Listeria And Erysipelothrix

Front 1

How to Identify Listeria?
- gram stain characteristics?
- catalase +/-?
- haemolytic on Blood Agar?
- motile?
- special tests?

Back 1

gram + small rods
Haemolytic on Blood Agar
Catalase +
Aesculin hydrolized
Motile
CAMP tests

Front 2

What does being Aesculin hydrolized mean?

Back 2

aesculin is added to agar with ferric citrate and bile salts. Hydrolysis forms aesculitin and glucose. A dark brown/black complex is visible with ferric citrate.

Streak and incubate 24 hours. A dark Halo= positive

Front 3

Listeria Habitat:

Back 3

can replicate in environment.
wide distribution: soil, water, vegetation

POOR QUALITY SILAGE

Front 4

What would be differentials to Listeria?

Back 4

Arcanopyogens (Trueperella) because catalase + and gram +.

** streptococci and Erysipelothrix rhusiopathiae are catalase -.

Front 5

Host-Pathogen-Environment

Back 5

relatively resistant.
Poor quality silage
* SHEEP affected sub clinically
* Many have immunity

Front 6

Listeria Pathogenesis
(overall)

Back 6

* ingestion of contaminated feed and may result in septicaemia, encephalitis or abortion
Penetrates intestine and spreads via lymph & blood
OR penetrates the nasal/oral mucosa/pulp cavity of teeth.
* Migrates via cranial nerves.
* can cross all three barriers
(intestinal, BBB and placenta)

Front 7

Listeria: Pathogenesis

Ingestion of contaminated feed results in what?
- which is most common?

Back 7

* encephalitis (most common)
septicaemia
abortion

Front 8

Listeria: Pathogenesis

Once Listeria is ingested, how does it penetrate?
(2 methods)

Back 8

1. Penetrates intestine and spreads via lymph & blood
OR
2. Penetrates the nasal/oral mucosa/pulp cavity of teeth.

Front 9

Listeria: Pathogenesis

Can Listeria migrate?
Can Listeria cross the BBB?

Back 9

* Yes- Migrates via cranial nerves.
* Yes it crosses all three barriers!
(intestinal, BBB and placenta)

Front 10

Listeria: Diagnosis

Back 10

*culture on BA
*cold enrichment
* PCR
*Serotyping (Strain typing)
-Serology, phage typing, genome analysis
* neurologic signs and abortion

Front 11

Listeria: Treatment and Control

Back 11

* cell mediated immunity
*antibiotics
encephalitis- poor response
septicaemia- responds well
* Make good silage
* live attenuated vaccine available in some countries

Front 12

L. Monocytogenes- pathogenesis.

Back 12

Migration via cranial nerves can invade both phagocytic and non-phagocytic cells.
Adheres iteranlins and receptors on phagocytes for lipoteichoic acids.
There is immune invasion where intracellular organismevades humoral immune response and escapes from the phagosome.
Can cross all three barriers in host. (intestinal, BBB and placenta

Front 13

HUMAN listeriosis

* major cause of food born illness!

Back 13

21 cases reported in Ireland 2007 and 11 in 2012. Septicaemia and miningitis if immunodeficient.
*minor skin infections
*infection by ingestion of extended shelf life refrigerated food (Soft cheese, pate)

Front 14

Listeria monocytogenes disease in Sheep

- the example from lab!

Back 14

* Neural Listeriosis "circling disease"
encephalitis, neural form.

Front 15

Listeriosis diseases

Back 15

* encephalitis (most common)
* abortion
* septicaemia
* Iritis and keratoconjunctivitis

Front 16

Listeria monocytogenes pathogenesis

Back 16

Internalin = adherance
LLO prevent lysosomal binding
Actin A tail sends it to a neighboring cell

Front 17

Listeria ivanovii

Back 17

causes abortion in ruminants

Front 18

Erysipelothrix rhusiopathiae: ID features

Back 18

slender G+ rods
No MAC growth
Oxidae/catalase -
TSA agar black line (H2S produced)

Front 19

Erysipelothrix rhusiopathiae: epidemiology

Back 19

Mainly pigs, some turkeys and sheep
Widespread in nature; infected by carrier animals of same spp.
* In tonsils, lymphoid tissues (skin/mucus memb)
* Contamination with feces
*survives drying, salting, smoking
* outbreaks in hot muggy weather
* Stress

Front 20

Erysipelothrix rhusiopathiae: diagnosis

Back 20

clinical signs
Response to AB
Isolation and ID
PCR (not routine)
Direct microscopy

Front 21

Erysipelothrix rhusiopathiae: control

What is advisable drug for treatment?
AMR? (antimicrobial resistance?)
Is elimination possible?
Can you vaccinate? If so.. live or dead?

