natural immunity! – Individual immunity |
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| Meningitis Treatment: |
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| -Penicillin G = DOC – Given IV for systemic infection like this, High doses |
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| Meningitis Prevention: |
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| Given to susceptible patients (like college dormers) -Prophylactic: Ciprofloxacin |
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| Pseudomonas aeruginosa Occurrence: |
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| Ubiquitous (all over all the time) -Opprotunists: Need an opportunity for it to enter body -Nosocomial infections: 9% |
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| Pseudomonas aeruginosa Resistance: |
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| Antibiotic sensitivity testing -Some doctors would rather treat you concurrently instead of testing -Pseudomonas aeruginosa sometimes grows in antibiotics! = Very resistant, Live in eye -Triclosan: Antimicrobial agent psesudomonas is (10-15% more resistant than it should be), Protein coagulator |
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| Pseudomonas aeruginosa Super infection: |
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| Resistant nonfermenter will grow even if antibiotics are present, Grow on top of another infection (Secondary infection) |
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| Pseudomonas aeruginosa Examples of Infections: |
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| Wound infections Superficial skin infections Genito-Urinary tract Eye "Others" |
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| Pseudomonas aeruginosa Examples of Infections: Wound |
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| Burn – Burnt skin is like open culture medium (Pseudomonas, Proteus, Staph) ?Septicemia: Poor prognosis b/c hard to clear out Pseudomonas, 75% death by infection (14% by pseudomonas infections) |
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| Pseudomonas aeruginosa Examples of Infections: Superficial skin |
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| /”Pseudomonas pyoderma”: Green pus/mucus, Smell like grapes Athlete’s foot Bed sores Eczema Hot Tub Dermititis: Rash when pores open up and go down hair follicles, Self-limiting b/c aerobic and can’t spread deep |
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| Pseudomonas aeruginosa Examples of Infections: Genito-urinary |
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| UTI, Nosocomial, Instrumentation (dirty catheter, ect.) Is this complicated or uncomplicated? Complicated = Reason you get this, Area plugged up |
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| Pseudomonas aeruginosa Examples of Infections: Eye |
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| Ulceration of eye attacks cornea Contact lenses |
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| Pseudomonas aeruginosa Examples of Infections: "Others" |
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| Pneumonia (intubation @ hospital) Meningitis Osteomyelitis – Bone infection Otic infections – Swimmer’s ear (pseudomonas, staph) |
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| Pseudomonas aeruginosa Treatment: |
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| Do an antibiotic sensitivity test (Kirby Baur, MIC) while treating patient concurrently UTI caused by pseudomonas – Ciprofloxacin (DOC) “Others” – Ticarcillin (cell wall) + Gentamicin (protein synthesis) Pipericillin (cell wall) + Gentamycin (protein synthesis) Synergistic: Work well together??? |
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| Bordetella pertussis: |
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| “Whooping cough,” Hard spasmatic coughing, Gasping for breath, More severe in children under 7 ?Lung collapse, Convulsions, Death [In children] ?Less severe cough [Older children to adults] |
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| Bordetella pertussis: Prevention |
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| DTaP (high dose) – Pediatric dose (Diptheria, Tetanus, acellular Pertussus), 5 shots, Tdap (booster) – 11/12 years old (adolescents), Replacement for adult vaccine Td (adult vaccine) – 16-64 years old, Given every 10 years |
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| Bordetella pertussis: Treatment |
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| Erythromycin, Azythromycin, Clarithromycin (any one of the three are DOC) |
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| Legonella pneumophilia |
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| “Legionnaire’s disease” (1976/Bicentenial) -Atypical pneumonia -Over 30 people died -GRAM – rod/bacullus = Legionella pneumo (lung) philia (loving) -Prefer cool water -Simbiotic relationship with amoeba -Droplet infection: ID50 = 1 rod -Dirty air conditioner -Individual resistance -Common in males over 50 years old (older servicemen) Cruise ship, Playboy party fog machine |
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| Legonella pneumophilia Treatment: |
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| Azythromycin (DOC) |
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| Salmonellosis |
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| Salmonella food poisoning/Gastroenteritis: Food infection (feces in it), Grow in small intestine lined with epithelial cells, which spread cell to cell causing septicemia -5 million deaths a year by diarrhea Very young, Very old – Lose fluids and electrolytes |
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| Salmonellosis Etiology: |
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| Salmonella enterica – Infect warm blooded animal Salmonella enteriditis (SE) - Found in chicken eggs, Get in before shell is formed Salmonella typhimurium – Most common (serovar of S. enterica) “Salmonella enterica serovar typhimurium” is best way to write “Salmonella enterica serovar enteriditis” |
