BIOM 250: Week 10 Notes
BIOM 250: Week 10 Notes BIOM 250
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This 7 page Class Notes was uploaded by Davis Notetaker on Tuesday April 12, 2016. The Class Notes belongs to BIOM 250 at Montana State University taught by Kari Cargill in Winter 2016. Since its upload, it has received 9 views. For similar materials see Micro Hlth Sci: Infect Disease in Biology at Montana State University.
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Date Created: 04/12/16
Mon 4/04 Bacterial Virulence Factors ToxinsTwo types Endotoxins seen in bacteria with gramnegative cell wall Targets specific cells, ex: enterotoxins, neurotoxins Exotoxins produced by variety Has a general target, ex: enterotoxins Enterotoxins Act on intestinal cells Ex: cholera, traveler’s diarrhea (E. coli), bacillary dysentery (bloody diarrhea, often due to destruction of intestinal lining) Neurotoxins Act on nervous system Ex: botulism, tetanus Disease: neurotoxin disease/infection Botulism etiologic agent clostidrium botulinum (caused by: name, type of m/o, G+ bacillus other characteristics) Forms endospores Anaerobe (doesn’t like oxygen) Produces a neurotoxin reservoir (where it is harbored spores in soil naturally) mode of transmission to contaminated food, when no oxygen is present: humans (& susceptible Improperly canned food people) spores can germinate, and cells produce toxin that is colorless, odorless and tasteless pathogenesis (progression of Ingested toxin leads to intoxication and affects brain signals disease within body, virulence to muscles (most toxic substance known) factors) symptoms Symptoms show ~1836 hours after eating contaminated food (ranges from 6 hours 10 days) Flaccid paralysis (muscles relaxed) Death from respiratory failure (in severe cases) Without treatment, botulism has 60% mortality rate, 3% in US with treatment treatment/prevention/control Treatment Start with an immediate antitoxin Maintain individual’s respiration Antibiotics not used, since harm is caused by toxin produced, not bacteria Infant Botulism ~10% of all honey contains botulism spores Recomm. No honey for babies <1 year old Wound botulism Spores contaminate a wound (that is deep enough) & toxins enter blood ~3% of US cases of botulism are from wounds Rates of wound botulism increase with increase of iv drug use (use of contaminated iv’s) Botulism in animals Ex: cattle, sheep, horses (prognosis poor if recumbent) Not uncommon in waterfowl & poultry Most dogs recover Botulinum toxin cosmetic uses: “Botox” Toxin given highly diluted & superficially, only lasts a few months Medical uses: Used to help relax muscles: ● migraines/tension headaches ● Overactive bladder Disease: neurotoxin disease/infection Tetanus etiologic agent Clostridium tetani (caused by: name, type of m/o, G+ bacillus other characteristics) Forms endospores Anaerobe Produces neurotoxin reservoir (where it is harbored Spores in soil naturally) Normal flora of horses, cattle, & 25% of people (can’t be eradicated from soil, because easily replaced via feces) mode of transmission to Puncture wound (deep enough to be anaerobic) humans (& susceptible people) pathogenesis (progression of Spore germinate in anaerobic wound disease within body, virulence Produces neurotoxin factors) symptoms Spastic paralysis Muscles contract, experienced as painful spasms “lockjaw” treatment/prevention/control Diagnosis: Based on symptoms Treatment: Antitoxin Maintain respiration & nutrition Prevention: Vaccine (boosters every 10 years) Impact ~1 mill cases/year/worldwide 300,000500,000 deaths US ~100 Neonatal tetanus ● Umbilical stump becomes infected if cut in insanitary circumstances ● Maternalneonatal tetanus (carrying mother becomes infected) Wed 4/6 West Nile Virus disease/infection West Nile Virus etiologic agent West nile virus (caused by: name, type of m/o, other characteristics) reservoir (where it is harbored Infected birds naturally) mode of transmission to Mosquito vector humans (& susceptible people) pathogenesis (progression of disease within body, virulence factors) symptoms Most humans are