Chlamydia And Clostridium Micro Lect 18+ 19Exam 2

Front 1

Chlamydial diseases

What's clamydiae trachomatis?
What serotypes do you see in the 4 specific cases?

Back 1

major cause of blindness, STDs
1. trachoma - see A, B, Ba, C serotypes A, B, Ba, C
2. inclusion conjunctivitis - serotypes A, B, Ba, D to K
3. non-gonococcal urtethritis: serotypes D to K
4. lymphogranuloma venerum- serotypes L1, L2, L2a, L3

Front 2

What does chlamydia begin as?
Describe the life cycle in an epithelial cell

Back 2

Begins as an elementary body (very small) that infects an epithelial cell.
- 12 hrs, creates a vacuole and in the next 36 hrs, gets converted into a retiuclar body.
-as a reticular body, it replicates and fills up the entire cell.
- up to 48 hrs, it converts back to the elementary body and releases all the organisms as the cell dies.

Front 3

How does trachoma manifest?

Name the 5 stages

Back 3

Begins as follicular hypertrophy with infections. (Trachomatous inflammation- follicular): drooping eyelides, red sticky painful. itchy eyes w/ white dots on inner lining of upper eyelid.

2) intense trachomatous inflammation - ahrd to see blood vessels in inner surface of upper eyelid due to extensive inflammation

3) trachomatous scarring - inner lining getsscarred, and feels like there's sand in the eye

4) trachomatous trichiasis - inner lining of eyelid thickens and shape of eyelid changes rinding lashes down to rub on eyeball results in corneal scarring

5) corneal opacity - eye looks white instead of clear. continued scarring leads to loss of vision.

Front 4

Describe inclusion conjunctivitis

Back 4

-can get it from spread of venereal disease but its very easily treated
-heals spontaneously w/o corneal abrasion
- in kids at birth, may have lesion that lasts for 1 year.
-often picked up in swimming pools that are inadequately chlorinated.

Front 5

What is the "grand daddy" of all venereal diseases?

Describe how you get it, and what are the clinical manifesations?

Back 5

Lymphogranuloma venereum.
-1 to 10 days following contact, see a lesion on the genitals.
-this heals w/o scarring but there is an invasion of the lymphatics, drain pus, and faciltate spreading.
-get arthrtic aches, anal stenosis, and various symptoms.

Front 6

Chalmydophila psittaci? What is the manifestation? Who catches it?

Back 6

Ornithosis - psitticosis.
-carried by birds from S. America. Infects people through domestication, and other birds that were outside.
-150-200 cases in NY, often in children that play in park. See nausea, vomiting, headache. may develop cyanosis, drop in BP, spinal cord fatality.
-take tetracycline that may abort infection quickly.

Front 7

Where can we see chlamydophila pneumoniae?

Back 7

1. known as TWAR - acute respiratory diease in immunocompromised pts.
2. implicated in coronary artery disease

-seen in many soldiers, and manifests as heart attacks due to CAD.

Front 8

Legionnaires' disease

Back 8

occurred in 1976 at american legion convention in Philly, there was approx. 5,000 attendees with 182 people infected.
-29 died.
-source: may be toxins, infectious agent, Cd Ni
-symptoms: headache, cough fever, pneumonia, liver degeneration, cardiac arrest..multisystem.

2 years earlier at same hote, there was a similar events of smaller mangitude occurred.

eventually isolated legionella pneumoniosa. Gram -, low Na, oxidation reduction potential, and it could be isolated from waters where ocean and spring water mixed together. Infected individuals at this hotel becuase of a/c leaking.

Front 9

Pontiac Fever?

Back 9

1968, 90% attack rate in health department building in michigan.
symptoms: flue syndome, allergic diesease, resolved in 2 to 5 days.
-also identified as Leigionella pnemophila once isolated from guinea pig pus.
- black background needs Fe to grow.

Front 10

How does Legionella grow?
What's the mechanism and clinical manifestations, and treatment?

Back 10

Grows in mononuclear cell.
Inhibits parts of cell that may attack the organism since it lives in an endocytotic vesicle.
As the cell is destroyed and organism is released, it goes on to lungs.
-attacks monocytes, neutrophils, caused microabsecces.

-Effector molecule is brought through outer membrane via Dot/Icm complex in bacterial cytoplasm, and this is squirted through the macrophage membrane.

-forms cavities in air spaces
-sensitized T cells and activated macrophages eventually abort infection
-can be treated with azithromycin.

Front 11

What is mycoplasma pneumoniae?

Back 11

mild to occasionally severe pneumonia in kids, young adults, and less so in older adults.
-takes about 2 - 3 weeks to be over with.

aka walking pneumoniae
chest xray will show particulate infiltratres
**see Clinical Micro made ridiculously simple**

Front 12

Describe the pathway of mycoplasma infection.

