What are the medically important Gram positive rods + most important disease?
Bacillus
B.anthracis -> anthrax, bioterrorism
B.cereus -> food poisoning (rice)
Clostridium
C.tetani -> tetanus
C.botulinum -> botulismus
C.perfringens -> gas gangrene, food poisoning
C.difficile -> antibiotic assoc. diarrhea
Corynebacterium
Listeria
Gardnerella
How do the medically important Gram positive rods grow?
All aerobic except Clostridium (anaerobic)
Which of the medically important Gram positive rods produce spores or Exotoxins?
Spores: Bacillus & Clostridium
Exotoxins: Bacillus & Clostridium & Corynebacterium
How do we deal with spores in medicine?
sterilization at 121°C more than 15 minutes
sporicidal disinfections
Can we use antibiotics on spores + reason?
Antibiotics ineffective because there is only low metabolism & coat of the spore impermeable for antibiotics
How do we see spores under miscroscope?
don´t stain with Gramstaining
hollow structures in bacteria
sometimes no spores in clinical samples bc already activated
What are soil bacterial spores & disease?
Clostridium tetani (Tetanus)
Clostridium perfringes (Gas gangrene)
What are the main important types of bacillus?
Bacillus anthracis
Bacillus cereus
What culture for B. anthracis?
blood agar culture -> no hemolysis (gamma)
-> aerobic condition
What are the virulence factors of B. anthracis
polypeptide capsule with poly D glutamic acid
secretes 2 Exotoxins: Edema & lethal factor
Explain structure of those 2 Exotoxins, how function + result
EF or LF (A subunit) always combined with protective antigen (B subunit)
Edema factor (EF) -> binds to Protein antigen on cell -> EF i cell -> EF binds Clmodulin (CAD) -> active adenyl cyclase -> incr. intracellular cAMP -> more fluid in extracellular space -> edema
Lethal factor (LF) -> cleaves MAPK (Mitogen act. phosphokinas) black eschar (necrotic lesion covered by crust)-> no cell growth
How can human get anthrax?
cutaneous (trauma to skin; cut. anthrax)
inhalation (pulm./inh. anthrax)
ingestion (contaminated meat: GIS anthrax)
injection (percutaneously; inj. anthrax)
Describe cutaneous anthrax
most common
spore enters via injury (rarely insect)
1-7 days incubation
20% mortality if not treated -> with treatment survive 100%
Describe Pulmonary/Inhalation anthrax
not communicable -> spores into lung but toxin rapid in mediastinal lymph nodes ->no transmission bc leaves lung
-> hemorrhagic mediastinitis
incubation 1-7 days (2months if small amount)
85-90% mortality ifno treatment (most deadly)
Describe GIS anthrax
vomiting, abdominal pain, bloody diarrhea
incubation time 1-7 days
mortality 50% if no treated
Describe Injection anthrax?
due to drug usage f.e. heroine
painless skin sore with black center after blisters/abscesses
What are the stages of anthrax?
Vesicular stage (day 5)
Eschar stage (day 12)
Ulcer stage (~2 months healed & scar)
How do we treat anthrax?
Prophylaxis & treatment
Ciprofloxacin
Doxycycline (alternative)
vaccination not effective & many doses
sterilization 120°C more than 15 min
2 hours disinfectant application
What is a disease that looks similar to anthrax & due to what & diference?
Orf ecthyma contagiosum
viral disease
self-limited & spontaneous resolution in 4-8 weeks
What bacteria causes food poisoning when f.e. reheating rice & why?
spores on grains when too much at room temperature -> germinate when repeated
Describe the Pathogenesis of Bacillus cereus
secretes 2 exotoxins
similar fct to cholera (watery diarrhea)
similar fct to Staphylococcal enterotoxin (super antigen)
2 syndromes
short incubation period (4h): nausea & vomiting
long incubation period (18h): watery nonbloody diarrhea
What do we do in Bacillus cereus infection?
no lab diagnosis
prevent by safe food consideration
symptomatic treatment
What disease due to Clostridium tetani & how inf.?
