Microbiology Flashcards
Give the 2 main species of mycobacteria
M. Tuberculosis (1/4th leading infection that results in death. - wasting, fever & bloody cough)
M. Leprae (affects skin, mucous membranes & nerves, can lead to disformaties and disfigurement in severe cases)
How do you stain for mycobacteria?
Ziehl-Neelsen stain
Their cell wall has a thick lipid layer which is pale staining in gram stains due to the mycolic acids in the wall.
Need acid fast stain
Ziehl-Neelsen: carbon fuchsin, acid alcohol, methylene blue.
AFB are resistant to destaining so stay pink/red
Explain how the immune system tries to prevent an infection due to a mycobacterium
Mycobacterium (AFB) phagocytosed by macrophages & enter a phagolysosome.
Host aims to degrade AFB and display the antigens for T-cells.
CD4 cells generate IFN-gamma for macrophages for intracellular killing. IL-12 stimulates T Helper and IFN-gamma.
Explain how a mycobacterium can lead to in infection
Signalling pathways are required to attract macrophages for killing.
Problems in the signalling pathways can lead to infection.
- genetic defects in IL-12/INF-g/signaling
- CD4 (HIV)
- TNF inhibitors (rheumatoid arthritis, inflammatory bowel disease)
- Immunosuppresed patients
Explain how granulomas form in mycobacterial infections
Lesions that try and contain mycobacteria
Macrophages:
- become epitheliod cells
- M0 fuse to form giant multinucleated cells ‘langhans giant cells’
Central part may necrose = caseating granuloma
Granuloma? Rule out TB
Which of the following is true?
a) Mycobacteria are not immunogenic
b) Mycobacteria are highly immunogenic
Mycobacteria are highly immunogenic
Due to mycobacterial lipids
How can you test exposure to TB?
Which is the most useful test and why?
Tuberculin skin test - intradermal injection of purified proteins, difficult to tell if immunitiy to BCG/TB
Interferon gamma release assays IGRAs - ELLISPOT/TSOT use antigens specific for M. tuberculosis. Demonstrate exposure but not active infection. - more useful
For the following give the main reason for the tissue damage
a) Tuberculoid leprosy
b) Lepromatous leprosy
a) Tuberculoid leprosy - too much immune response -tissue hypersensitivity and granulomata
b) Lepromatous leprosy - Too little immune response - tissue damage to uncontrolled bacilli & poorly formed granulomata
What are the principles of mycobacterial treatment?
Prolonged treatment as slow growing bacteria
Can grow in different locations - intra/extracellular
Combination of drugs
Resistance (big problem) - need to target all populaions and mutants - MDR & XDR
Compliance is essential
In primary tuberculosis where are the bacilli most likely to settle and why?
a) Carina of trachea
b) Apex of lung
c) Lower legft and right lobes
d) Right main broncus
Bacilli settle in the apex of the lung and form granuloma.
This is because the apex has more air and less blood supply (fewer defending WBC)
With TB which doesn’t makes up the primary complex?
a) granuloma
b) lymphatics
c) lymphnodes
d) capillary beds
Primary Complex = Granuloma + Lymphatics + Lymph nodes
Describe how laten TB can become active
Latent TB = no clinical disease
Vigorous T cell control
Detectable cell mediated immunity of IGRA/tuberculin test
May become active if there is a compromise to the immune system - aging, HIV, malnutrition, diabetes
Control lost by the T cells
Which bacteria is being described?
Purple on gram stain. Negative catalase test with chains of cocci. Appears yellow on a haemolysis test.
a) Beta haemolytic stretococcus
b) Streptococcus pneumoniae
c) Staphlococcus pneumonia
d) Staphlococcus aureus
Beta haemolytic stretococcus
Purple on gram stain = +ve
Negative catalase test with chains of cocci = Streptococcus
Appears yellow on a haemolysis test = beta haemolytic
Which of the following are being described?
Purple on gram stain. Clusters of cocci that are catalase +ve and coagulase +ve.
a) Beta haemolytic stretococcus
b) Streptococcus pneumoniae
c) Staphlococcus pneumonia
d) Staphlococcus aureus
Staphlococcus aureus
Purple on gram stain = gram postive
Clusters of cocci that are catalase +ve = Staphlococcus
Coagulase +ve = S. aureus
Which of the following are being described?
