Bordetella & Mycoplasm

Front 1

What does Bordetella Pertuisis need to survive?

Back 1

Requires human respiratory tract (ciliated) - humans are the only carriers

or

special agar (Nicotinamide & other stuff) to grow Gram (-) coccobacilli

Front 2

How does Bordetella grow?

Back 2

Slowly (3-5d) in specialized medium

Front 3

How is the diagnosis of bordetella pertusis made?

Back 3

Diagnosis is made clinically and confirmed by the slow growing culture. (gram - coccobacilli)

Rapid DFA & serology can confirm clinical suspicion.

Absolute lymphocytosis above 40K can aid in confirmation

Front 4

What are the adherence factors(4) & Toxins(4) of Bordetella Pertusis

Back 4

Adherence Factors (4) [PPPF]
Pilli=fimbrae
Pertactin
FHA (filamentous hemeagluttin)
Pertusis Toxin - acts both as a toxin & an attachment factor

Toxins (4) [PEAT]
Tracheal Cytotoxin (TCT) (Dermonecrotic toxin) - destroys ciliary escalator
ACT - activated by host CaM to raise cAMP & inhibits phagocytic cells
Endotoxin (LPS)
PT (see above) - inhibits Gi activation

Front 5

How does pertusis toxin work?

Back 5

An AB toxin

S2-S5 act as B portion for uptake
S1 is the A part - ADPR Inhibits the Gi function (increase in cAMP)

Front 6

Clinical signs of PT in blood?

Back 6

Absolute lymphocytosis (40K)
Hypoglycemia

Front 7

What does Adenylate Cyclase Toxin (ACT) do?

Back 7

[PAHCO]
[A]CT is a bacterial cyclase which is activated by host calmodulin to convert ATP->cAMP

Some [h]emolysis activity. This **inhibits [p]hagocyte cells**, [c]hemotaxis, cell signaling & leads to 2y bacterial infections. Blocks formation of [o]xidative burst chemicals (PMN)

Front 8

What is and what does Tracheal CytoToxin (TCT) do? How does it compare to Endotoxin?

Back 8

TCT - secreted fragemnted portions peptidoglycan layer of BP.

TCT - causes cytotoxicity of ciliated tracheal cells. This destroys the mucociliary escalator which takes 12wks to regrow.

Front 9

Where do you catch Whooping Cough? What is the infectivity rate? What is the reason for the recent resurgence?

Back 9

1. Strict human pathogen. Some partially immunized adults carry but DO NOT have symptoms. They spread the pathogen
2. 80-100% infectivity rate to exposed.
3. Recent resurgence do to fear of vaccines

Front 10

Which Bordetella Pertussis Ag have antibodies(4)?

Back 10

Ab form against FHA, PT, Pilli, Pertectin [FPPP]

?CMI is not stimulated possible reason requires boosters?

Front 11

Bordetella Pertussis

Back 11

infection localized to UR tract & remains superficial binding to cilia. It does NOT directly invade.

Toxins rather than the bacteria will have systemic effects.

Front 12

What are the stages and Clinical symptoms of Bordetella Pertusis disease?

Back 12

Overlapping phases

Catarrhal (1-2wks) - rhinorrhea, nonspecific malaise & fever this is when it is most communicable (flu like)

Paroxysmal (2-4wks) - Cough 50x/day, coughing followed by whooping and occasional vomiting. Marker LYMPPHOCYTOSIS (>40k)

Convalescent (3-4wks) - Cough decreases severity & frequency

Front 13

Can you treat whooping cough?

Back 13

No, once the cough has started all therapy is supportive or to decrease spread to others.

Treat with erythromycin or clarithromycin.

Front 14

How does bordetella pertussis enter and cause diseases in humans? What does it secrete?

Back 14

It is airborne, binds to ciliated respiratory epithelium via pertectin (PRN) + PT + FHA. This immobilizes the cilia. -> does NOT invade rather it superficially secretes

ACT - which causes hemolysis & disables PMNs
PT - paralyzes PMN/macrophage, may stimulate insulin secretion, CAUSES lymphocytosis (>40K)
TCT - Kills ciliated cells causing the persistent cough

Front 15

How can pertussis be prevented? How was the vaccine improved?

Back 15

Vaccine is available that always uses purified Petussis Toxoid & FHA and some use Pernectin and Pilli. (Acellular)

The old vaccine used whole cells which had serious SE similar to GN shock

Front 16

What makes mycoplasma unique? What are it's growth requirements?