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| Salmonellosis Transmission: |
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| ID50 = 10^5 (100,000 to 1 billion) but acid can kill them before infect -Disease of “lower animals” (not human-human), Dogs and cats spread it via feces, In food Birds – Turkey, chicken, Put dead bird in vat with feces coming out, Defeather Reptiles – Wild turtles w/salmonella, Zoo petting animals |
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| Salmonellosis Symptoms: |
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| 3 days -Diarrhea, Vomiting, Severe abdominal cramps -Headache b/c septicemia |
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| Salmonellosis Treatment: |
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| None Young children, Immunocompromised (AIDs) – Ceftriaxone, Cefotaxine Will spread Salmonella for up to 6 months after cure b/c still in cells |
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| Salmonellosis Complications: |
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| Replace fluids and electrolytes lost |
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| Typhoid Fever Etiology: |
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| Salmonella typhi “Salmonella enterica serovar typhi” = New -Humans are only host (must have ingested human feces) 1,000 to 10,000 bacilli (small dose) |
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| Typhoid Fever Symptoms: |
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| -Diarrhea, Vomiting, Headache, Fever, Severe abdominal cramps -Ulcerations: Perforations, Actual holes 15% mortality rate |
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| Typhoid Fever Treatment: |
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| Ciprofloxacin (DOC), Ceftriaxone (DOC) -Keep from becoming carrier |
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| Shigellosis Etiology: |
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| Bacillary dysentery - GRAM – ROD/BACILLUS, Blood and mucus sloughed off in diarrhea Shigella sonnei – Northern US Shigella flexneri – Southern US Shigella dysenteria – Asiatic strain, Shigatoxin (hemorrhagic bleeding, danger in blood loss) *Most dangerous* -GRAM – BACILLI -Endotoxin -Exotoxin: Enterotoxin |
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| Shigellosis Transmission: |
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| ID50 = 200 bacilli (resistant against stomach acid) -Food/water contaminated with human feces Symptoms: Incubation period = 1-14 days -Large intestine irritated: Job is to absorb water, so if interrupted water comes out w/stool, blood, mucus, Shigatoxin -Does not cause septicemia (stays in one area of body) |
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| Shigellosis Treatment: |
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| 1/3 cases require Hospitalization due to diarrhea = Shigella -Fluids, Electrolytes DOC: Ciprofloxacin |
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| Escherichia coli |
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| Look in water analysis -Coliform: GRAM -, Bacillus, Ferment lactose to produce gas (CO2) -Enteric: GI tract of mammals Can get into watershed (source of water) from nearby animals’ feces getting into water -Stool tool: Can tell if there is feces in the water -Strains: Over 150 strains, Differentiate strains through serology |
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| E. coli Strains: |
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| Over 150 strains, Differentiate strains through serology Most are not pathogenic Some opportunistic – 24% Nosocomial infections from people not washing their hands Some pathogenic - Enterotoxigenic (ETEC) = Strain of E. coli, Enterotoxins present to irritate bowels, Lots of water loss through diarrhea (Cholera) LT = Heat labile ST = Heat stable Enteroinvasive (EIEC) = Invade large intestine, (Shigella) Enteropathogenic (EPEC) Enterohemorragic (EHEC) = Lots of bleeding due to Shigotoxin EC0157:H7 = Strain of eneterohemoragic variety |
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| E. coli Infections: |
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| Cystitis Epidemic diarrhea/Summer diarrhea/Infantile Traveler’s diarrhea/Tourista Peritonitis "Others" |
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| E. coli Infections: Cystitis |
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| UTI in the bladder Uncomplicated – Does not involve patient on antibiotics (wiping out normal flora like E. coli), No instrumentation (catheters), No obstruction (mucus, dirt) -E. coli causes 85% uncomplicated cystitis infections -Proteus is #2 Complicated – -Proteus is #1 cause -Females more likely to get these diseases anatomically |
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| E. coli Infections: Epidemic diarrhea |
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| Epidemic diarrhea/Summer diarrhea/Infantile: Hot in the summer, Bacteria grow well, Baby wearing cloth diaper -Enteropathogenic, Enterohemorrhagic (specific strain) |
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| E. coli Infections: Traveler's Diarrhea |
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| Traveler’s diarrhea/Tourista: Don’t drink water in foreign country -Enterotoxigenic strain |
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| E. coli Infections: Peritonitis |
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| Peritoneum = Lining on inside of body -If intestines or appendix is perforated, leaks out peritonitis -Appendicitis: Blind pouch can be blocked with feces or objects, Inflamed and burst, E. coli is one cause |
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| E. coli Infections: "Others" |
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| E. coli is opportunist, Will cause infection wherever it enters |
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| E. coli Treatment: |