Back 12

New antigen develops in host epithelial cells that causes an autoimmune reaction.
-loss of cilia on cells, damaged protective mechanism
- can be treated by microorganisms, polypeptides, azithromycin, tetracycline, erythromycin

Front 13

Describe the appearance of clostridium.

Back 13

has a large terminal spore. Good gram straining.
-anaerobic organisms, 10-12 microns in length.
-may cause gangrene. release toxins, destroy tissues, vasculatures, generate gas, blood cells
-cause death by pulmonary, renal, and cardiac failure

Front 14

What happens in a gas gangrene infection? (Clostridium perfringens)

Back 14

1. wound interrupts blood supply
2. you see inflammation and anoxia
3. you see increase tissue lactic acid, anaerobic glycosis
4. now organism shifts to anaerobic area and starts to grow. oxidation reduces rapidly.
5. ph of tissues drop to 4. you see spore germination, and eventually wound colonization.

Front 15

Describe the following toxins produced by C. perfringens in gas gangrene. What enzymes or toxins are these associated with?

1. alpha
2. kappa
3. mu
4. theta
5. Nu
6. Beta
7. iota
8. enterotoxin
9. epsilon

Back 15

1. Alpha: lethal necrotizing lecithinase

2. Kappa: collagenase

3. Mu: hyaluronidase

4. Theta: hemolysin

5. Nu: deoxyribonuclease

6. Beta: releases catecholamines

7. Iota: similar to alpha toxin

8. Enterotoxin: alters membrane permeability

9. Epsilon: increases permeability of GI tract

Front 16

What are the differential effects of botulism and tetanus?

Back 16

Botulism: get flaccid paralysis. No matter how many messages you send to the brain nothing is activated
2) tetanus toxin interacts with GABA inhibitor. causes spastic paralysis. GABA inhibitor blocks the message that's coming down.

Front 17

What results in opisthotonos?

Back 17

Opisthotonos is arching of the body and is a manifestation of advance tetanus with spastic paralysis.
-usually from puncture wounds (often seen in soldiers).

Front 18

What causes botulism?

Back 18

Spore found in soil that makes its way into food. Germinates and produces a toxin; A, B, E, and F affects humans.
-Toxin is very potent!

Front 19

Describe how botulism affects the release of Ach.

What are the symptoms?

Back 19

H chain and L chain is taken in by cholinergic neurons. this then blocks the release of Ach, which inhibits muscle contraction.

Botoulinum neurotoxins (BoNT) A, E, B, D, F, C - all made by different strains of botulism. Designed to attack certain animals; each toxin attacks a different animal that will effect the release of Ach vesicle.

-associated with double vision, dry mouth, constipation.
-toxin is absorbed by gut. may take years till its released totally from pt.

Front 20

What is Bacillus stearothermophilus?

Back 20

Most heat resistant organism that is used as a test organism for detecting how many other organisms in a particular can are particularly viable.
-good for testing in cans. Need to make sure that heating process is sufficient to kill microorganisms.

Front 21

Pseudomembrane colitis? What do you see in the colon? What is it caused by?

Back 21

Caused by clostridium diphicil. Can see white patches or lesions through entire length of the colon through endoscopy.

Clostridium diphicil:
Inhabitants of the colon, and on occasion given antibiotics may survive and cause this disesae. produces enterotoxin resulting in fluid loss, and cytotoxin that alters morphology causing pseuomembranous colitis. Sometimes appears with pts treated with cephalosporins.
-treated with vancomycin

Front 22

What do you see microscopically for pseuodomembrane colitis?

Back 22

See volcanic lesions, tha tmakes a pseudomembrane around it. When this pops off though, RBCs rush out and there's a lot of blood loss.

Front 23

Where can we see clostridium dificil?

Back 23

Caused by antibiotics taken in pts, which permits it to grow. But its taken care of easily with other antibiotics. need to prevent toxin production, that results in pseudomembrane colitis.

Front 24

Describe anthrax (bacillus antracis)

Back 24

1st bacterial disease discorvered by koch.
-large 1X 3 micron, facultative anarobe. 3 capsular genes w/ exotoxins and detected in specimens but not in cultures.
-causes large black lesion.
-edema factor
-considered a war weapon, esp if its pulmonary or GI anthrax via inhalation of ingestion of spores.

-prevented by vaccination or ciprofloxacin.

Front 25

What is bacillus cereus?

Back 25

infectious, gram positive, responsbile for food borne disease.
-opportunisitic. may cause vomiting, diarrhea. spore former.
-spores can germinate and make heat resistant toxin (in RICE!)
-diarrheal form caused by toxins made by spores.

Front 26

What bacterial toxin has been used beneficially to treat a patient?

Back 26

Botulin