Bio 326M Flashcards Ch 15-19

Front 1

What four highly virulent Clostridiums?

Back 1

difficile
perfringen
tetani
botulimim

Front 2

What are anaerobic spore forming gram positive rods, motile, able to grow very rapidly, and are mostly non-virulent saprophytes (organisms that feed on dead/decaying organic matter)?
--some species have aerotolerance

Back 2

Clostridium

Front 3

In the virulent clostridium perfringen, which one of the five different strains is most responsible for human infections?

Back 3

Type A

Front 4

What are some characteristics of the clostridium perfringen?

Back 4

It is not motile, has rapid growth and has a low rate of spore formation. Also has a very wide distribution and primarily infects the GI

Front 5

clostridium perfringen produces alot of toxins what are four of these toxins

Back 5

Alpha, epsilon, iota, and entertoxin

Front 6

Which one of the toxins of clostridium perfringen has neurological effects, forms a pore in cell membranes, allowing potassium ions to diffuse out, and is activated by trypsin?

Back 6

Episilon toxin-permease

Front 7

What toxin of the clostridium perfringen is a binary toxin whose active agent is an ADP ribosylase and target is the monomeric actin.The protein acts as an enzyme, adding ADP to actin monomers. This prevents actin polymerization, disrupting the cytoskeleton?

Back 7

Iota toxin

Front 8

What is a permease?

Back 8

general term for a membrane protein that increases the permeability of the plasma membrane to a particular molecule, by a process not requiring metabolic energy.

Front 9

Entertoxin are superantigens that are produced from C. perfringens, what is the effect?

Back 9

Entertoxin is a superantigen, brings permease activity and it is produced during sporulation.

Front 10

Entertoxin is usually seen where?

Back 10

The intestinal cells

Front 11

What toxin produced from C. perfringens is a lecithinase/phospholipase and give a brief description?

Back 11

Alpha toxin
-Makes gas gangrene
Lyses cells(responsible for necrosis)
-Phospholipid → phosphate + Diacylglycerol. Diacylglycerol is a strong activator of protein kinase C
Protein kinase C does lots of things, overactivation of PKC is really bad.

Front 12

How do you treat C. Perfringens?

Back 12

Hyperbaric chamber
Aggressive debridement (removal of dead, infected tissue)
IV Antibiotics, usually high dose penicillins

Front 13

How do you diagnose C. Perfringens?

Back 13

Growth on blood plate will show large colonies with full and partial hemolysis
Large numbers of rectangular gram positive bacteria and absence of WBC

Front 14

What are some diseases from C. Perfringens?

Back 14

Cellulitis
Clostridial food poisoning
Gas gangrene/myonecrosis/necrotizing myositis

Front 15

What is cellulitis

Back 15

discoloration of the skin
Gas production
Localized swelling and non-painful

Front 16

Describe the process of gas gangrene?

Back 16

Pain is first symtom
Spread very rapid
Edema, skin turns bronze, then blue/black then develop a peculiar sweet oder.

Front 17

What myonecrosis?

Back 17

A premature death of muscle fibers.

Front 18

What are the later systemic effects of gas gangrene?

Back 18

Later systemic effects can include massive muscle necrosis, shock, renal failure, tachycardia

Front 19

What are some things that makes the body more sucesikbtible to gas gangrene?

Back 19

Heavy trauma (surgery, open fractures, hematomas, deep punctures)
Also diabetes makes increase risk because diabetics have poorer circulation, resulting in lower O2 levels.

-Also to be noted gas gangrene has a short incubation period.

Front 20

Clostridial food poisoning, is an intoxication not an infection is from ________ , mediated by ________ and can cause:

Back 20

Contaminated meat products
Enterotoxins (Enterotoxin is heat sensitive. Cases usually result from food prepared too far in advance – spores germinate, grow, produce enterotoxin which causes GI symptoms).

Cause- Rapid onset cramps, diarrhea, BUT NO FEVER, VOMMITTING OR NAUSEA

Front 21

Give some basic characteristics of C.tetani?

Back 21

It is highly sensitive to oxygen.
Motile, characteristic drumstick shape in culture due to spore formation
Ubiquitous, spores found in soil, frequent colonization of animal GI tracts

Front 22

How is C. tetani treated?

