diseases

pertusis

Diaphteria

primarily affect the upper respiratory tract

symptoms

swollen neck glands

pseudomembrane

sore throat

skin infections(cutaneous diaphteria)

1-5 years

info

gram positive and club shaped bacteria, non motile and non encapuslated ,arobic

it have metachromatic granules that stored inorganic phosphate for ATP synthesis

culture by tellurite blood agar

gravis

intermedius

mitis

large grey colonies

black colonies with grey periphery

small, dull gray to black colonies

virulence factors

basically the top gene is from the bacteriophage once it insert the viral chromosome into the bacterial chromosome

A-B toxins

ADP ribose transfer

membrane insertion

receptor binding

how does iron regulate the synthesis of the diaphteria toxin

when there is a high amount of iron it will bind to the diphtheria toxin repressor and bind to the tox gene and act as a transcriptional repressor, and inhibit the synthesis of diphtheria toxin

pathogensis

mechanism

treatment

where

direct infection

contaminated objects

droplet infection

uptake of the toxin by the receptor mediated endocytosis

formation of the endocytic vescicle

the toxin B domain will bind to the specific receptor

acidification in the vesicle will lead to the conformational change of the toxin and A subunit will be cleaved and reach cytosol and will be active toxin

protein synthesis is stoped

ADP ribose transfer will take the ADP ribose from NAD and give to elongation factor 2 that will inhibit the transaction and will lead to the cell death

systemic effects

myocarditis

demyelinating neuritis

anit-toxins

passive immunization

give when you suspect the disease and do not wait for the diagnosis results

antibiotics

to kill the bacteria to prevent it from toxin production

antibiotics who are on contact in with people who have disease or carriers

bordatella pertussis

culture

complications

virulent factors

pertussis stages

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uncontrollable cough and paroxysms

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can affect under 10 years primirly

stage 2

stage 3

stage 1

catarrhal

paroxysmal

convalescent

highly contagious

violent cough with whoop

6 or 10 weeks

recovery

1-2 weeks

2-3 weeks

apnea

seizures

pnemonia

brain damage

gram negative small ovoid bacilli

non motile and non sporing form and obligate aerobic

metachromatic granules can be seen if there is toludine blue stainin

it lives in the cilia of the respiratory tract

Regan Lowe

bordet gengou

charcoal blood agar

small and glistening white/grey colonies

mercury drops

bisected pearl

adhesion factors

toxic factors

pertactin

fimbriae aggulitogens

filamentous hemaglutinin (FHA)

lipooligosaccaride

surface protein

it will adhere to the ciliated respiratory cells and colonize

pertussis toxin

tracheal cytotoxin

adenylate cyclase toxin

dermonecrotic toxin

heat labile toxin

AC domain

pore forming domain

the toxin will enter to the cell by pore forming domain and then bind to the calmodulin in the cell and toxin will be activated and the cAMP generation will increase

secretion signal

cAMP important for sugar and lipid metabolism and growth and differentiation

it is composed of AB5

ADP ribosyltransferase activity

binding to the receptor and entering the cell

mechanism of action

the G inhibitory can inhibit the activation of AC and decreases cAMP

the pertussis toxin will bind to the Gi and cause the inhibition of the Gi and it will lead to the accumulation of the cAMP

colonizing factor

an bind to the cilia and cause ciliary stasis

peptidoglycan like molecule

it will attach to the cilia of the respiratory cells

ciliostasis

pathogensis

secrete toxins that will affect first the cilia by the pertussis toxin and tracheal cytotoxin

AC toxin

adhere to the ciliated epithelial cells

pertussis toxin wil be secreted

trasmittion via cough

accumulation of mucuos

will lead to the acummaltion of cAMP levels and cause anti-inflammatory and anti-phagocytosis and damp the immune system

affect myeloid cells

lead to absence of fever

bind to the cell

endocytosis

endosome

cause the secretion of the cytosolic toxin domain

pertussis toxin

will lead to delay the inflammation

by inhibiting the chemokine synthesis

pertussis toxin

lymphocytosis

histamine release

respiratory tissues are hypersensitive to the histamine

leakage of BV contents

and inflammation of tissues and swollen airways

pertussis toxin will access growth factor that is sensed by lymphocytes and they will divide about 2-3 times higher than normal

treatment

erythromycin

azithromycin

clarithomycin

vaccination

DTP

DTaP

from 6 weeks to 6 years

5 doeses

TDap

10 -64 years

one dose