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| Ceftriaxone, Cefotaxine, Cefepime -What if they don’t identify this and realize it’s uncomplicated GI tract infectionBactrim (Sulfamethoxazole, Trimethoprim) |
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| Klebsiella Etiology: |
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| Klebsiella pneumonia – Enteric (intestines), Coliform (grows slowly in water analysis), Capsule (looks like someone sneezed if on plate) |
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| Klebsiella Diseases: |
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| Diseases: Nosocomial pneumonia: 10% of cases, Sticks to things like intubation tube and will grow Pediatric wards: Septicemia cause (from not washing hands) |
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| Klebsiella Treatment: |
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| Cefalosporin = Ceftriaxone, Cefotaxime, Cefepime |
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| Proteus Group |
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| Drug companies look for plants to use -Very resistant based on antibody testing Diseases: |
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| Proteus Group Diseases: + Treatment |
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| Proteus mirabilis – Cystitis, #1 strain isolated, #1 in burn patient infections Treat = Ampicillin Proteus vulgaris – Less commonly isolated, Cause cystitis and burn patient infections Morganella morganii/Proteus morganii – Infantile diarrhea Providencia stuartii/Proteus inconstans – Involved in burns Treatment for these three = Cefalosporin like Ceftriaxone, Cefotaxime, Cefepime |
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| Proteus Proteus mirabilis Disease + Treat |
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| Proteus mirabilis – Cystitis, #1 strain isolated, #1 in burn patient infections Treat = Ampicillin |
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| Proteus Proteus vulgaris Disease + Treat |
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| Less commonly isolated, Cause cystitis and burn patient infections Cefalosporin - Ceftriaxone, Ceftoaxime, Cefepime |
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| Proteus Proteus/Morganella morganii Disease + Treat |
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| Infantile diarrhea Cefalosporin - Ceftriaxone, Ceftoaxime, Cefepime |
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| Proteus Proteus stuartii/Providencia inconstans Disease + Treat |
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| Involved in burns Cefalosporin like Ceftriaxone, Cefotaxime, Cefepime |
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| Haemophilus influenzae |
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| -Flu is caused by virus: When trying to grow out on plate, virus wouldn’t multiply, but this would grow GRAM – Rod, Capsule, Chocolate agar to grow out (enriched), Capneic incubation (increase CO2, decrease O2) -Found in respiratory tract |
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| Haemophilus influenzae Diseases: |
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| Meningitis Otitis media Acute bacterial epiglottitis "Other" |
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| Haemophilus influenzae Diseases: Meningitis |
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| Caused by (#1) Streptococcus pneumonia, (#2) Neisseria meningitides, (#3) Haemophilus influenza (old people) -Decreasing b/c of antibiotics and vaccinations -Cases today are increasing for people who didn’t vaccinate their kids in fear of autism -90% mortality rate 25-35% Sequalae (consiquences) after disease (deafness, mental retardation) |
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| Haemophilus influenzae Diseases: Otitis media |
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| Middle ear infection, Can lead to deafness, Children sniffle mucus back damaging ear Caused by (#1) Strep pneumo, (#2) Haemophilus influenza |
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| Haemophilus influenzae Diseases: Acute bacterial epigottitis |
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| Epiglottus = Flap reflex to keep food out of lungs, May swell and suffocate you Within 24 hours can cause death |
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| Haemophilus influenzae Diseases: "Other" |
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| Does this cause flu? NO! Pneumonia/Upper respiratory infection |
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| Haemophilus influenzae Treatment: |
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| Life threatening = Ceftriaxone, Cefotaxine Non-life threatening = Bactrim (Sulfamethoxazole, trimethoprim) |
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| Haemophilus influenzae Diseases: Those extra ones + Treatment |
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| Haemophilus aegyptius: Pink eye, Eyelid swelling, Spread by Fingers, Fomites (microscope eyepiece) Treat = Tetracycline, Sulfonamide Haemophilus ducreyi: Tropics/warm areas, Cause Chancroid (STD) = Soft chancre Treat = Ceftriaxone |
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| Vibrio cholera |
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| -Still considered spirochete, though it looks like a rod with a bend -Cholera: Severe diarrhea Pandemic: 19th century (1800s), On every continent Endemic (today): Persistently found in certain area-Parts of Asia -Like salty, alkaline water -No spore, but hardy and will survive Epidemic: Pass from one area to another (get on a plane) |
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| Vibrio cholera Transmission: |
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| Feces in water, food |
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| Vibrio cholera Symptoms: |
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| CT (Cholera Toxin) produced – Enterotoxin (exotoxin) -Rice water stools produced: Water -Vomitting, diarrhea |
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| Vibrio cholera Mortality: |
