Actinbacillus

Question 1

ACTINOBACILLUS
* Small Gram-negative coccobacillus
– filaments may occur
* Fermentative without gas
* Some species grow on MacConkey agar

Question 2

Question 3

• Colonies may be sticky
• Some species are beta-hemolytic
• Obligate parasite of mucosal surfaces
• Some are host-specific

Question 4

Question 5

Major Species and Hosts
* A. lignieresii
* A. pleuropneumoniae
* A. suis
A. equuli subsp. equuli
subsp. haemolyticus (horses only)

Question 6

Other Species and Hosts
* A. actinomycetemcomitans
– periodontal disease,
endocarditis
* A. capsulatus
– Arthritis, bacteremia
* “A. seminis”
– Epididymitis, orchitis

Question 7

Questions
* The most likely etiologic agent of this disease is:
– A. Pasteurella multocida
– B. Actinobacillus suis
– C. Actinobacillus pleuropneumoniae
– D. Streptococcus suis
– E. Haemophilus parasuis

Question 8

A. pleuropneumoniae
– absolutely specific for pigs
– Biovar 1 requires V factor (NAD; like
Haemophilus) so needs chocolate agar
for isolation
– Biovar 2 does not require NAD
– hemolytic
– >15 serotypes: 1, 5, & 7 most common in
United States

Question 9

Specific Diseases
* Swine pleuropneumonia
– fibrinous pleuritis and pneumonia
– lesions are hemorrhagic and necrotic
– infections are subclinical to acute
– chronic infections and carriers common
and spread disease to
– nonimmune herds

Question 10

Question 11

Clinical signs
– trembling, anorexia, dyspnea, fever, and
hemorrhage from nose and mouth
– animals that recover may continue to carry
bacteria and be a source of new infections

Question 12

Question 13

A. pleuropneumoniae Virulence
Properties
* Capsule
* Lipopolysaccharide (endotoxin)
– contains O side chains like enteric bacteria
* Four RTX exotoxins (lytic for red and/or white blood
cells).
– RTX toxins are directly responsible for the
hemorrhagic and necrotic lesions seen in swine
pleuropneumonia
– similar to E. coli and M. haemolytica toxins
* Adhesions (LPS and proteins)

Question 14

Question 15

Question 16

Compromising Factors
* Some serotypes are highly virulent (not all
produce the same exotoxins); compromising
factors are still needed.
* Disease is always more severe due to stress,
previous infection, and overcrowding
– disease can be controlled by management (e.g.
use closed herds, separate animals at different
production stages)

Question 17

Immunity to Ap
* Protection predominately provided by
NEUTRALIZING antibodies to RTX (repeats in
toxins) toxins
* contain C-terminally located glycine and aspartate-rich
repeat sequences of nine amino acids
– neutralize toxicity and prevents lesions
* Antibodies to capsule and somatic antigens
enhance opsonization and clearance

Question 18

Vaccination
* Current bacterins cannot induce neutralizing
antibodies to the exotoxins
– exotoxins are labile, and not stable
– Porcilis® APP is based on the outer membrane
protein (OMP) and three toxoids ApxI, ApxII and
ApxIII, collectively produced by all Actinobacillus
pleuropneumoniae strains.
* Live attenuated vaccines most effective as
long as they induce neutralizing antibodies
to toxins.
– e.g., non-encapsulated mutant was commercially available
through Boehringer-Ingelheim Vetmedica; no longer sold
– Can control this disease through management (all in all out
farm practices)

Question 19

Question 20

The agent most likely responsible for the
infection in these foals is:
– A. Actinobacillus suis
– B. Actinobacillus equuli
– C. Actinobacillus lignieresii
– D. Actinobacillus pleuropneumoniae
– E. Actinobacillus arthritidis

Question 21

A. equuli
* Two subspecies: equuli and haemolyticus
– equuli
* Resides primarily in tonsils, and intestinal and reproductive tracts of
horses and pigs
* Most important infection is sleepy foal disease (acute bacteremia), which
may become chronic resulting in purulent nephritis and arthritis
* May also infect pigs, and more rarely other animals such as dogs,
monkeys, calves, rabbits, and people
* Grows on MacConkey agar
* Nonhemolytic, but still has RTX toxin
– haemolyticus
* Infects primarily horses
* Primarily in respiratory tract
* Less common as a pathogen that equuli
* Haemolytic (RTX toxin)

Question 22

Question 23

Primary disease is foal bacteremia or “sleepy
foal disease”
* Obtained in utero or during birth
* If co-infected with Strongylus
vulgaris, aneurysms may result

Question 24

Answer 24

The larvae of S. vulgaris migrate extensively
in the cranial mesenteric artery and its
branches, where they may cause parasitic
thrombosis and arteritis.