Purple on gram stain. Catalase test -ve. Green haemolysis test. Optochin sensative.
a) Beta haemolytic stretococcus
b) Streptococcus pneumoniae
c) Staphlococcus pneumonia
d) Staphlococcus aureus
Streptococcus pneumoniae
Purple on gram stain = +ve
Catalase test -ve = Streptococcus
Green haemolysis test = alpha haemolysis
Optochin sensative = S.pneumoniae
Name the sterile parts of the body?
Sterile parts of the body
Blood, CNS, joints, peritoneal cavity, pleura fluid, lower respirary tract, urinary tract
Which of the following could be being described here?
Pink on gram film. Yellow appearence on MacConkey agar. Oxidase test +ve.
a) Shigella / salmonella
b) Pseudomonas
c) E.coli
Pseudomonas
Pink on gram film = -ve
Yellow appearence on MacConkey agar = non-lactose fermentors
Oxidase test +ve = Pseudomonas
Which of the following could be being described?
Pink on gram stain. Pink/red appearence on MacConkey agar
a) Shigella / salmonella
b) Pseudomonas
c) E.coli
d) Staphlococcus
Pink on gram stain = GNB
Pink/red appearence on MacConkey agar = lactose fermentors = enterobacteriaceae = E.coli
What are protozoa?
Protozoa are single cells eukaryotic organisms
Consumers of bacteria, algae + microfungi
What type of infection is malaria?
Parasitic protozoa
Sporozona -> plasmodium spp.
How is malaria transmitted?
On the bite of an anophele mosquito
Which is the most dangerous type of malaria?
Plasmodia falciparum
Explain the life cycle of malaria
Malaria bites an infected human - takes up gametocytes
Gamaetocytes to sporozoites in mosquito salivary gland
Mosquito bites human
Human liver into merozites - released into blood stream
Merozites invade RBC, divide and destroy them
Explain the difference in lifecycles of P.ovale and P.vivax
P.ovale & P.vivax have an additional hypnozoite stage in the liver
They are also not eradicated by conventional anti-malarial treatments
P.falciparum is known as ‘cerebral malaria’ and can be fatal.
Explain how it can cause tissue hypoxia.
The parasite matures in RBC and forms knobs on the surface.
These bind to receptors on endothelial cells & other RBC (rosetting)
Sequestration in small vessels (including brain, lung)
= Microcirculation obstructed: tissue hypoxia
A 32 year old presents with fever, chills and sweats, fatigue, headaches and diarrhea.
On history you find that they have been in Kenya 2 months ago.
What could be the diagnosis?
Malaria
Fever and they have been to a tropical contry… think Malaria
What are the following clinical features describing?
Fever, coma, ARDS, renal failure and shock
P.falciparum malaria
Broadly explain how antimicrobials work
Antimicrobials work by binding to target sites on a bacteria.
Defined as points of bichemical reactions that are crucial to the survival of the bacteria.
The crucial binding site varies with each class of antimicrobials.
Give examples of beta lactams and explain how they act as antimicrobials
Beta-lactams:
Penicillin based - penicillin, amoxicillin - cephamycin, cephalosporins …
They bind to penicilin binding proteins in the cell wall and prevent cell wall synthesis
Glycoptpties also work by this mechanism
Give the correct antimicrobial mechanism of action for the fluroquinolones
a) Inhibition of ribosomal acivity & protein synthesis
b) Interference with nucleic acid synthesis/function
c) Binding to cell wall and inhibiting cell wall synthesis
d) Inhibition of DNA gyrase (topoisomerase II)
The antimicrobial mechanism of action for the fluroquinolones =
Inhibition of DNA gyrase (topoisomerase II)
Give the correct antimicrobial mechanism of action for the aminoglycosids and tetracyclins
a) Inhibition of ribosomal acivity & protein synthesis
b) Interference with nucleic acid synthesis/function
c) Binding to cell wall and inhibiting cell wall synthesis
d) Inhibition of DNA gyrase (topoisomerase II)
The antimicrobial mechanism of action for the aminoglycosids and tetracyclins =
Inhibition of ribosomal acivity & protein synthesis
Give the correct antimicrobial mechanism of action for metronidazole & rifampicin
a) Inhibition of ribosomal acivity & protein synthesis
b) Interference with nucleic acid synthesis/function
c) Binding to cell wall and inhibiting cell wall synthesis
d) Inhibition of DNA gyrase (topoisomerase II)
The antimicrobial mechanism of action for metronidazole & rifampicin =
b) Interference with nucleic acid synthesis/function
