Haemophilus, Actinobacillus, Pasteurella Flashcards

1
Q

HAEMOPHILUS (were haemophilus)
–> Characteristics
* Gram- _______, ______
* weakly ______
* Originally based on whether requires _____ or blood _____. Now based on genetic relatedness.
* Normally X factor (hemin) or V factor (NAD) coenzyme in electron transport chain for
respiration. Found in UPR, urogenital tract; will not be found in environment.
* obligate parasite of host mucosal surfaces
* each species is host specific
* taxonomy is in state of flux

A

negative, coccobacillus, fermentative, blood, factors

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2
Q

Haemophilus” spp and their host
* Avibacterium (H.) paragallinarum
* Glaesserella (H). parasuis
* Histophilus (H.) somni

A

Used to be haemophillus, now this.

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3
Q
A

things in red = important

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4
Q

What disease do you think these pigs have?
* A. Atrophic rhinitis
* B. Swine cholera
* C. Glässer’s disease
* D. Erysipelas
* E. I don’t have a clue

A

C

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5
Q

What is (H.) parasuis?

A
  • specific for swine
  • requires V (NAD) factor only.
  • Nonhemolytic; does not produce an exotoxin
  • More than 15 serotypes may occur, based on capsule or lipooligosaccharide
    (LOS), or are untypable; usually a herd issue, which is why you want to know the serotypes.
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6
Q

Where do pigs with PRRS usually come from? What is the typical age of the pig? What can be seen clinically/ post mortem?

A

Pigs that have been infected with PRRS or are from SPF herds are particularly susceptible.
* Usually occurs in young pigs (important cause of nursery mortality; develop early on in development)
** fibrinous inflammation of serous surfaces (e.g. pleura or
joints)
“Purple ears are often a feature. Bacteria can readily be isolated from the blood and lesions at post-mortem examination. Chronic cases may be more difficult to
diagnose and may require P-M to look for joint and heart valve lesions.”

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7
Q

What can be seen in this image?

A

Glasser’s Disease (polyserositis)

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8
Q

What can be seen in this image?

A

Fibrin on paricardium and liver

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9
Q

What can be seen in this image?

A

Blood clot in trachea

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10
Q

What can be seen in this image?

A

Pericarditis;

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11
Q

Specific Diseases due to G. (H.) parasuis?

A
  • Respiratory Disease
  • Usually occurs in older pigs
    following previous infection
    (mycoplasma or virus)
  • Chronic pleurisy
  • Differential:
  • P. multocida, Bordetella,
    Actinobacillus spp., others
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12
Q
A
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13
Q

What are the virulence factors of G. (H.) parasuis ?

A

Virulence Properties
* Capsule
* Lipooligosaccharide
* Adherence factors
* Membrane proteins, no known exotoxins

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14
Q

What are the Adherence Factors of G.(H) parasuis?

A
  • required to colonize the host
  • bacteria attach to mucosal epithelial cells
  • Usually mediated through pili, LOS, or membrane proteins
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15
Q

What is important about the haemophilus species in terms of bacterial composition?

A

Lipooligosaccharide
There are no O side chains (polysaccharide) in the LPS of Haemophilus species examined, and therefore it can be called an LOS
* The Lipid A still has endotoxic properties
** Causes inflammation
* Core oligosaccharide is antigenic

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16
Q

What are the Compromising Factors?
* Viral Infection: associated with respiratory disease
* Stress: associated with Glasser’s disease, but not required as
newborn pigs are already compromised
The disease is predominately the result of HOST INFLAMMATION-trying to remove a pathogen it cannot

A
  • Viral Infection: associated with respiratory disease
  • Stress: associated with Glasser’s disease, but not required as
    newborn pigs are already compromised
    The disease is predominately the result of HOST INFLAMMATION-trying to remove a pathogen it cannot
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17
Q

How is Immunity to G. (H.) parasuis formed?

A
  • Protection is usually mediated by antibodies to capsule; however,
    there are at least 15 capsule types
  • Protective antibodies may also be made to LOS, membrane proteins,
    and other somatic antigens.
  • Humoral immunity most important
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18
Q

What is the Vaccination, treatment and prevention of G. (H) parasuis ?

