Bacterial/Parastitic Lecture Flashcards
Prokaryotes
No membrane bound nucleus
Gram staining
Gram positive: thick cell wall of peptidoglycan
Gram negative: peptidoglycan sandwiched between two membranes
Classification
Shape
Anerobic/anaerobic
Mechanisms of bacterial injury
Adhere to host cells, invade or deliver toxins
Virulence genes confer these properties
- Pathogenicity island (genes are bound together)
Biofilms
Within extracellular polysaccharides that adhere to host tissues or devices as catheters
Makes them inaccessible to immune systems
Adhesins
Surface molecules on bacteria that bind to host cells
Entry into host?
Opsonization (coated with antibody and taken in) and phagocytosisinto macrophages
Inside the host?
Replicate, inhibit host protein synthesis, lyse hotst cells
Bacterial toxins?
Endotoxins (components of bacterial cells):
Lipopolysaccharids (gram - bacteria) which activate protective immunity but can cause septic shock
- Exotoxins (secreted by bacteria): enzymes, intracellular toxins and neurotoxins (superantigens)
Injurious effects of host immunity?
Granulomatous reaction in TB (tries to engulf the bacteria but it is hypersensitive so you have huge influx of macrophages that form granulomas)
Antibodies react against strept proteins begin to act against heart
Poststrep glomerulonephritis
— Type 3 hypersensitivity (lots of antibody/antigen complexes forming) deposit in the joints
Gram Positive Bacterial Infections
Diptheria Listeriosis Anthrax Streptococcal infection Staphylococcal Infections
Diptheria
corynebacterium diptheriae
- Produce toxin that blocks host cell protein synthesis
- Immunization: protects against leathal effects of toxin
- EF2 (elongation factor): conversion from RNA to protein is blocked
Listeriosis
Listeria monocytogenes
Food borne
Causes menigitis
ACTA: allows it to escape the lysosomes and move to adjacent cells
IFN-gamma activates macrophages to phagocytose and kill bacteria
- Internalins + E-cadherins: internalization
Anthrax
Bacillus anthracis
Has a polyglutamyl capsule: prevent anthrax toxins
Two parts: can’t act without B
Heptamer: interacts with edema factor or lethal factor –» forms an acidic pH
Edema fact: interacts with calmodulin convert AMP to cAMP causing water efflux leading to edema
Lethal factor: protease that works on MAPK and causes cell death
Steptococcal infections
Rheumatic fever, glomerulonephritis
Pneumonia and meningitis
Dental caries
Rheumatic fever, glomerulonephritis
S. pyogenes
Pneumonia and meningitis
S. pneymoniae
Dental caries
S. mutans
Staphylococcal infections
Multiple toxins and enzymes
Superantigens
Antibiotic resistance
Multiple toxins and enzymes
S. aureus
Superantigens
Huge release of antigens causing shock
S. aureus and S. pyogenes
Antibiotic resistance
MRSA
Methicillin resistance
Gram negative bacterial infections
Neisserial Infections Whooping Cough Pseudomonas Infections Plague Chancroid Granuloma Inguinale (donovanosis)
Neisserial Infections
N. menigitidis and V gonorrheae
Whooping cough
Bordetella pertussis
Inspiratory whoop
PCR
Infects bronchial epithelium and macrophages
Pertussis toxin- paralyzes the respiratory cilia –> inactivates G proteins
Whooping Cough mechanism
Virulence factors: BVGS is activated and phosphorylates BVGA
BVGA regulates transcription of mRNA for adhesions and toxins