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| 50% die w/o support (fluids & electrolytes) |
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| Vibrio cholera Treatment: |
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| Tetracycline, Doxacycline |
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| Yersinia Pestis |
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| -“Black Death” |
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| Yersinia Pestis Transmission: |
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| Fleas of rats, rodents, prairie dogs jump off and transmit -Flea bites, spread to lymphatic system, Darkening -100 million people died! (1/4-1/3 of world population) -“Bubonic Plague” |
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| Yersinia Pestis Mortality: |
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| 70-90% death rate -“Pneumonic plague”: Next step after the black plague doesn’t kill you, In lungs, Spread by droplet infection Delta 32 Mutation of the CCR5 gene may have protected people from plague Still happens today in CA or NV, from prairie dogs |
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| Yersinia Pestis Treatment: |
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| Streptomycin (DOC) (+/- Tetracycline) |
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| Rickettsial Infections |
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| -Domain: Bacteria -Phylum: Proteobacteria -Prokaryotic -Hypotrophs: Obligate parasites, Grow on chicken eggs |
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| Rickettsial Infections Transmission: |
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| Bite of arthropod vector (ticks, fleas, mites) Incubation: 1-2 weeks -Circulatory, lymphatic systems |
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| Rickettsial Infections Symptoms: |
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| Alternate b/w chills and fever, Rashes, ?Can cause death through circulatory collapse (overwhelmed by so many organisms-failure) |
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| Rickettsial Infections Diagnosis: |
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| Serology – Check blood to see if producing antibodies against these diseases |
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| Rickettsial Infections Treatment: |
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| Tetracycline (Doxacycline) |
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| Rickettsial Infections Louse-born |
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| Epidemic typhus – Body lice, Spread in homeless/during war/prison (no shower) -Mortality: 50%, especially in older individuals |
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| Rickettsial Infections Flea-born |
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| Endemic typhus/Marine typhus – Rat fleas, Atlantic and Gulf Coast -“Endemic” b/c confined to waterfront areas -Mortality: Mild, no deaths reported |
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| Rickettsial Infections Tick-born |
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| Rocky Mountain Spotted Fever- Ticks (off dogs, whatever), Common in spring when ticks wake from winter, Occur through summer and fall -Wrist rash, Ankle rash -Mortality: 20% w/o treatment 5% w/treatment |
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| Rickettsial Infections Mite-born |
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| Scrub typhus/Chiggers – Mice -Chigger = Baby mite, Larvae -US has chiggers, but they do not carry this Scrub typhus (Australia, Asia have) -Mortality: 50% untreated |
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| Rickettsial-like Infections |
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| Q-Fever: Coxiella burnetii Cat Scratch Fever: Bartonella henselae |
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| Coxiella burnetii |
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| Q-Fever – Coxiella burnetii: Unpasteurized milk, Ticks -Many get infected, few get symptoms -People constantly exposed most likely to get it Treatment: Tetracycline (doxacycline) |
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| Bartonella henselae |
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| Cat Scratch Fever – Bartonella henselae -Pus filled sores -AIDs indicator ? Become systemic, Septicemia Treatment: Azythromycin |
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| Chlamydial Infections: |
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| Chlamydia trachomatis Nongonococcal utethritis Ocular trachoma Inclusion conjuncitivitis Chlamydophila psittaci |
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| Chlamydial Infections: Chlamydia trachomatis |
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| -Domain: Bacteria -Phylum: Chlamydia -Prokaryotic -Hypotroph: Obligate parasite -Grow out in chicken eggs |
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| Chlamydial Infections: Nongonococcal urethritis |
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| UTI not caused by Neisseria gonnorhoeae Post gonococcal urethritis: Same thing, depends on timing, From STD Adult treatment for STD: Tetracycline (doxacycline) or Azythromycin |
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| Chlamydial Infections: Ocular trachoma |
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| Adult, touch genitals then eyes, Leading cause of preventable blindness -BOTH involve Chlamydia trachomatis in eye Treatment: Azythromycin |
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| Chlamydial Infections: Inclusion conjunctivitis |
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| Baby through birth canal (Opthalmia nenonatorum), Picks up bacteria and damage eye -BOTH involve Chlamydia trachomatis in eye Treatment: Erythromycin |
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| Chlamydial Infections: Chlamydophila psittaci |
