GPB Flashcards
What cellular structure do the genera Bacillus and Clostridium have in common?
large GPB & Spore forming
How could you easily differentiate between an aerotolerant Clostridium sp. and a facultative Bacillus sp.? (hint: bench top test)
Catalase test
Pos: Bacillus sp.
Neg: Clostridium sp.
What do the terms “coryneform” and “diphtheroids” normally describe in a routine clinical laboratory?*
GPB non-pathogens
If a gram smear result was described as pallisading GPB, what does this mean? (i.e. what would you see?)
Pallisading: form groups (III = V L)
List 5 identifying lab. characteristics of Listeria monocytogenes? How could you distinguish between Group B Streptococcus and L.monocytogenes.
- Short non-sporing GPB in pairs & pallidasing
- narrow zone of B haemolysis (similar to GBStrep)
- Catalase pos (unlike GBStrep. catalase neg)
- Tumbling motility at 25ºC but not at 37ºC
- Needs enrichment media (NG on MAC)
What lab. characteristic would help to distinguish C.perfringens from almost all other members of the genus Clostridium?
- Double zone of haemolysis on BA: inner zone B, Outer zone a
- non-motile
List the causative organisms for anthrax, gas gangrene, Botulism and tetanus?
Anthrax: Bacillus anthracis
Gas gangrene: Clostridium perfringens (80%)
Botulism: Clostridium botulinum (spores or toxin)
Tetanus: Clostridium tetani
a) What is pseudomembranous colitis?
b) Describe the pathogenesis (how the organism gains entry to humans and the processes involved in causing human disease/symptoms) and
c) list the most likely causative organism.
a) Inflammation of colon
b) Pathogenesis: Exposure to organism in food (spores not cooked properly); or Hx of antibiotic therapy = encourage resistant strains. Release of enzymes and exotoxins/enterotoxins => gut symptoms
c) Caused by Clostridium difficile, C. perfringens
What is the designated protocol for treating diagnosed clostridial colitis?
- Stop antimicrobial therapy
- Initiate fluid & electrolyte replacement therapy
- Treat mild diarrhoea w/ MTZ, and severe diarrhoea w/ Vanc.
- Faecal transplant from donor: Inc microbial diversity in colon
What clinical history would suggest the possibility of pseudomembranous colitis?
Hx of antibiotic therapy = dec NF + overgrowth of Cl. difficile/ Cl. perfringens
What is the normal vaccination schedule for tetanus? i.e how often is it given and to who?
5-dose schedule: 2, 4, 6, 18 months and 4 years
Booster: 1 injection every 10 years
Clostridium species cause many of their disease effects through powerful toxins. Are these toxins exotoxins or endotoxins and what are the differences between these two types? (hint: review slides from Fermentative GNB lecture).
- Enterotoxins are harmful to the digestive system
- They are exotoxins: high toxicity, strong antigenicity, not heat stable and not produce fever
What is the difference between short and long incubation food poisoning with B.cereus?
Short: 1-6hrs. caused by preformed heat stable exotoxin in food (Consume toxin)
Long: 8-16hrs: Consume spores from improperly cooked food = in vivo enterotoxin (exotoxin) production (heat labile=alter)
If you isolated a Bacillus species in the clinical laboratory, how could you easily determine if it was B.anthracis? List three features that would differentiate it from the other members of this genera.
- motility: neg
- Encapsulated in vivo: pos
- Lysis by gamma phage: pos
- haemolytic: none (B.subtilis V b/w B and none)
- LV test: pos (B. cereus also pos)
Features to consider when you have a GPB
- AnO2, dec O2, aerobic
- non-/ branching
- Acid fastness
- catalase
- spore forming
Who is primarily affected by Listeria monocytogenes and common pathogenesis?
- pregnant women, newborns and immunocompromised
- Contamination in food processing (salads, cheese) w/ spores => meningitis
- grows at 4ºC
Lab features if Bacillus cereus
- GPB
- Produce spores: R to pasteurisation of milk
- Catalase pos
- Large feathery colonies
- B haemolytic*
- Motile*
- facultative*
Lab features if Clostridium perfringens
- GPB brick-shaped, may be encapsulated
- Double zone of haemolysis on BA: inner zone B, Outer zone a
- non-motile
- LV & Nagler pos
Lab features if Clostridium tetani
- thin long GPB
- easily decolourised
- Tennis racquet spores
- narrow a or B zone
- Motile = swarms lace-like
Lab features if Clostridium difficile
- GPB
- easliy decolourise
- Spores variable position in bacteria
- Motile
- Selective medium (CCFA)
- Detect toxin in faeces using commercial kits
Which species of mycobacteria cause tuberculosis?
Mycobacteria tuberculosis
How is tuberculosis transmitted?
Most Droplets/aerosol except M.bovis transmitted via infected milk
Name two staining methods for visualising mycobacteria under the light microscope.
- Ziehl Neelson or Kinyoun stain for AFB
2. Fluoroscent staining - Rhodamine or rhodamine auramine
Why are mycobacteria slow growing?
bc they have a hydrophobic cell wall = hard access for nutrient into cell= hard to absorb nutrients
What makes Mycobacterium so resistant to acids, alkalis, antibiotics and desiccation?
Bc the cell wall is hydrophobic due to high lipid content
Why would immune status affect the initial outcome of infection with TB organisms?
A healthy person can get infected w/ TB organisms and not get symptoms maybe bc their immune sys is good, and also bc organism is slow growing. When immune system is poor it can allow organism to multiply.
