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BIOM 250: Week 10 Notes

by: Davis Notetaker

BIOM 250: Week 10 Notes BIOM 250

Marketplace > Montana State University > Biology > BIOM 250 > BIOM 250 Week 10 Notes
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Week 10 notes, only up to what will be on exam 3. Topics include: bacterial virulence factors, superinfection, drug resistance. Diseases: Botulism, Tetanus, West Nile Virus, UTI, MRSA
Micro Hlth Sci: Infect Disease
Kari Cargill
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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 difficil​thought 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 S​taph 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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