Back 16

Does not stain. It has a trilaminar membrane with Sterols from the host/environment. It acts parasitic

Smallest self replicating bacteria that requires Special mycobacteria agar to slowly grow.

Front 17

How is mycoplasma pneumoniae spread? and to whom?

Back 17

Only reservoir is humans. It is spread by few as 100 droplets, generally causing symptoms in 5-15yo's in close quarters (prisons, military)

Front 18

How does mycoplasma pneumoniae enter the body?

Back 18

Binds to the cilia of bronchial epithelium. It then attaches at the base of the cilia using P1 tip attaching adhesion. This blocks the cilia function. This leads to desquamation and inflammation.

Front 19

How does mycoplasma pneumoniae present in a patient?

Back 19

atypical "walking" Pneumonia

2-4days of fever, HA & malaise. Physical exam will show patchy/unilateral pneumonia. Prior to respiratory symptoms of cough & mild tracheobronchitis.

Front 20

How is mycoplasma pneumoniae diagnosed? What is the culture appearance?

Back 20

Gram stain of sputum show no organisms, or cells lacking cell wall. It requires special media cultures "fried egg appearance"

Serological tests are best, w/ a 4fold rise in the titer

Front 21

How is mycoplasma pneumoniae treated? Here does it persist?

Back 21

No cell wall targeted drugs can be used. Erythromycin & tetracycline may shorten the duration but the bug may persist longer in the nasopharnyx.

Front 22

How are bordetella pertusis and mycoplasma pneumoniae similar? Different?

Back 22

Both bind to cilia in the trachea and move from there. Are spread by droplets.

Myco pneu produces no toxins
Bord Pertus produces many toxins

Front 23

How does bordetella pertussis and mycoplasma pneumoniae immunity compare?

Back 23

mycoplasma pneumoniae - host CMI may cause damage, the humoral immune response is induced. IgM, IgA and 2wks later IgG are formed. (may xreact-autoimmune w/ RBCs, brain, heart leading to anemia & systemic sx (arthritis))

Bordetella Pertussis - possibly uses CMI, IgG forms but will wane w/ time. 2nd infection will be more mild

Front 24

What are the mycoplasma that cause STDs? How are they spread? How are they differentiated from each other?

Back 24

Ureaplasm urealyticum & Mycoplasma Hominis

spread through sexual contact. Ureaplasm urealyticum is identified by the production of urea.

Front 25

Describe the different manifestations of both unique mycoplasms in males? females?

Back 25

1. men - urethritis, dysuria, urgency, & urethral discharge (Nongonococcal urethritis)
2. female - often asx but may have Salpingitis (Nongonococcal Salpingitis)

Front 26

What is the most common complication of Mycoplasma Pneumoniae?

Back 26

CNS in about 25% of the cases

Front 27

Is Xray alone enough to diagnose Mycoplasma Pnuemoniae? If not, what would be required?

Back 27

No, though lower lobe Xray would be consistent with the disease. Xrays will show patchy/unilateral pneumonia.

Serology would confirm diagnosis. Stains are of little help with absence of a cell wall.

Front 28

What are the CXR findings in mycoplasma pneumoniae?

Back 28

It often looks worse then the symptoms would suggest. Xrays will show patchy/unilateral pneumonia.

Front 29

Is there a vaccine for mycoplasma pneumoniae?

Back 29

No

Front 30

What is hemagglutination?

Back 30

Hemeagluttination is a specific form of agluttination of RBCs. Agluttination describes clumping.

It is used to diagnose mycoplasma pneumoniae.

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Front 31

Describe the mycoplasma pneumoniae bacteriology?

Back 31

[CPRBC]

No [c]ell wall, marked [p]leomorphism, [r]esistant to [b]eta lactams, No gram stain. Have [c]holesterol in trilaminar membrane

Front 32

What are the common causes of atypical pneumoniae?

Back 32

[MLCV]
mycoplasma
legionella
chlamydia
viruses

Front 33

What are the different symptoms for atypical pneumoniae compared to classical pneumoniae?

Back 33

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Front 34

What population is most at risk for Whooping Cough?

Back 34

Neonates, often mom's immunity has waned and does not transfer to the neonate. Vaccinations are given starting @ 2mo.

This is a dangerous window

Front 35

What are the major sequelae from whooping cough in neonates?

Back 35

Life threatening in children w/ heart or lung problems. Otherwise neurological sequelae from hypoxia

Front 36

How does TCT compare to Endotoxin?

Back 36

Endotoxin is lipid A which is a part of the outer membrane in GN cells. TCT is from the peptidoglycan layer that is just deep to the outer membrane.