Bacteriology - Test Ii Lecture (7-8)

Front 1

Is Salmonella a good pathogen or poor pathogen?

Back 1

good pathogen

Front 2

Salmonella classification is based on what?

Back 2

-serological classification based on "O", "H" and Vi" antigens
-Kauffman-White scheme

Front 3

What syndromes are caused by Salmonella?

Back 3

(1) enteritis
(2) septicemia +/-localization
(3) carrier state

Front 4

What does Salmonella commonly cause?

Back 4

diarrhea in domestic species and humans
-host adapted strains are less likely to cause diarrhea, but can be very difficult to eradicate as they frequently result in long term carrier states

Front 5

Is Salmonella normal flora in the mare?

Back 5

no

Front 6

What is the pathogenesis of diarrhea caused by salmonella?

-what about localized infections in the joint?

Back 6

-Salmonella cause opportunistic infections, therefore need a predisposing factor

-factors include pregnancy/transportation/antibiotics/surgery/young animal

Front 7

Where do Salmonella come from?

Back 7

-GIT of mammals (carrier animals), birds, reptiles, insects ; fecal contamination of feed/water; long-lived in the environment

Front 8

What is the route of infection of Salmonella infections?

Back 8

feco-oral or recrudescence

-a large number of Salmonella MUST be ingested to produce GIT colonization

Front 9

If Salmonella is ingested, how does it then go about and cause diarrhea?

Back 9

-adhesion to M cells in the lower ileum and large intestine
-invade these cells and multiply
-bacteria are then released into the lamina propria
-virulence factors cause the diarrhea

Front 10

What are the virulence factors of diarrhea?

Back 10

(1) Enterotoxins - only some have them
(2) cytotoxins - inhibit protein synthesis and cause cell death
(3) endotoxin
(4) inflammation causes release of prostaglandins which cause increase in cAMP

Front 11

What is the cause of hemorrhage and fibrin in the diarrhea of horses affected with Salmonella?

Back 11

-exotoxins
-endotoxins
-hypersecretory component due to prostaglandin release

Front 12

What is characteristic of diarrhea in horses affected with Salmonella?

Back 12

hemorrhage and fibrin

Front 13

One salmonella is localized in intestinal epithelial cells, how often are the shed?

Back 13

3-6 weeks intermittently

Front 14

If ingested Salmonella does not cause diarrhea, what does it alternatively do (both this and diarrhea can be done in conjunction)?

Back 14

-can localize in phagocytes (macrophages) --> facultative intracellular parasites

-once inside, they traffic to local lymph nodes, liver, and spleen and remain there for weeks to years as a carrier state

Front 15

What are three outcomes of ingestion of Salmonella?

Back 15

(1) diarrhea
(2) become a carrier
(3) septicemia - with localization in organs (lungs, joints, kidney, heart, spleen)

Front 16

When septicemia occurs as a result of Salmonella, who does it most often occur in?

Back 16

young animals

Front 17

What serotype of Salmonella has been shown to cause infection in both animals and humans?

-who is most at risk for infection?

Back 17

S. typhimurium

-young, old, immunocompromised

Front 18

What two methods should an owner take if their animal comes down with Salmonella infection?

Back 18

-isolate (don't transfer to other horses)
-biosecurity (don't transfer to people)

Front 19

What type of Salmonella MAY be involved in infections?

Back 19

-multi-drug resistance

Front 20

ALL Enterobacteriaceae require WHAT to cause disease?

Back 20

host component

Front 21

What type of animals does cystitis caused by E. coli normally occur?

Back 21

young, speyed females (short urethra)

Front 22

What are other predisposing factors to an animal developing cystitis as a result of E. coli infection?

Back 22

-urolithiasis
-metabolic disease
-neoplasia
-obstructive lesions

Front 23

What is the most common bacteria to cause cystitis in the dog?

Back 23

E. coli

Front 24

What important virulence factors are involved in E. coli causing cystitis in the dog?

Back 24

(1) pili - attach to uroepithelium
(2) capsule
(3) hemolysins - to cause cell damage
(4) Fe acquisition systems
-intracellular survival/slime layer
**(5) Endotoxin

Front 25

Where do Klebsiella live?

Back 25

-environmental organism that likes wood shavings
-commensal in GIT

Front 26

What are the virulence factors of Klebsiella?

Back 26

-fimbriae
-capsule * - highly encapsulated
-hemolysin
-Fe acquisition system
-endotoxin *

Front 27

What diseases do Klebsiella cause?

Back 27

(1) cystitis
(2) pneumonia (usually secondary)
(3) mastitis
(4) equine endometritis - specific strains
(5) septicemia/naval ill
(6) nosocomial infections

Front 28

How do you diagnose Klebsiella?

Back 28

-isolate from sterile sites

Front 29

How do you treat Klebsiella - what would you do first?

Back 29

-sensitivity testing required b/c there is a lot of resistance

Front 30

Where does Proteus live?

Back 30

In the environment it is ubiquitous, transient in intestinal tracts

Front 31

What are the virulence factors of Proteus?

Back 31

(1) fimbriae
(2) IgA protease
(3) Fe acquisition systems
(4) hemolysin
(5) endotoxin
(6) swarming motility
(7) UREASE - get alkanisation of urine

Front 32

Why might there be an increase in urolith production in cases of cystitis caused by proteus?

Back 32

-because of urease - get alkanisation of the urine

Front 33

What disease does proteus cause?

Back 33

cystitis

Front 34

What type of motility does Proteus have?

Back 34

swarming motility

Front 35

Other than cystis, what diseases does proteus cause?

Back 35

-otitis externa
-prostatitis
-diarrhea
-wound infections (a common contaminant)

Front 36

How do you diagnose proteus?

Back 36

with care, because it is often a contaminant
-repeat culture often

Front 37

Where is yersina found?

Back 37

intestinal tracts of a wide range of mammals and birds

Front 38

Does yersina cause cystis?

Back 38

NO

Front 39

What are virulence factors of Yersinia?

Back 39

(1) facultative intracellular parasite
(2) endotoxin
(3) motile (not Y. pestis)
(4) adhesins/invasins
(5) capsule (Y. pestis)
(6) plasminogen activator (Y. pestis)

Front 40

What bacteria causes bubonic plaque?

Back 40

Y. pestis

Front 41

What diseases does Y. pseudotuberculosis cause?

Back 41

enteritis, sporadic abortion, septicemia (mostly ruminants; birds and lab animals)

Front 42

Which is more virulent, Y. pseudotuberculosis or Y. pestis?

Back 42

Y. pestis

Front 43

What are the clinical signs of cats in endemic regions that have Yersinia?

Back 43

-increased lymph nodes and severe depression

Front 44

How do you diagnose a Yersinia infection?

Back 44

with care because it is zoonotic
-send aspirates to specialized labs

Front 45

Which bacteria typically cause endotoxemia?

Back 45

Gram neg rods

Front 46

What is endotoxemia?

Back 46

-the presence of endotoxin in the blood
-the clinical syndrome observed when endotoxemia is present

Front 47

What is endotoxin?

Back 47

-endotoxin is a component (75%) of the outer cell wall of gram negative bacteria
-also called LPS

Front 48

What is another word for endotoxin?

Back 48

Lipopolysaccharide

Front 49

When is endotoxin released?

Back 49

-upon bacterial death during proliferation/multiplication
-LPS bound to bacterial cell wall is 20x< biologically active
-in its free state, it induces the clinical syndrome of endotoxemia

Front 50

Which is more harmful - LPS bound to bacteria cell wall OR in its free state circulating in the blood?

Back 50

-FREE endotoxin

Front 51

How many structural domains does each LPS molecule have?

Back 51

3

Front 52

What are the 3 structural domains of each LPS molecule?

Back 52

(1) O-antigenic chain (Polar polysaccharide)
(2) Core region
(3) Lipid A

Front 53

What doe the polar polysaccharide O side chains do?

Back 53

-these sugars project into the aqueous extracellular mileu
-this region is highly variable and antigenically specific for each bacterial strain

Front 54

What part of the LPS molecule are protective AB normally directed?

Back 54

Core acidic monosaccharide region

Front 55

Is the center, core acidic monosaccharide region conserved between gram negative bacteria?