Back 22

There are vaccinations given DTP
Toxin-specific immunoglobulin (Passive immunization)
Debridement
Metronidazole

Front 23

Why is Metronidazole used instead of penicilin?

Back 23

Penicillin is contraindicated due to GABA inhibition – one side effect of penicillin is an inhibition of GABA on its receptors. Usually this effect is small enough to ignore (some patients will have convulsions when given large doses of penicillin). Tetanospasmin decreases release of GABA, thus penicillin and tetanospasmin form a sequential blockade on the action of GABA.

Front 24

What toxin is produced by C.tetani?

Back 24

Tetanospasmin , is a single polypeptide and is broken down by host protease. Will then become two disulfide peptides.
-The heavy chain B is used at binding to the cell
-The light chain A is used for neurotic activity

Front 25

Describe the pathway of c.tetani?

Back 25

Tetanospasmin is produced and released once bacteria lysed.
The A chain(light chain), a zinc metalloproteinase, enter neurons and moved to CNS via retrograde axonal transport. The heavy chain (B) is used to bind and enter cells.
Cleaves proteins that are used in release of synaptic vesicles, release of GABA and glycine are also stoped.---It uses the Zn to cleave proteins
The firing rate of neurons increased lockjaw, smiling, drooling, sweating, tachycardia, irritability and other symptoms. Constant firing of motor neurons – rigid paralysis.

Front 26

What are some basic characteristics of C.botilism?

Back 26

Ubiquitous found in soil
Binary toxin
--
Complexed with accessory proteins, survives passage through stomach
B toxin mediates entry, A toxin enters synapse at neuromuscular junction
A toxin (metalloprotease) remains at synapse (up to months) and prevents release of acetylcholine, preventing stimulation of muscle (flaccid paralysis)

Front 27

What are the three kinds of botuillism?

Back 27

Food, Wound, Infant

Front 28

What are some results of food botulism?

Back 28

Vomiting, constipation, abdominal pain, nausea, but no fever
Respiratory paralysis may lead to death
Symptoms may persist over months (toxin may persist)
Mortality ~10% with treatment (ventilation)

Front 29

What botuillism doesn't have GI symptoms?

Back 29

Wound botulism

Front 30

What has the lowest mortality rate in botullism?

Back 30

Infant

Front 31

What is the leading cause of noncomial diarrehea and antibiotic is leading risk ascoiated?
Also give some characteristics:

Back 31

C. difficile is a strict anaerobe, fastidious growth
Bacterium is largely in spore form
Some strains are non-toxigenic and do not cause disease

Front 32

Which Clostridium has:
Toxins
--Enterotoxin – toxin A
Chemoattractant, proinflammatory, fluid accumulation
Animal models show that this toxin alone can replicate many disease symptoms
-----Exotoxin – toxin B
Binary toxin, depolymerization of actin (similar to iota toxin of C. tetani)

Back 32

C. Difficle

Front 33

Pseudomembranous colitis presents as ______ and _______ with greenish, mucoid __________

Back 33

cramping
abdominal pain
diarrhea

Front 34

Pseudomembranous colitis is a infection of the large colon due to what occuring?

Back 34

The antibiotics kill off normal flora leads to overgrowth of C. difficile

Front 35

How do you treat Pseudomembranous colitis?

Back 35

Give yogurt
Withdraw Antibiotics
Use Metrazinodiale if cannot withdraw antibiotics

Front 36

What is the diagnosis for Pseudomembranous colitis?

Back 36

Antibiotic-induced nosocomial diarrhea should raise suspicion of C. difficile.

Growth is evident as tan/yellow/green/black nodules, 2-10mm loosely adherent to colon walls, patchy in mild forms, nearly confluent in advanced disease.

Pseudomembranous tissue composed of dead cells, fibrin

Presence of toxins in stool (ELISA/EIA or in cytotoxicity assay)

May also cause diarrhea without forming pseudomembrane (probably a much less severe disesase)

Front 37

Give some a description of mycobacterium?

Back 37

Gram positive bacteria, sometimes called acid-fast positive

Non-motile, no spores

Highly complex cell wall

Slow growing, and fastidious(difficult to be cultured)

Front 38

What are some relevant species of mycobacterium?

Back 38

Tuberculosis
Leprae
Avium
Cosmeticum

Front 39

Describe the cell wall of mycobacterium?

