week 11

C. diptheria, legionella,

Typical pneumonia

caused by strep. pneumonia

Atypical pneumonia

caused by Legionella

all strains of C. diphtheria are _________ meaning what?

lysogenic; lyse with the liberation of bacteria phage particles

What does the A fragment of C. diphtheria do?

A subunit inhibits protein synthesis via ADP-ribosylation of the Elongation factor 2

What does the B fragment of C. diphtheria do?

mediates the translocation of A into the cell cytosol

C. diphtheria causes what symptoms?

* pseudo membrane formation
* sore throat
* fever, malaise
* shortness of breath (dyspnea)
* arrhythmia (irregular heart rate that causes heart failure)
* bull neck

C. diphtheria causes heart failure and neurological symptoms why?

they have the same receptors so diphtheria toxin can bind

What atom is required for the toxin production of the C. diphtheria toxin?

iron

Walking pneumonia

you have minor symptoms but aren’t bed ridden

B. pertussis causes what disease

whooping cough

B. pertussis, four adhesins

* Filamentous hemagglutinin
* Pertusis toxin
* pili
* pertactin

Filamentous hemagglutinin (FHA) types

* ciliated cells= binds to galactose residues on sulfated glycolipids
* PMN= binds to CR3 receptor. induces phagocytosis

What toxins are present in B. pertussis

1. Pertussis toxin
2. Adenylates cyclase toxin
3. tracheal toxin
4. Dermonectrotic toxin
5. LPS

How does tracheal cytotoxin work?

* causes the whooping part of the cough
* causes an increase in cAMP and therefore increase of mucous in the lungs
* Kills respiratory ciliated cells with 1,6 anhydromuramic acid N-acetyl-glucosamine- tettrapeptide

How does LPS work in B. pertiussis?

* has lipid X which is more toxic than lipid A

What happens when there is an increase in cAMP?

causes an Cl and Na to increase outside of the cell membrane causing an osmotic gradient and loss of water, making more mucous build up in the lungs and airway

Adenylate cyclase toxin does what

1. Extracellular ligand binds to the GPCR
2. Receptor associated with heterotrimeric G protein, stimulating GDP release
3. Nucleotide exchange (GDP → GTP), leading to Gsalpha GTP dissociation
4. Gs alpha subunit binds to adenylate cyclase, results in increased cAMP
5. GTP to GDP hydrolysis Gs alpha- GDP dissociation followed by its reassociation with Gs beta and Gs gamma

When cystic fibrosis transmembrane is phosphorylated it opens a channel and causes

increase in Chloride and water secretion

Pertussis toxin: ADP-ribosylation of Gi alpha does what?

* prevents the dissociation of GDP, preventing Gialpha from binding GTP
* forces the cAMP to increase and prevents the inhibition of the G protein regulation

Pertussis: Phosphorylates BvgA is activated

Stages of B. pertussis:

1. Catarrhal
2. Paroxysmal
3. Convalescent

What stage of B. pertussis is the most contagious?

Catarrhal

B. pertussis: What stage is the coughing stage?

Paroxysmal; has the tracheal toxin working hard

Paroxysms are violent and lead to

detached retina and prolapsed rectum

Antibiotic treatment of B. pertussis is best when?

* in the early stages, when it is hard to diagnose Catarhal stage
* paroxysmal stage reduces severity and duration but the damage is done, usually just reduces communicalbility

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B. pertussis toxin is weird because

it cause lymphocytes to go crazy and increase outside of the lymph

90% of deaths from B. pertussis are to

infants