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| Psittacosis Ornithosis “Parrot fever” Atypical pneumonia – Inhale bird droppings in lungs Treatment: Tetracycline (doxacycline) |
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| Chlamydial Infections: Chlamydophila pneumoniae |
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| -CAP = Community acquired pneumonia 3 causes: Chlamydophila pneumonia, Streptococcus pheumoniae, Mycoplasma pneumonia Treatment: Tetracycline, Azithromycin, Erythromycin, Clarithromycin |
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| Are viruses alive? |
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| No: Cell Theory = Smallest unit of living thing is a cell Cell membrane, Cytoplasm w/ ribosomes, Nucleus/Nucleoid, DNA |
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| Virus Structure |
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| Nucleic Acid Core Protein Coat/Capsid Envelope Helical Icosahedral/Polygon |
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| Virus Structure Nucleic Acid Core |
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| RNA or DNA (not both) -Single stranded or double stranded |
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| Virus Structure Protein Coat/Capsid |
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| Contained in container, Protection, Host recognition (what to infect) -Capsomeres: Individual building blocks of capsids Rod shaped Triangular -Nucleocapsid: Combination of Nucleic Acid Core and Capsid, All contain |
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| Virus Structure Envelope |
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| Lipids, proteins, carbohydrates (found in cell membranes), As virus leaves cell it picks up these from animal cells, Protection -Spikes: Extend from envelope, Host cell recognition |
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| Virus Shapes |
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| Helical Icosahedral/Polygon Complex |
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| Virus Shapes Helical |
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| Rod shaped capsomere, Looks cylindrical -Rabies (bullet shape), Flu, Measles |
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| Virus Shapes Icosahedral/Polygon |
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| 20 sided, Herpes, HIV |
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| Virus Shapes Complex |
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| Don’t fit one category or another, Bacteriophage-Infect bacteria -Head looks like polygon -Body looks helical -Legs |
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| Virus Size |
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| -Filters standard 0.2µm/200nm supposed to remove all prokaryotes (and things larger), But not all viruses Filterable: Viruses are 20nm-450nm – Smaller viruses will pass through filter -Giant Viruses: Missing critical enzymes so not alive |
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| How classify virus? |
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| -Viruses don’t have all those enzymes so can’t use regular tests DNA or RNASingle or Double StrandedEnvelope or noHelical or polygon or whatSize? |
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| Herpes Viruses |
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| -Not all are important in human viruses -Cell Fast: Once virus enters body, Stay for life, Cannot clear it out Goes into DNA and incorporate its genome into your DNA -Grow latent: Symptomatic individuals, Symptoms go away but are still there, Can be reactivated (low immune response causes it to flare up) |
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| Human Herpes Virus Type I Common Name |
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| “Herpes simplex 1” |
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| Human Herpes Virus Type I Cause |
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| Fever bliters, Cold sores, Herpes labialis (lips) -Milder blisters |
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| Human Herpes Virus Type I Transmission |
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| Easily transmitted, Children (1-5 yrs old), Saliva, Not washing hands -90% of us will test positive for the antibodies -US: 4 million people symptomatic |
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| Human Herpes Virus Type I Symptoms |
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| Itching/Tingling in skin (mildest form of pain, nerves), Blisters (fluid leaking out), Crusting lasts 2-3 weeks -Stress lowering immune system induces: Fever, cold/flu, sunlight |
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| Human Herpes Virus Type I TREATMENT |
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| Acyclovir (reduce symptoms by half a day) |
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| Human Herpes Virus Type I Complications |
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Herpetic gingivostomatitis: Lips, gums, throat, More painful Herpetic keratitis: Eyes, Common in AIDs patients -Vision loss depending on immune system 30% Neonatal encephalitis: Infects brain, STROCH, From simplex1 -H=Herpes simplex, Caused by 1 and 2 -Cause retardation, death |
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| Human Herpes Virus Type II Common name |
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| “Herpes simplex 2”, “Genital Herpes” (Goes adult to adult) |
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| Human Herpes Virus Type II Occurrence |
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| CDC: 1 in 5 adults infected from age 12 up |
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| Human Herpes Virus Type II Symptoms |
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| Pain, Malaize (nausea) before blisters, Blisters begin in genitals and go down buttocks and legs -More severe than herpes 1 |
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| Human Herpes Virus Type II Complications |