Back 39

Has mycolic acids, arabinose and glycolipids

Also made of mannose and LAM(lipoarbinomanan)

Cell wall is also made of peptidoglycan

Front 40

Describe in more detail parts of the mycobacterium cell wall?

Back 40

60 % of cell is lipid so it is hydrophobic

15% is transport proteins, porins and other proteins

Mycolic acids- are branched chain fatty acids, responsible for the ropy apearance
--Helps exclude hydrophobic antibiotics

Front 41

Why is mycobacterium considered acid fast?

Back 41

It retains the fuchsin dye following acid-alcohol wash
-small red rods in microscopic field

Front 42

What is the therapeutic target of mycobacterium and what is the presentation of mycobacterium?

Back 42

Target is the synthesis of mycolic acids and is inhibited by isoniazid

Presentation is through CD1 to Tcells.
--CD1 is like MHC I in structure but presents exogenous antigens like MHC II
--Expressed by professional APC's (DC, macro, B cells)

Front 43

There are 5 steps of a tuberculosis infection, give those five steps.

Back 43

Step 1 Inhalation
-May infect any part of body, but pulmonary infections are most common by far

Step 2: 7-21 days following initial reaction
-Phagocytosis by alveolar macrophages
Fusion of phagosome and lysosome blocked by bacterial protein
unchecked growth within unactivated macrophages, they eventually burst

Step 3- Tubercles
-Large granulomas form which can prevent the spread of bacteria, however they can cause necrosis. Which will cause a formation of a wall of fibrin, preventing macrophage action. Bacteria may become dormant due to hypoxic conditions.

Symptoms include cough, fever, weight loss and chest pain

Surrounding macrophages may fuse to form multinucleated giant cells

Other phagocytic cells are attracted to the infection
-macrophages and Tc attracted by C5a
-Activation of macrophage and CTL through Cytokine production (IFNgamma, IL-1, TNF)


Step 4-Spread
-Spread mostly by granulomas
-sometimes called miliary tuberculosis

Step 5 necrosis
-Liquification of granulomas and necrosis of lungs

Front 44

Tuberculosis has little or no toxin production, slow growing, fastidious and can co-infect with what virus?

Back 44

HIV
-immune depression leads to longer treatment
-PPD reaction depressed as well. PPD reaction is mediated by TH cells
Type IV hypersensitivity – TDTH and Macrophages.

Front 45

What is the importance of CD1 with tuberculosis?

Back 45

CD1 is structually to MHC I but is functionally similar to MHC II. They present hydrophobic antigens

Front 46

What is milary tuberculosis?

Back 46

This is when the xray is done there are hundreds of granulomas seen

Front 47

What diagnosis done for tuberculosis?

Back 47

PPD
-bacterial proteins from cell wall injected subcutaneously
-Positive test from asymptomatic carriers
Reaction may be suppressed in immune compromised patients (false negative)

Chest XRays are done

Culture-effective but takes long time

Direct examination of sputum(mucus of respiratory system)

Front 48

What are some drugs used for treating TB?

Back 48

Rifampin-RNA polymerase inhibitor
Isoniazid
Pyrazinamide- prodrug, not effective against other Mycobacteria
Ethambutol-inhibtor of arabinose transferase. Arabinose transferase is necessary for cell wall formation

Front 49

What is vacine for TB?

Back 49

BCG
-Live M.bovis strain
-Vaccine will make PPD test useless
-Effectiveness at preventing pulmonary infections vary with location.Good north bad by equator
-Efffective at preventing progression to millary disease and encephalitis but not so effective at preventing infection

Front 50

People are drug resistant to rifampicin and isoniazid, what is this?

Back 50

Multidrug Resistant- For TB Drugs

Front 51

People are drug resistant to at least rifampicin and isoniazid as well any member of the quinolone family and one other second line drug is called what?

Back 51

Extensively Drug Resistant

Front 52

What is the transmisson of leprosy?

Back 52

Person to person

Front 53

What mycobacterium disease only infects 1% of human population, infects both externally and internally(internally infects schwann cells and macrophages). This is also heavily dependent on T cells, including Tdth and CTL?

Back 53

Leprosy

Front 54

wHAT HAPPENS IN THE EARLY INFECTION OF LEPROSY?

Back 54

Skin lessions
Hypopigmentation
Hypohydrosis

Front 55

What happens in lepromatous leprosy?

