Haemophilus, Actinobacillus, Pasteurella Flashcards
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
negative, coccobacillus, fermentative, blood, factors
Haemophilus” spp and their host
* Avibacterium (H.) paragallinarum
* Glaesserella (H). parasuis
* Histophilus (H.) somni
Used to be haemophillus, now this.
Other species of less importance
* H. influenzae
Meningitis, (leading cause of bacterial meningitis in children under 1 year of age; significantly reduced with vaccine) otitis media, bronchitis, etc.
* H. felis respiratory disease
* H. haemoglobinophilus
causes Neonatal mortality in puppies
* Taylorella equigenitalis
causes Contagious equine metritis (S.E. Asia, Austraila, New Zealand).
Said won’t be focusing on this
things in red = important
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
C
G. (H.) parasuis
* 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.
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.”
Glasser’s Disease (polyserositis)
Fibrin on paricardium and liver
Blood clot in trachea
Pericarditis; differential?
Specific Diseases due to G. (H.) parasuis
* Respiratory Disease
* Usually occurs in older pigs
following previous infection
(mycoplasma or virus)
* Chronic pleurisy
* Differential:
* P. multocida, Bordetella,
Actinobacillus spp., others
G. (H.) parasuis Virulence Properties
* Capsule
* Lipooligosaccharide
* Adherence factors
* Membrane proteins, no known exotoxins
*Adherence Factors
* required to colonize the host
* bacteria attach to mucosal epithelial cells
* Usually mediated through pili, LOS, or membrane proteins
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
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
Immunity to G. (H.) parasuis
* 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
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
Make sure to get correct serotype.
Don’t necessarily need to be long lasting in the case of Glaccier’s disease
Avibacterium (H). paragallinarum
* Specific for avian species
* Requires V factor only
* Nonhemolytic
Specific Diseases due to A. paragallinarum
Fowl Coryza (acute rhinitis)
* inflammation of turbinates and sinus epithelium
* air sacculitis
* primarily a disease of chickens
Depressed, discharge near beak, painful, hunched over
High morbidity, but not
mortality
Inflammation of air sacs
Inflammation, pus
Virulence Properties of A.
paragallinarum
* Capsule
* Lipooligosaccharide
* Adherence factors
* Membrane proteins?, exotoxins not recognized
Compromising Factors
* Viral or mycoplasma infection
* Stress
Again, disease is predominately due to host
inflammation
Immunity to A. paragallinarum
* 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
Vaccination
* 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
- 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
C
Histophilus somni
* 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
Need CO2 and yellow = key characteristic
- 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
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
TME
Eyes drooping, inflammed (key of TME)
Laying down; unwilling to get up
Pneumonia
Myocarditis
Acute, necrotizing myocarditis; bacteria are
in biofilm-like aggregates and adherent to venous
endothelium, with fibrin and neutrophils
Biofilm formation
* 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
Filaments, fibirn material
polysa, protein, extracelluar dNA = components of biofilm.
Virulence Properties of H. somni
* 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.
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.
Virulence factors
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
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.
Causes vasculities, enabling bacteria to penetrate host BBB ad enter blood stream.
Third image on right = cell that does produce binding protein.
Compromising Factors
* Infection with virulent, as opposed to “commensal”, isolates
* Stress
* Previous infection
Disease is due to host inflammation
Immunity to H. somni
* 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
Vaccination
* 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.
Host specificity
* 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.
Diagnosis of Haemophilus spp.
*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)
*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
Treatment
* Susceptible to most antibiotics
* Use least expensive and most appropriate drugs
* Antimicrobial resistance can occur; may need susceptibility test
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