A

Make sure to get correct serotype.
Don’t necessarily need to be long lasting in the case of Glaccier’s disease
Vaccination, treatment and prevention
*Bacterins are effective against homologous serotype (and somewhat against
others), but may not be long lasting
* Attenuated live vaccine also available and effective
* Antimicrobials
* Intentional exposure at 3-5 days of age with low dose of less virulent
serotypes (RISKY)
* Protection also through maternal antibodies

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19
Q

What is Avibacterium (H). paragallinarum?

A

Avibacterium (H). paragallinarum
* Specific for avian species
* Requires V factor only
* Nonhemolytic

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20
Q
A
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21
Q

What diseases are Specific due to A. paragallinarum?

A

Fowl Coryza (acute rhinitis)
* inflammation of turbinates and sinus epithelium
* air sacculitis
* primarily a disease of chickens

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22
Q
A
23
Q

What is seen here?

A

Depressed, discharge near beak, painful, hunched over

24
Q

What is seen here?

A

High morbidity, but not
mortality

25
Q

What is seen here?

A

Inflammation of air sacs

26
Q

What is seen here?

A

Inflammation, pus

27
Q

What are the Virulence Properties of A.
paragallinarum?

A
  • Capsule
  • Lipooligosaccharide
  • Adherence factors
  • Membrane proteins?, exotoxins not recognized
28
Q

What are the Compromising Factors of A paragallinarum?

A
  • Viral or mycoplasma infection
  • Stress
    Again, disease is predominately due to host
    inflammation
29
Q

How is Immunity to A. paragallinarum formed?

A
  • Protection is usually mediated by antibodies to capsule
  • Protective antibodies may also be made to LOS, membrane proteins,
    and other somatic antigens.
  • Humoral immunity most important
30
Q

What is important about Vaccination for A. paragallinarum?

A
  • Bacterins (to serotypes A, B, and C) are effective
  • Designed to raise antibody to cell components
  • Antibodies to capsule are protective, but only against 1 serotype -
    purified capsules nonimmunogenic
  • Other serotypes may be present
31
Q
A
32
Q
  • What is the most likely etiologic agent of this outbreak?
  • A. Pasteurella multocida
  • B. Mannheimia haemolytica
  • C. Histophilus somni
  • D. A virus
  • E. Any or all of the above
A

C

33
Q

What is Histophilus somni?

A
  • Includes Haemophilus somnus,
    H. agni, and Histophilus ovis
  • Specific for bovines and sheep
  • Requires neither X or V factor, but does require blood and CO2
  • Most have yellow pigment
  • Weakly hemolytic or nonhemolytic
  • **Colonies are yellow **when picked up with a white
    swab
34
Q

What is seen here?

A

Need CO2 and yellow = key characteristic

35
Q

What is the normal habitat of histophilus somni?

A
  • Normal habitat is the ruminant genital and respiratory tracts
  • Disseminates via the bloodstream and localizes at other
    sites (brain, heart, joints, etc.)
  • Reasons for dissemination are not clear
  • Probably due to inflammation of endothelium (vasculitis is a
    hallmark of this pathogen)
  • Stress and viral infection are required; primarily a feedlot disease; rarily see it in cattle that live out on passure
36
Q

What specific diseases are due to H. somni?

A

Specific diseases due to H. somni
* First disease documented by this organism = TME (thrombotic meningoencephalitis)
* *Pneumonia (BRDC or shipping fever)
**
Myocarditis (biofilm formation)
* Reproductive failure (abortion, infertility)
* Arthritis
* Bacteremia
* Others

37
Q

What is seen here?

A

TME
Eyes drooping, inflammed (key of TME)
Laying down; unwilling to get up

38
Q

What is seen here?

A

Pneumonia

39
Q

What is seen here?

A

Myocarditis
Acute, necrotizing myocarditis; bacteria are
in biofilm-like aggregates and adherent to venous
endothelium, with fibrin and neutrophils

40
Q

How is the Biofilm formed for H. Somni?