Back 55

This is a result of defect in cellular response.
-High number of bacteria
-Bacteremia nearly constant
-Infection at cooler distant parts of body, eyes, legs, hands
-There is nasal stuffiness, los of hair and teeth
-Then loss of motor control and sensation and clawed hands

Front 56

What happens in Tuberculoid leprosy?

Back 56

There is granuloma formation, low numbers of bacteria and sometimes called paucibacillary(means low bacteria count) leprosy

Front 57

What is unique concerning lepromatous and tuberculoid leprosy and Lepromin test (like the PPD)?

Back 57

You will see a false negative in lepromatous
Tuberculoid works

Front 58

Beside the lepromin test how else can someone be evaluated for leprosy?

Back 58

Microscopic examination
Lepromin test

Front 59

What are the three classical symptoms for leprosy?

Back 59

Pin pricks, hpopigmentation, hypohydrosis

Front 60

What does Ubiquitous mean?

Back 60

existing or being everywhere

Front 61

What are the two Mycobacterium Avium Complex?

Back 61

M. avium and M. intracellulare

Front 62

What people are usually infected with MAC?

Back 62

immunecompromised patients

Front 63

MAC is usually just in the lungs, but spreads due to what infection...usually M. avium is seen to be with this virus?

Back 63

HIV

Front 64

The Mlung infection of elderly female non-smokers have patients with what characteristics?

Back 64

Fastidious (Overly concerned about tidiness and cleanliness.)
They do voluntary cough suppresion which leads to mucus accumulation

Front 65

Sputum is

Back 65

is matter that is expectorated from the respiratory tract, such as mucus or phlegm, mixed with saliva, which can then be spat from the mouth.

Front 66

What is the diagnosis for a Mlung infect?

Back 66

Culture of sputum

Front 67

What was the complete 180 degree turn around found in the science article?

Back 67

That the old TB vaccine was ineffective, beacause it was too wimpy and over-attenuated It was just certain traits made it less effective in evoking a immune response, take away these traits and we have a greater response

Front 68

How was the old TB vaccine created?

Back 68

Weaken a strain from a cow, that causes TB and is related to humans

Front 69

Why did researchers feel BCG was weak afterawhile?

Back 69

It was grown in culture for years, so it is proposed it probably changed and became less effective in preventing pulmonary infection

Front 70

What was the real reason the BCG was not working?

Back 70

The BCG was producing antioxidants, same thing TB makes which suppress the immune responses

Front 71

How was the modified BCG better than the parent BCG?

Back 71

the modified BCG induced greater cytokine (immune regulatory factor) production during the early phase of the immune response, more CD8 cell-killing T cells at the peak of the primary response, and more CD4 helper T cells during the memory phase.

Front 72

Why do vaccines against TB have to be greater in invoking an immune resonse in effectiveness than the natural infection?

Back 72

Because the regular TB infection does not provide subsequent immunity, maye due to immunosuppresion

Front 73

What test have been done to create a vaccine that is stronger at invoking an immune resonse in effectiveness than natural infection?

Back 73

Replace BCG-use recombinant virus that expresses TB antigens

Subunit based, usually in conjunction with BCG

Front 74

Crohn's disease is characterized by inflammation of GI tract, due to _____ and ____ responses

Back 74

TH1 and TH17
TH1-IFN gamma
TH17-IL-17

Both cytokines are seen in high levels of patinets

Front 75

For Chron's disease there are two modes of treatment, antibiotic and immunosupression, describe both?

Back 75

Antibiotic-Ciprofloxacin (a flouroquinolone-inhibitor of DNA gyrase) or Metranidazole

Immunosuppresion-Corticosteroids and/or 6 mercaptopurine

Front 76

What causes Crohn's disease?

Back 76

Mycobacterium avium subspecies paratuberculosis

Front 77

What is used to treat Mycobacterium avium subspecies paratuberculosis?

Back 77

All antibiotics used against Crohn's disease and 6-mercaptopurine inhibits MAP

Front 78

What are some targets for viral drugs?

Back 78

The viral drug targets are the :
Receptors
Nucleic acid polymerases
Other specific viral genes (HIV Protease. Influenza (NEuraminidase and proton ionophores)
Non specific targets

Front 79

What does neuraminidase do in influenza?

Back 79

Helps take influenza from the plasma membrane of a cell