Back 21

Penicillin for treatment and prophylaxis

AMR- Tetracyclines, aminoglycosides, sulphonamides

Clean and disinfect (elimination not possible)

Vax (pigs, sheep, turkeys)- dead vax protect for 6 months

Front 22

E. rhusiopathiae: pathogenesis

Back 22

1. Tissue colonization (adherence)
2. Immune evasion (capsule, spaA protein)
3. Tissue invasion and damage (hyaluronidase, vascular damage, immunopathology)
4. Disease production (varies with strain, carriers contaminate environment, infection/infestation of abraded skin.
5. Adherence to epithelium and penetrates bloodstream (neuraminidase)

Front 23

E. rhusiopathiae: Disease production
- know localization and septicaemic

Back 23

varies with strain
carriers contaminate environment
infection by ingestion or abraded skin
adherence to epithelium
penetrate blood stream and then is either localized or septicaemic

Front 24

Turkeys (turkey erysipelas)

Back 24

Turkeys (turkey erysipelas)
- septicaemia
- arthritis
-valvular endocarditis

Front 25

Sheep erysipelas

Back 25

- polyarthrjtis in lambs
- post-dipping lameness
- pneumonia
- valvular endocarditis

Front 26

Pigs (swine erysipelas)

Back 26

- septicaemia
- 'diamond skin' lesions
-chronic valvular endocarditis
- abortion

Front 27

If the E. rhysiopathiae disease is localized, what are the effects?

Back 27

vascular damage
arthritis
endocarditis
skin lesions

Front 28

If the E. rhusiopathiae disease is Septicaemic, what are the effects?

Back 28

vascular damage
Thrombosis
Fever

Front 29

In Swine E. rhusiopathiae - what are the 3 forms/ (4 syndromes)

Back 29

SWINE:
"hyperacute" = sudden death
acute = diamonds (skin lesions)
chronic: polyarthritis, vegetative endocarditis

Front 30

What is E. rhusiopathiae called in Man ?

Back 30

erysipeloid

Front 31

LAB: steps to ID Listeria and Erysipelothrix

Back 31

Growth on BA and CNA and NO GROWTH on MAC
Gram + rods- small
small glistening colonies and haemolysis= Listeria or possible Erysipelothrix

Front 32

LAB Diagnosis: Listeria

Specimens

Back 32

visceral (septicaemic) form- lesions from liver, kidneys or spleen

abortions- foetal abomasal contents and cotyledons

neural form- spinal fluid or tissue from medulla oblongata

Front 33

Lab Diagnosis: Direct microscopy

Back 33

stained histopath sections are important in neural form to demonstrate microabscesses and perivascular cuffing

Front 34

LAB Diagnosis: Listeria
Isolation:
Abortion and visceral forms

Back 34

blood agar, aerobically at 37c for 24-48 hours

Front 35

LAB Diagnosis: Listeria
Isolation:
Neural form

Back 35

COLD ENRICHMENT.
Homogenized brain tissue in NB, incubated at 4c. Subculture from broth to Blood AGAR once weekly, for up to 12 weeks

Front 36

LAB Diagnosis: Listeria
Identification

Back 36

main characteristics
Histopath in neural syndrome (microabscesses and perivascular cuffing in brain)
definitive id by API 20 STREP

Front 37

LAB Diagnosis: E. rhusiopathiae
direct microscopy

Back 37

acute- gram + rods
chronic- gram + filaments

Front 38

LAB Diagnosis: E. rhusiopathiae
isolation

Back 38

blood agar aerobically at 37c for 24-48 hours

Front 39

LAB Diagnosis: E. rhusiopathiae
identification

Back 39

small, non haemolytic colonies at 24 hours
partial haemolytic colonies at 48 hours

microscopic appearance: smooth colonies: