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Microbiology Exam 4 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

What are the general characterisitcs of Corynebacteria?

A

1) theyre gram+
2) Aeoribic or faculativly anaerobic
3) non motile

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2
Q

What is the shape of corynebacteria?

A

Rodlike; Pleomorphic
-Can apear as cocobacilli, club shaped or exclamation points.

-Little tendancy to branch

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3
Q

Why does the corynebacteria dipetheria has a V shape?

A

Because of an incomplete separation of sibling bacterias during fission

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4
Q

Whats the phylum of corynebacteria? Catalase postive or negative?

A

Its from the phylum Actinobacteria which includes other closeley related Hugh G and High C genera. such as mybacterium, nocardia and streptonyces

  • Metachromatic granules
  • Does not form spores

Catalase Postive

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5
Q

What are metachromatic granules in corynebacteria?

A

Inclusion bodies for phosphate storage

-

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6
Q

Does the genus corynebactrium affects humans only? part of normal floura?
Where is its natural habitat in the body?

A
  • Its diverse so it affects; humans, animals and plants
  • Some corynebacteria such as diptheroids are part of the normal flora for humans
  • They usually reside in the oropharynx, mucosa and skin of humans or animals
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7
Q

What is the most widley studied pathogenic species of corynebacteria?
What are the non-diptheria coryne bacteria often refered to as?

A
  • THe widles studied one is corynebacterium diptheria (Has the causual agen diptheria)
  • Non- diptheria corynebacteria is known as diptheroids.
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8
Q

What is the clinical significance of corynebacteria?

A

Mostly none pathogenic but theyre oppurtuinistic pathogens: If theryre introducued via installation of a device or an implant they will cause parthenogenesis.

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9
Q

What is pathogenisis of corynebacterium Jeikeium?

A

-Transported via the unwashed hands of medical personell. Highly Antibiotic resisitant and its an implants or bone marrow transplant related infection.

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10
Q

What is the pathogenisis of C. Haemolyticum?

A

-Causes sore throat, bacterimia, generalized rash and chronic skin ulcers.

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11
Q

What is the pathogenicis of C.Urealyticum? Is it urease postive?

A

UTI, Bactermia, endocarditis, periotonitis and oseteomylititis.

UREASE POSTIIVE

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12
Q

What is the pathogenisis of C.Ulcerans?

A

-associated with drinking unpasteurized milk; causes toxin producing strains that leads to diptheria like symptoms

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13
Q

What did the FISH probe of supragingival plaque reveal?

A

Framework primarily of corynebacterium Matruchoti filaments.
-The corynebacterium filaments create a favorable microenviroemnt favorable to cocci

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14
Q

What is the history of Corynebacteria Diptheria??

A
  • one of the most studied human bacterial diseases.
  • The study of diptheria follows the development of modern medical microbiology, immunology and molecular biology

-Prior to immunizations (Before 1920) about 150k cases and 13k fatalitites.

Since 1990’s 0-5 cases per years mostly in none immunized individuals but its still an endemic in developing countries.

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15
Q

What are the 2 clinical form of corynebacteria diptheria and what is the virulence level?

A

very highly virulent.
-capable of causing severe illnessses or death in unvaccinated hosts. It causes diptheria

1) classical diptheria or pharyngeal was most common in pre vaccine era
2) the Cutaneous diptheria which is what is most common now in the U.S

Humans are the only known reservoir of Diptheria

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16
Q

How is diptheriae transmitted?

A
  • Person to person via droplet inhalation. or exudate from infected skin lesions.
  • Asympomatic respiratory carriage in endemic areas of none immunized individuals.
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17
Q

Classical or pharyngeal diptheria have 2 distinct phenomenas; what are they?

A

1) Noninvasive infection of respiratory tract- Stays in superficial layers of respiratory tissues; induces inflammatory response
2) Toxigenisis: production of diptheria toxins (DT). THe toxin is very virulent because it causes inhibiton of protein synthesis.

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18
Q

When is the toxigenisis induced in C.Dipterhaia?

A

When there is a specific virus bacteriophage carrying the tox gene.

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19
Q

What are the symptoms of the respiratory tract infection of diptheria?

A

-Low grade fevers in the first 1-5 days but if left untreated it will progress to a forming a grayish yellowish pesudomembrane covering the soft palate.

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20
Q

Where does the name diptheria come from?