Tetanus
spores in soil; also when contaminated umbilicus or circumcision wound (neonatal tetanus)
Describe the pathogenesis of C.tetani
Exotoxin: Tetanospasmin
carried intraaxonally to the CNS -> Blocks release of inhibitory mediators at the spinal synapses (glycine and GABA)
results in muscle spasms, lockjaw, paralysis (majority spastic)
How do we diagnose & treat C. tetani?
Microscopy: terminal spore-tennis racket shape
No culture
Tetanus immunoglobulin TIG -> neutralizes
prevention: Tetanus toxoid vaccine; clean & contaminate wound
What bacteria causes inf. after eating food from contaminated cans & which food high risk & prevention?
Clostridium botulinum -> Botulismus
high risk: green beans, mushrooms, smoked fish
prevention: sterilize cans, sufficient cooking
Describe the pathogenesis & result of clostridium botulinum infection
Botulinum toxin = Protease
-> blocks release of acetylcholine by cleaving needed proteins
Paralysis, descending weakness, diplopia (double seeing)
Dysphagia (swallowing pain)
No fever
How many immunogenic types of botulismus & which common?
8 types
A B E most common human illness
A used for botox
What are special botulismus cases?
wound botulismus
due to injecting drugs -> skin popping
infant botulismus
spores in honey dangerously for children <1
How do you diagnose & treat botulismus
no culture
test uneatened food & patiens serum
Food industry: mouse protection test
treat with Antitoxin & Respiratory support
What disease due to Clostridium perfringens & how inf.?
Gas gangrene or food poisoning
spores in soil, due to war, accidents, septic abortions
Describe the pathogenesis of gas gangrene?
Alpha toxin (lecithinase) damages cell memebranes (also erthrocytes -> hemolysis) -> produce gas in tissues -> myonecrosis
What are clinical findings of gas gangrene & treatment?
pain, edena, crepitation (crackling sound when palpating wound due to gas), hemolysis, jaundice, death
Blood agar culture: Gram positive bacilli (α and β hemolysis)
Treatment immediately when suspected bc risk of death
Wound debridement
Penicillin G
Hyperbaric oxygen
What are the symptoms of food poisoning due to C. perfringens & treatment?
8-16 hr incubation period (Watery diarrhea, Cramp, Vomiting)
No lab diagnosis, just symptomatic treatment
Resolves in 24h
What disease due to Clostridioides difficile & symptoms & how?
pseudomembraneous colitis
-> antibiotic assoc. nosocomial diarrhea (often during hospitalization)
non-bloody diarrhea, fever, abdominal cramp, toxic megacolon
dispiosis in microbiota due to antibiotic -> C. difficile survives & multiplies -> secretes 2 exotoxins
What are the 2 Exotoxins secreted by Clostridioides difficile & similarity & function?
both glucosyl-transferase
Exotoxin A: Enterotoxin (potent neutrophil chemoattractant)
Exotoxin B: Cytotoxin (depolymerization of actin ->disrupt cytoskeleton -> death of enterocytes)
disrupt epithelial-cell barrier
What are high and medium risk antibiotics possibly Clostridioides difficile?
High risk: Clindamycin, Ampicillin, Cephalosporins, Fluoroquinolones, Amoxicillin-cotrimoxazole
Medium risk: Macrolides, Tetracyclines
How do we diagnose Clostridioides difficile?
toxin detection
EIA (Enzyme immunoassay) for exotoxins
EIA stool antigen detection
PCR toxic gene DNA detection
cytotoxicity assay
colonoscopy
How do we treat Clostridioides difficile?
Fluid replacement
remove colon in life threatening cases
fecal transplantation (rare)
stop causative antibiotic and switch to f.e. Vancomycin, Methronidazol, Fidaxomycin
those still have low risk for causing disease
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