asymptomatic Those with symptoms might experience: WN fever: fever, joint pain, lasts 710 days treatment/prevention/control Diagnosis: Blood test to screen for antibodies to virus Treatment: No cure, symptoms are treated Prevention: Mosquito control & avoid mosquito contact Vaccine for horses Microbial Control Part 2 superinfection occurs through overuse of antibiotics which can result in destruction of the normal flora allowing pathogens to flourish Disease: superinfection disease/infection AntibioticAssociated Diarrhea etiologic agent Clostridium difficilthought to cause 20% of diarrhea, (caused by: name, type of m/o, commonly referred to as Cdiff) other characteristics) G+ rod Anaerobe Endospores Exotoxins reservoir (where it is harbored Endogenous can be naturally internal/”opportunistic” naturally) Environmental spores mode of transmission to Opportunistic: superinfection humans (& susceptible As a results of broadspectrum antibiotics, leads to loss of people) normal intestinal flora but endospores survive and germinate Clindamycin,ampicillin,cephalosporins,..., have been most highly associated with cases in superinfection pathogenesis (progression of Two exotoxins that cause inflammation and fluid loss disease within body, virulence May progress to pseudomembranous colitis, which has factors) 12% mortality rate especially in the elderly symptoms Diarrhea, cramps, fever (up to 106 deg F) Perforation of colon possible (can lead to life threatening complications) treatment/prevention/control Diagnosis: Isolate organisms from stool Identify toxins that may be present Endoscope observation of pseudomembranes in colon Treatment: Stop antibiotic treatment & monitor for improvement Switch antibiotic treatment: vancomycin,metronidazole (more of an anticarcinogenic but, targets anaerobes) In severe/extreme cases: treat with fecal transplant to restore normal flora Introduced as enema, or through tube Donations very rigorously screened for safeness 25% of cases recur Not due to drug resistance, results from germination of residual spores Epidemiology #1 cause of nosocomial diarrhea Drug resistence MRSA First recognized in 1961 Resistance to betalactam drugs drugs that affect peptidoglycans Ex: penicillin, amoxicillin, methicillin, cephalosporins 2 Types ● HAMRSA : hospital associated, accounts form 85% of cases today ● CAMRSA: disease/infection MethicillinResistant Staphylococcus Aureus “MRSA” etiologic agent Staphylococcus aureus (caused by: name, type of m/o, other characteristics) reservoir where it is harbored 2530% of people are colonized with Staph aureus naturally) ~1% colonized with MRSA mode of transmission to Direct contact and fomites humans (& susceptible people) pathogenesis (progression of Further spread is potentially lifethreatening, esp infection disease within body, virulence of: factors) Blood, lungs, bones Virulence factors: Drug resistance genes USA300 strains has a leukocidin associated with pneumonia + necrosis USA300 most common in CAMRSA symptoms Red bumps, resemble pimples, boils or spider bites Quickly turn to deep abscesses treatment/prevention/control Treatment: Other antibiotics Vancomycin (antibiotic of “last resort”) Drain & clean abscess & monitor for recovery Control; Handwashing Sterile iv’s and catheters Awareness of 5 C’s & countermeasures: Don’t share personal items Keep wounds covered Sanitize clothing & linens Wash hands Get tested for any skin infection needing treatment The 5 C’s Crowding Skintoskin Contact Compromised skin (cuts) Contaminated items (fomites) Lack of Cleanliness Fri 4/8 Antimicrobials for other microbes Antivirals More recent development Creating antivirals is difficult because viruses are prone to high mutation rates Phage therapy Using bacteriophages (viruses that infect bacteria) to treat bacterial infections Advantages: Specific to the pathogen Harmless to host and beneficial bacteria Bacteria don’t become “resistant” to viruses Researched & used in former soviet Georgia for ~100 yrs Recent clinical trials in US Administered topically/orally
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