A

-its from the greek work for leather hide and that describes the defining aspect of the disease which is the leathery pharyngeal membrane.

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21
Q

What is the pesudomembrane that is the hallmark of c.diptheria composed of?

A
  • Its composed of bacteria, fibrin, inflammatory cells and it extends all the way to the larynx and trachea.
  • The organisms remain in the membrane without invading the throat tissues.
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22
Q

What are the systemic symptoms of corynebacteria diptheria?

What causes death in C.Diptheria classical?

A
  • Production of toxins causes severe systemic symptoms.
  • Targets heart, kidney and peripherial nevres

-Suffocation due to the pseudomembrane or systemic effects of toxin

23
Q

What is Cutaneous diptheria associated with?

A
  • Poor hygiene
  • Can enter skin via a cut or an abrasion
  • the pathogen develops into none healthing ulcerated skin lesions that turn into grey membrane that are non progressive
24
Q

Is cutaneous diptheria associated with systemic intoxication?

A

RARE when it comes to systemic intoxication. can induce high antitoxin levels but does not make patients too ill and NO DEATH.

25
Q

Diptheria Toxin or DT. What is that?

A
  • Its encoded by lysogenic gene. so it has to be incorperated into the bacterial genome. the Beta- bacteriophage incorprates the tox gene.
  • Since its lysogenic via a specific phage so its not found in all strains.
26
Q

What is the structural and chemical properties of the diptheria toxin?

A
  • Its a heat labile exotoxin (Sectreted toxin).
  • Its a prototype of the A/B toxin family (Includes anthrax toxin, tetnus toxin and botulinum toxin)
  • A subunit is an enzyme functional domain (Source of toxicity)
  • B is the binding domain to the cell wall receptor and aids in the translocation of the A subunit
27
Q

In short what are the function of the A and B subunits of the Diptheria toxin?

A
  • A is the enzyme and functional toxin
  • B is the binder to the cell wall and aid in translocating A
  • A/B toxin gets into cell by cell mediated endocytosis and acidify in the endosome.
  • The Sulfide bond between A and B is broken in endosome it leads to the A subunit translocation
  • A subunit goes into cytoplasm and causes blocking of protein synthesis leading to cell death (By causing ADP ribolysation of host eEF-2)
28
Q

How can you treat DT?

A

DAT diptheria antitoxin which is made from immunized horses. Hyptersensitivity to horse proteins caused the decrease in production.

-Antibiotics: Penicillin, erthyromycin if allergic to penicillin

Support measures is intubation (breating support.

29
Q

What is the diptheria vacccine?

A
  • its the diptehria toxoid which targets the toxin not the bacteria it self.
  • Immunization almost completely eliminated Diptheria colonization in humans.
  • immunization given to children adults recieve a booster
30
Q

What is herd immunity?

A

As long as a high percentage of the population is vaccianated other unvaccinated people are protected as well

-Herd immunity is not applied to teranus toxoid vaccine. It only protects the vacinee

31
Q

Phylum firmcutes includes what bacteria?

A
  • Bacillus (aerobic)

- Clostridium (anaerobic)

32
Q

What are the general charcateristics of firmcutes ( Bacillus and clostridium)?

A
  • both are gram postive
    -Both rod Shaped
    both produce endospores.

HOWEVER;
-Clostrdium is catalase negative while bacillus is catlase postive.

33
Q

What do certain species of bacillus produce? Are they ubquitous?

A

Sometimes they produce:

  • Toxins (e.g Bacillus anthrax toxin)
  • Antibiotics (e.g Bacitracin)
  • Amylase

They are ubquitous which means theyre found in many areas and survice in wide variety of areas.
-Transmission via water, dust and materials of plant or animal origin.

34
Q

Medical importance of the genus Bacillus:

A

1) Ubiqutous and forms endospores that are eventually released.
2) heat resistant, strong acid and disenfection
3) VERY DURABLE AND CAN survive many years in dormancy.
4) When enviroment stress is gone they become vegative cells.

35
Q

What is 4 problomatic aspects of bacillus?

A
  1. contamination of surgical equipments
  2. Bacillus cerus and Bacillus subtillis can cause infection in heavily contaminated wounds
    3/ B. Cereus can also cause severe occular infection after trauma.
36
Q

What is the Bacillus cereus food poisoning features?

A

1) Emetic type
- Very short incubation and upper GI Tract. causes vometting and nausea.
- Caused by heat and trypsin resistant enterotoxin that is plasmid encoded.