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| -Associated with Cervical Cancer: Human Papiloma Virus (STD) Can auto inoculate self by touching one are and then the other -Not always lead to cancer, but when combined with herpes, doubles risk factor of getting it -70% Neonatal Encephalitis -Cesarean section: As baby comes out of birth canal it can get herpes Prevent through c-section |
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| Human Herpes Virus Type II Reactivation |
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| -Stress -Lower immune system -Menstruation |
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| Human Herpes Virus Type II TREATMENT |
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| Acyclovir |
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| Human Herpes Virus Type III |
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| Chicken Pox – Varicella Shingles – Zoster / “Herpes zoster” |
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| Human Herpes Virus Type III Chicken Pox – Varicella Morbidity |
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| 90% by age of 10 have been exposed |
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| Human Herpes Virus Type III Chicken Pox – Varicella Transmission |
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| Easy to transmit making it common, Breathe in through respiratory tract -Sputum/saliva/coughing, Microaerosals during eating (clang utensils on plate) -Blisters on sheets and towels inhaled -Can transmit 1-3 days before symptoms, All throughout, Up to 6 days after crop of blisters (long time) |
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| Human Herpes Virus Type III Chicken Pox – Varicella Incubation |
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| 1-3 weeks |
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| Human Herpes Virus Type III Chicken Pox – Varicella Symptoms |
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| -1-2 days blisters -Blisters with straw-like fluid -6 days of crops of blisters on body (painful, infectious) Crater: Scratching causes E. coli to get into blister |
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| Human Herpes Virus Type III Chicken Pox – Varicella Reduce Symptoms |
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| Oral acyclovir |
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| Human Herpes Virus Type III Chicken Pox – Varicella Complications |
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| Reye’s Syndrome – Inflammation of brain, Swelling, Lead to death -Not give Aspirin b/c increase chances of getting this |
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| Human Herpes Virus Type III Chicken Pox – Varicella Immunity |
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| -Vaccine provides long term protection, Maybe even against shingles -Rare to get Chicken Pox twice |
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| Human Herpes Virus Type III Shingles – Zoster / “Herpes zoster” What it is and Morbidity |
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| -Reactivation of Chicken Pox 10-20% get Chicken Pox, then Shingles -Older people get it, but some young people as well -Reactivated by decreased immune system (stress) |
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| Human Herpes Virus Type III Shingles – Zoster / “Herpes zoster” Symptoms |
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| One side of the body, hide in the nerves (Up shoulder, along arm, ) Painful (burnt by a lit cigarette, hurts to wear clothes) -You can’t give someone Shingles, but you can give someone Chicken Pox and spread that which may reactivate |
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| Human Herpes Virus Type III Shingles – Zoster / “Herpes zoster” Complications |
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| Post herpetic neuralgia – When blisters disappear, still feel pain (up to 1 year) |
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| Human Herpes Virus Type III Shingles – Zoster / “Herpes zoster” Treatment |
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| Acyclovir |
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| Human Herpes Virus Type IV (4) Name |
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| Epstein-Barr Virus “Infectious mononucleosis” = Spread by saliva, “Kissing disease” |
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| Human Herpes Virus Type IV (4) Symptoms |
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| Sore throat, fever, Lymphadenopathy (swollen), Lymphocytosis (? WBC) ?Burkett’s Lymphoma: B cell malignancy (cancer), Africa, -Swollen cheek area, belly |
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| Human Herpes Virus Type V (5) |
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| CMV – Cytomegalovirus CMV Mononucleosis Congenital CMV Disseminated CMV |
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| Human Herpes Virus Type V (5) CMV – Cytomegalovirus |
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| -Most are asymptomatic (Everyone has it and the antibodies) |
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| Human Herpes Virus Type V (5) CMV Mononucleosis |
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| -Symptoms: Sore throat, fever, lymphadenopathy, lymphocytosis, NO cancer |
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| Human Herpes Virus Type V (5) Congenital CMV |
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| -STOR”C”H=Cytomegalovirus through placenta Death, Mental retardation |
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| Human Herpes Virus Type V (5) Perinatal CMV |
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| -As baby comes through birth canal, picks up CMV -Less severe |
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| Human Herpes Virus Type V (5) Disseminated CMV |
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| -No resistance against CMV -Common in immunocompromised patients (HIV+ ? AIDs) |