A
  • H. somni forms a biofilm under most growth conditions and in host
    tissues. When in a biofilm, bacteria are more resistant to antibiotics
    and host defenses
    , but induce less inflammation
41
Q

What is seen here?

A

Filaments, fibirn material
polysa, protein, extracelluar dNA = components of biofilm.

42
Q

What are the Virulence Properties of H. somni?

A
  • Endotoxin (Lipooligosaccharide)
    Phase variation of lipooligosaccharide in vivo
  • Antigenic epitopes change and
    enable bacteria to evade host
    immunity; some are identical to host
    oligosaccharides
  • In the host, the bacteria take up sialic
    acid and decorate their surface with
    sialic acid
    Their whole defense mechanism is to hide from the host.
43
Q

What is seen here?

A

short chains; can phase vary. Can resist host defenses; host makes antibodey repsonse to Lipo, organisms cleared and those that have changed their oligo now persist.

44
Q

What are some additional Virulence factors for H. Somni?

A

Produce a very large protein: IgG Fc receptors (immunoglobulin binding protein [IbpA]
on bacterium
* bacterium binds Fc region of IgG, protecting the bacterium
from host defenses (fibrillar network of IbpA)
** (there is a toxic fic motif in IbpA)
**Survives within phagocytic cells by inhibiting
phagosome-lysosome fusion
* LOS causes apoptosis of endothelial cells, leading to
vasculitis
* Adherence factors-many

45
Q

Region within gene of immmunogobluni binding protein that produces a Toxin/Exotoxin (has not be categorized yet)
H. somni produces a cytotoxin as part of a motif of the
IgG binding protein A. This motif has been shown to be
toxic for bovine endothelial cells and macrophages.

A

Causes vasculities, enabling bacteria to penetrate host BBB ad enter blood stream.

46
Q

What is seen in this image?

A

Third image on right = cell that does produce binding protein.

47
Q

What are the Compromising Factors of H. Somni?

A
  • Infection with virulent, as opposed to “commensal”, isolates
  • Stress
  • Previous infection
    Disease is due to host inflammation
48
Q

How is Immunity to H. somni developed?

A
  • Antibodies to the bacterium are normally present in
    animals and should be protective, but no direct
    evidence for this yet; can survive in phagocytic cells
    *** Virulence is largely due to avoiding the host
    immune response
  • Protective components not well defined, and likely
    require cellular immunity
  • Antibodies to fic motif protective in passive
    immunity studies
49
Q

What are the vaccination strategies for H. Somni?

A

Bacterins are limited in effectiveness due to phase variation
and IgG binding proteins; best against TME
* An effective vaccine against BRD has not yet been developed. Need an intelligen vaccine that recognizes antigens expressed in the host.

50
Q

What is the Host specificity of H. Somni?

A
  • Host specificity is mediated by adherence and iron acquisition
  • Host-specific bacteria obtain iron from host transferrin. Species
    that can only utilize transferrin of one host cannot infect other animals.
51
Q

How do you Diagnose Haemophilus spp.?

A

*Culture:
* Need to isolate from sterile site or in pure culture – chocolate agar = blood agar heated to 80 degrees
* Most isolates from animals require NAD only (blood for H. somni)
* Some species may require CO 2 (H. somni, some G. (H.) parasuis)

52
Q

Is serology used to diagnose Hemophilus species i? What is the most common tests? What are not very sensitive?

A

Serology (not usually used):
* Complement fixation test most common
* Slide or tube agglutination tests easy to do, but are not very sensitive
or specific
* others that are more sensitive and specific include ELISA.
* Outer membrane protein preps or exopolysaccharide

53
Q

What are the treatment options for hemophilus spp?

A
  • Susceptible to most antibiotics
  • Use least expensive and most appropriate drugs
  • Antimicrobial resistance can occur; may need susceptibility test
54
Q

Summary
* A. paragallinarum - Fowl coryza
*Birds only
* G. (H.) parasuis - Glasser’s disease, pneumonia,
septicemia
*PIGS ONLY
* H. somni - TME, pneumonia, myocarditis, abortion,
arthritis
*BOVINES, and occasionally sheep, ONLY

A