Back 55

yes!

Front 56

Where is the hydrophobic, Lipid A region located in the LPS molecule?

Back 56

-largely buried in the bacterial outer membrane

Front 57

Which part of the LPS molecule mediates most of the toxic effects of endotoxin?

Back 57

-the hydrophobic Lipid A region

Front 58

The hydrophobic Lipid A region is highly conserved, but variation in what confers the degree of toxicity?

Back 58

-variation in number and length, saturation and position of FAs

Front 59

What are the 6 steps to endotoxemia?

Back 59

(1) physical barriers are breached
(2) initial contact between LPS and blood
(3) macrophage activation and dependent processes
(4) neutrophil activation and dependent processes
(5) clinically apparent circulatory insufficiency and organ damage
(6) death or recovery

Front 60

Where is endotoxin normally restricted to in the healthy host?

Back 60

-lumen of the GIT due to existence of a very efficient intestinal barrier

Front 61

What makes the intestinal barrier so efficient at protection from endotoxin?

Back 61

-mucosal epithelial cells and their secretions (mucus)
-resident bacterial population
-SMALL amount that is absorbed is cleared by Kupfer cells in the liver

Front 62

How does endotoxin gain access to the body from the GI tract?

Back 62

-if protective integument or mucosae are damaged
-if absorption exceeds the capacity of the Kupfer cells to clear it
-if endotoxin is directly absorbed into the lymphatics
-other enteric diseases that cause a breech

Front 63

What enteric diseases can cause a breech in the GI system and allow endotoxemia to occur?

Back 63

-bacterial enteritis (Salmonella)
-alteration of the integrity of the bowel
(1) Ischemia (bowel torsions, infarcts)
(2) inflammation (proximal enteritis)
(3) mechanical trauma (rectal perforation)
(4) intraluminal acidification (grain overload)

Front 64

What percent of colics present with endotoxaemia?

Back 64

30-50%

Front 65

What non-enteric disease cause breaches to the GI tract?

Back 65

-Gram negative infections
-Pleuropneumonia
-wound infections
-placentitis/metritis
-septicemia
-omphalitis

Front 66

What must endotoxin do to be toxic to mucus membranes?

Back 66

enter blood stream
-it is rarely DIRECTLY toxic

Front 67

Where is the one place where endotoxin may be directly toxin to mucus membranes?

Back 67

respiratory tract

Front 68

When endotoxin first enters the blood, what two things happen?

Back 68

(1) some is neutralized by anti-LPS antibody (from previous exposure)
(2) most is bound by LPS-binding protein (LBP)

Front 69

What binds endotoxin when it first enters the blood?

Back 69

LPS-binding protein

Front 70

LPS binding protein is the equivalent of a what for the LPS?

Back 70

A taxi!! Ha HA

Front 71

What does LPS-LBP complex bind to?
How does it bind?

Back 71

-binds to cell surface receptors with high affinity and specificity

EX: CD14 on intravascular macrophages

Front 72

What is the key initiating event from which almost everything else flows in the development of the signs of endotoxemia?

Back 72

-the interaction of endotoxin with macrophages

Front 73

Once LPS-LBP attaches to CD-14 receptors on intravascular macrophages, what does this activate?

Back 73

-activates intracellular signaling pathways and transcription factors

Front 74

Within 30 minutes of LPS binding, what happens?

Back 74

-processing of MO plasma membrane arachidonic acids into vasoactive lipid mediators (thromboxane A2)

-don't see this clinically

Front 75

When the macrophage plasma membrane arachidonic acid is processed into a vasoactive lipid mediator (thromboxane A2), what does this act locally to cause?

Back 75

-aggregation of platelets
-elaboration of additional thromboxane and serotonin
-initial vasoconstriction
-DON'T see this clinically

Front 76

When endotoxin stimulates macrophages, there is intese synthesis and secreation by LPS stimulated macrophages of a small group of extremely potent cytokines (inflammatory peptides). When this happens, what do you see clinically?

Back 76

fever

Front 77

What stimulates neutrophils?

Back 77

-macrophage cytokines

Front 78

When TNF and IL-1 (cytokines) act on PMNs and endothelial cells to cause adhesion and margination, what will you see clinically?
When?

Back 78

-leucopenia

-1 hour post LPS

Front 79

What do TNF and IL-1 cytokines do to PMNs and endothelial cells?

Back 79

cause adhesion and margination

Front 80

What does the second wave of macrophage cytokines do and when?

Back 80

--the second wave of cytokines produced by macrophages brings in circulating neutrophils and stimulates further production
-contributes to lethality

-this occurs 24 hours post LPS

Front 81

What will you see clinically after the second wave of macrophage produced cytokines?

Back 81

-leucocytosis

Front 82

During phase 4 of endotoxemia, MO cytokines activate PMNs which result in what?

Back 82

-increased sensitivity to complement products
-release of cell contents and toxic oxygen metabolites onto the endothelium --> increased vascular permeability and leakage from blood vessels
-release of potent lipid-containing mediators
-synthesis and release of nitric oxide

Front 83

What are the net result of the effects of endotoxin?

What does this look like clinically?

Back 83

systemic arterial hypotension and thrombosis --> inadequate tissue perfusion

-DIC and hemorrhage

Front 84

Once organs stop being perfused, what happens and what are the signs?

Back 84

impaired organ function --> stupor and in coordination (CNS), oliguria (kidney-renal failure), ileus and colic (intestine), icterus (liver), laminitis (hoof), and respiratory distress (lung)

Front 85

Does endotoxemia always lead to death?

Back 85

NO

Front 86

How does the host get rid of the infection (enterobacteriacea)?

Back 86

-antibody mediated immunity (to pili or capsule or the O side chains (LPS) - BUT serotype specific)
-cell mediated immunity (salmonella)

Front 87

Are enterobacteriaceae predictable sensitive to antibiotics?

Back 87

no - because drug resistant plasmids are readily transferred

Front 88

Which of the Enterobacteriaceae are particularly known to be drug resistant?

Back 88

-E.coli
-Salmonella
-(Klebsiella)

Front 89

For non-enteric diseases, what is the most important aspect of treatment?

Back 89

-antibiotics (first do a sensitivity test)
-aminoglycosides
-third generation cephalosporins
-trimethoprim/sulphonamides
-fluroquinolones

Front 90

What is the most important aspect of therapy for treatment of enteric diseases?

Back 90

-replacement of fluids and electrolytes
-given orally if still bright and alert or systemically if evidence of systemic disease
-adequate nutrition (milk) and nursing care

Front 91

Is antibiotic treatment needed for treatment of enteric disease caused by enterobacteriacea?

Back 91

-it is controversial
-if young and severely leucopenic

Front 92

What three things are important in all species when treating endotoxaemia?

Back 92

(1) reducing movement of endotoxin into circulation
(2) neutralizing endotoxin before it interacts with inflammatory cells
(3) general supportive care

Front 93

What three things are important in just horses when treating endotoxemia?

Back 93

(1) preventing synthesis and release of pro-inflammatory mediators
(2) interfering with action of pro-inflammatory mediators
(3) preventing endotoxin-induced cellular activation

Front 94

In preventing endotoxemia, how do you reduce movement into circulation?

Back 94

-focal infection: cut it out or drain it; antibiotics effective against gram - bacteria
-diffuse infection: LESS indication for antibiotics; if severe - bacterial translocation

Front 95

If you want to neutralize endotoxin to prevent interaction, what two parts of the LPS are BEST to target?

How does this work?

Back 95

-antibodies to the core region and or lipid A
-bind to LPS and prevent interaction with MO

Front 96

In neutralizing endotoxin to prevent interation of the LPS with the macrophages, how do antibodies get to the core region and or the lipid A part of the LPS?

Back 96

mutant bacteria that don't have O side chains - BUT not sure if it really works although it is widely used

Front 97

What is the best type of supportive care you can give to treat endotoxemia, even if there is no diarrhea?

Back 97

-fluid therapy to combat hypotension and hypoperfusion
-AND ID and correct any electrolyte and acid-base abnormalities

Front 98

How do we control enterobacteriaceae infections?

Back 98

-they are management diseases, so have to strengthen the host (colostrum) and decrease exposure to large numbers of organisms
-ISOLATION is key