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| Human Herpes Virus Type VI (6) |
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| “Human T-lymphotrophic virus” -Infants less than a year old get Roseola Rash, fever Self limiting May lead to Multiple Sclerosis |
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| Human Herpes Virus Type VII (7) |
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| Orphan virus = Doesn’t cause disease, just a rash Kaposi’s Sarcoma – AIDs patients get purple hemorrhagic tumors (cancer) Not as common anymore b/c medications today |
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| Hepatitis (A-G) |
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| -Hepa = Liver -Alcoholic hepatitis from drinking too much -INH, used for Tuberculosis, can cause severe Hepatitis Liver produces too much bile - Fever, jaundice (yellow skin), brown urine |
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| Hep A |
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| RNA "Infectious Hep" Fecal/Oral Acute: 2-3 weeks |
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| Hep B |
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| DNA "Serum" -Needles -Mosquito -ST”O”RCH Blood- Last dry for at least a week (Mosquito, passive vector, can pass on dried blood)Chronic: 6% Mortality: 2% -Hepatoma (cancer) Vaccine prevents TREATMENT:Alpha interferon -Side effects -“Cure” = Can’t detect virus particles Tenofovir (AIDs drug, Oral)[DOC] |
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| Hep C |
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| RNA "Classic non A non B" Blood- Post-transfusion Hep -70-80 day delay detecting antibodies 1/100,000 chance -Firefighters get blood on Chronic (75-85%) TREATMENT "Cure" = Suppress virus particles Peg interferon + ribavirin [DOC] +Telaprenovir (Protease inhibitor) |
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| Hep D |
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| RNA "Delta Agent" Blood- Alone: Not infectious Coinfection with other Hep (like B)= -Increased liver damage Vaccine for B will protect against D -Treatments don’t always work |
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| Hep E |
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| RNA "Infectious non A non B" Fecal/Oral Same symptoms as Hep A Pregnant women = higher death rate |
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| Hep G |
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| RNA Blood1995 Mild to death -Flu ? die G+C or HIV will slow down progression/damage |
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| HIV: Human Immunodeficiency Virus Etiology: |
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| HIV1 – Most common HIV2 – Africa, Less virulent, Longer incubation period (live longer) AIDs – Acquired Immune Deficiency Syndrome 2-15 years before show severe symptoms |
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| Hep F |
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| Actually just a variant of C |
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| RNA Retrovirus |
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| HIV Multiplies by reverse transcriptase -Take single stranded viral RNA and make double stranded viral DNA |
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| HIV Structure |
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| -2 single strands of RNA -Enclosed by Capsid -Surrounded by Envelope -Spikes sticking through Envelope (how attach to cells) |
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| HIV Morbidity |
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| 30-60 million world 45 million 12 million children (through placenta) |
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| HIV Mortality |
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| 5% don’t progress – Delta 32 mutation of CCR5 coreceptor 95% turn into AIDs -63% individuals die (1995) -18% mortality (1998) |
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| HIV Transmission |
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| Bloodborne pathogen – If spilled need significant amount of blood -Outside cell: 6 hrs survive -In macrophage: 1.5 days survive Unprotected sexual contact: Semen, vaginal secretions = 10-50 viral particles/mL Parenteral: Blood, Transfusions, 1000-100,000 particles/mL Placenta Breast milk Not dangerous: Sweat, saliva, perspiration, tears, vomit, feces, <1 virus/mL (according to CDC and OSHA) |
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| HIV Incubation + What happens |
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| 8 year, average -Virus particles attacked by dendritic cells (engulf and modify but not kill virus) -Dendritic cells hand virus off to WBCs, where virus can multiply CD4 Cells: “T-Helper Cells,” Macrophages, Major cells virus multiplies in 500-1,000/mL = Normal levels -When down to 200 CD4 cells/mL: HIV+ ? AIDs (highly symptomatic) |
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| HIV Stages of Infection |
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| Category A Category B Category C |
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| HIV Category A |
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| First 3 years of infection, Mononucleosis-like symptoms for few weeks, Asymptomatic Viremia: Septicemia of a virus, Can transmit to others |
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| HIV Category B |
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| ”Early symptomatic” Year 4-8 -Chronic lymphadenopathy, Cadidiasis (Candida albicans), Thrush, Plaque in back of throat |
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| HIV Category C |
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| 200 CD4 cells/mL ? AIDs |
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| CD4 Cells |
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| “T-Helper Cells,” Macrophages, Major cells virus multiplies in 500-1,000/mL = Normal levels -When down to 200 CD4 cells/mL: HIV+ ? AIDs (highly symptomatic) |
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| AIDs Indicators Viral |
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| -Extrapulomonary TB – Mycobacterium avium -Herpes zoster – Shingles multiple times -Herpes simplex outbreaks over and over -Cytomegalovirus (CMV) becomes systemic b/c immune system can’t control it |
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| AIDs Indicators Protozoa |
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| -Toxoplasmosis – Cat litter sickness, Goes systemic in AIDs patients ? Encephalitis (infect brain) |
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| AIDs Indicators Fungi |
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| -Candidiasis – Candida albicans -Pneumocystis jiroveci (carinii) pneumonia (PCP) – Pneumonia, used to be leading cause of death -Cryptococcosis – Cryptococcus neoformans, Level 3 danger, Cause meningitis, Yeast -Penicillinosis – Penicillium marneffei In Asia, most common infections are Extrapulmonary TB, Cryptococcosis, Penicillinosis |
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| AIDs Indicators |
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| -Kaposi’s Sarcoma: Hemorrhagic tumors due to Herpes 8, Interferon use fights it |
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| AIDs Life cycle |
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| Adsorption: First step -Spikes on HIV fit into Receptors on WBC to dock Penetration (fusion): Get through membrane -Enzymes at every step Replication: Make more Nucleic Acid and Capsid -Made separately Maturation: Put together -Put NA in Capsid (done by enzymes) Release/Budding: Get out of cell |
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| AIDs Prevent Adsorption |
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| -Maraviroc (MVC) -Binds to CCR5 Coreceptor, making non-functional -CXCR4 strain hits that coreceptor instead, and this drug is not going to help (mutation) |
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| AIDs Prevent penetration |
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| Fusion inhibitor -Enfuvirtide (ENF)/Fuzion GP (Glycoprotein) 41 on spike blocked from transforming membrane and gaining entry |
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| AIDs Reverse Transcriptase Inhibitors |
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| NRTI/NaRTI: “Nucleoside analogue reverse transcriptase inhibitor” NNRTI: Non-nucleoside reverse transcriptase inhibitors |
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| Reverse Transcriptase Inhibitors NRTI |
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| NRTI/NaRTI: “Nucleoside analogue reverse transcriptase inhibitor” -Chemically similar to nucleoside but modification puts wrong chemical in making different/bad RNA -Azidothymidine, Zidovudine (AZT): Naive patients that are pregnant, Give at birth to prevent AIDs from transferring to fetus -Lamivudine (3TC): Well tolerated (few treatment toxicities) -Emtricitabine (FTC): Naive patient treatment -Tenofovir (TDF): Also used for Hep B, Naive patients |
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| Reverse Transcriptase Inhibitors NNRTI |
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| Non-nucleoside reverse transcriptase inhibitors -Bind to enzyme and change structure to turn non-functional -Efavirenz (EFV) -Nevirapine (NVP) |
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| Azidothymidine, Zidovudine (AZT) |
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| NRTI Naive patients that are pregnant, Give at birth to prevent AIDs from transferring to fetus |
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| Lamivudine (3TC) |
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| NRTI Well tolerated (few treatment toxicities) |
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| Emtricitabine (FTC) |
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| NRTI Naive patient treatment |
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| Tenofovir (TDF) |
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| Also used for Hep B, Naive patients |
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| AIDs Protease inhibitor |
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| Blocks maturation step of assembling nucleic acid with capsule with protease -Indinavir (IDV) -Ritonavir (RTV) BOTH for Naive patients: Never treated before |
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| AIDs Interferon |
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| Blocks Budding, Virus can’t get out of cells |
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| HAART |
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| Highly Active Anti-Retroviral Therapy (cocktail) AZT + Reverse Transcriptase Inhibitor + Protease inhibitor |
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| AIDs -Naive patient treatment |
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| Tenofovir, emtricitabine (NRTI) and Efavirenz (NNRTI) -Patients who use this get a decrease in number of viral particles -Decrease virus becomes resistant to drugs -Increase in number of CD4 cells (less other infections) |
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| Influenza |
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| 1 strand RNA Hemagglutinin H1, H2, H3 Neuraminidase N1, N2 |
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| Influenza Treatment |
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| Amantadine, rimantadine, Zanamivir (Relenza), Tamiflu |
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| Mumps |
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| Epidemic parotitis (Paramyxovirus) |
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| Measles |
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| Rubeola from mribillivirus Koplik's spots |
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| Rabies |
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| HDCV = Human diploid cell vaccine HRGI = Human rabies immune globulin (put in wound to slow spread) |