  • Toxin in food primarly associcated with fried rice and is known as the fried rice syndrome.
  • The vegrative cells and spres are found on rice.

-The spores can surivive cooking.

37
Q

What is the bacillus cereus diarrheal type features?

A
  • Incubation is 8-16 hours after eating. causing cramps, watery diarrhea
  • has the enterotoxin that is heath and trypisn labile oxin
  • Toxin genes must be present in bacterial chromosome.
38
Q

Do you need treatment usually for Bacillus cereus food poisoning?

A

No usually self limiting to no more than 24 hours.

39
Q

ANTHRAX! What is the structure of anthrax?

A

Large bacillus with squared off ends. “Boxcar shaped.

-transmission via spores not person to person but spores are viable for years.

40
Q

What are the 3 forms of human anthrax?

A

1) cutaneous
2) Inhalation
3) gastrointestinal

41
Q

What are the facts on Human cutanous anthrax?

A

95% of human anthrax is cutaneous.
-Due to handelling the skin of carcasses and occurs moslty in developing country without veternatiy public health measures/

-Transmitted via flies

  • Spores are subcutanously grown rapidly and form vesicles which develops to black eschar
  • lesions are painless and pussless serous drainage.

-CAN BE FATAL IF UNTREATED

42
Q

What is an eschar and what is it a hallmark of?

A

-Eschar is black wound and its a hallmark of cutanous anthrax.

43
Q

Facts about gastrointestinal anthrax?

A
  • Minor cases
  • Never been reported in US
  • Similar effects as cutanous anthrax but only occurs on intestinal mucosa.

HIGH MORTALITY rate.

44
Q

Facts about inhallation anthrax:

A

Minority of cases associated with industrial workers at wool, hair and animal products facotries.

  • Not from contact with infected animal but its due to inhalaing spores carried on animal hair or fur. Thats why its sometimes called “Wool sorters disease”
  • ITs also dangerous weapon in bioterrorism.
45
Q

What is the pathogensis of inhallation anthrax?

A

-It starts with high fever and chest pain then it progressses to systemic hemorrage and often fatal.

46
Q

What are the two large plasmids Isolated from the Bacillus anthracis?

A

pXO1 and pXO2.

pXO1 harbors genes fro the anthrax toxin that kill immune system and promote edema.

pXO2: harbors genes for poly-D-Gamma-glutamic acid capsule.

  • Capsule provide immunoresistance
  • Immunosupressive attributes.
47
Q

What are the anthrax toxins produced into?

A

Anthrax produces two extracellular toxins A&B.

-The toxina are producd as three separate polypeptides.

1) PA (protective, and major virulence factor) (B subunit)
2) EF or edema factor
3) LF which is lethal factor

48
Q

So Anthrax toxin function in adding the different types of toxins and that would result in different outcomes. Whats an example of that?

A
  • Edema factor + Pag A factor will results into edema .
  • LF or lethal factor + Pag A will results in cell death and thats what is known as “anthrax toxin”
  • PA is the protective factor and its the main active ingredient in the anthrax vaccine. (Because its found in both)
49
Q

So Anthrax functions by binding PA into the cell wall then EF or LF will be inserted. What are the outcomes of that?

A

1) Disrupts cell signaling and migration
2) initiates cell lysis.

RECENT Work by sellman and mourez constructed mutant PA that does not assemble with EF and LF.

50
Q

How is anthrax treated?

A

At early stages its easily treated with anitbiotics. such as penicliln
-Later stages is when its fatal because toxins will be released and antibiotics cannot reverese the effects of the toxins.

51
Q

When anthrax wasnt anthrax. What was that case?

A

A patient came in with inhallation anthrax type symptoms but they were significantly severe and died. The findings showed that he did B. Cereus that had a plasmid of pOX1 which harbors anthrax toxins.

-This lead to the anthrax like symptoms and ultimatly the death of the patient.

52
Q

How often does steam autoclaves and chemical vapor sterlization equipments require spore testing?

A

Weekly.

-and the organism used with spore testing is bacillus stearothermophilus.

53
Q

Dry heat and ehtylene oxide sterilization requires spore testing every how often? and what organism is used?

A

Weekly as well

- Bacillus subtilis.

54
Q

Why use different spore strips for different equipment?

A

Because each species have different heat tolerances.

Microbiology Exam 4 (9 decks)

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