Question 25

Question 26

Bacteremia/septicemia may result in death in 1-4
days
* Animals dying in 24 h may only present with
enteritis
* Abscesses and lesions may be present in kidneys
and joints in less acute infections

Question 27

Answer 27

Facial cellulitis
in a neonate

Question 28

Question 29

A. equuli in pigs
* Can Vet J. v.51(11); Nov 2010
* Death of over 300 sows in 2 months on a 3000 sow
farrow-to-wean operation in Manitoba
* In addition 1- to 4-day-old piglets from rooms that had
been populated by sows affected by A. equuli suffered
pyrexia, arthritis, and mortality.

Question 30

Diseases caused by A. equuli subsp.
haemolyticus
– Adult horses primarily (probably associated
with stress), but can cause sleepy foal disease
* abortion, stillborn fetus, metritis, mastitis,
meningitis, respiratory disease, wound infections,
bacteremia, arthritis, endocarditis, and inflamed
wounds
* These and other species have been
isolated from human wounds
following horse bites

Question 31

Virulence Properties
* LPS (endotoxin)
* Adherence factors
* RTX toxin (weak)

Question 32

Compromising Factors
* Mare carrying A. equuli in genital tract prior to
delivery
* stress, infection, climate
– parasitism (S. vulgaris), overtraining, exposure to
bad weather

Question 33

Immunity to A. equuli
* Vaccination of mares should provide passive
immunity to foals, but not commercially
available
* Greater attention to sanitation in the birthing
environment can reduce infection; maternal
antibodies in colostrum are often protective
* Prebreeding culture screening may be more
effective at prevention
* Attempts at passive immunity with antiserum
have not worked

Question 34

Antibiotic Treatment
* Chloramphenicol, gentamicin, or third-
generation cephalosporins
* β-Lactam antibiotics and sulfonamides have
been recommended, but widespread
resistance to both antibiotics has been
reported.

Question 35

Question 36

This disease is commonly called:
– A. Wooden tongue
– B. Actinobacillosis
– C. Stemy silage disease
– D. A and B
– E. B and C

Question 37

A. lignieresii
* Predominately in cattle and sheep, but may
cause infections in other species, even
humans
– Commensal of oral cavity
– Requires serum or blood + CO2 for initial isolation

Question 38

Actinobacillosis or “wooden tongue”
– tumor-like lesions of tongue and oral cavity that
ulcerate (except tongue)
* Lesions occur following trauma
* Bacteria may spread to internal organs and to skin
following ulceration

Question 39

Answer 39

Actinobacillosis or “wooden tongue”

Question 40

Answer 40

Actinobacillosis or “wooden tongue”

Question 41

Infection may become chronic and form
granules
* Lesions with granules appear similar to those
caused by Actinomyces bovis, but smaller

Question 42

Answer 42

granules

Question 43

Question 44

Granuloma formation
“A granuloma is a compact (organized) collection of
mature mononuclear phagocytes (macrophages and/
or epithelioid cells), which may or may not be accom-
panied by accessory features such as necrosis or the
infiltration of other inflammatory leukocytes”
(Adams DO)

Question 45

Question 46

Question 47

Question 48

Virulence Factors
* Lipopolysaccharide
* RTX exotoxin (weak)
* Capable of disseminating
* RESISTANCE TO HOST DEFENSES (Results in
induction of chronic, granulomatous
inflammation)

Question 49

Compromising Factors
* Invades tissues following wounds or trauma
– Part of normal flora
– Self-inoculation of buccal epithelium by foreign
material

Question 50

Immunity to A. lignieresii
* granulomatous reaction is characteristic of
chronic inflammatory response
* cellular immunity is most important
(predominately a Th1 response)
* antibodies are made, but role in resistance is
unclear?

Question 51

Vaccination
* Based on the host immune response, a live
vaccine would be expected to be optimal, but
none are commercially available
* A bacterin has been used experimentally
during an outbreak that reduced relapses and
prevented new cases
* Disease is sporadic; can be prevented by good
management

Question 52

Treatment
* A. lignieresii
– Sodium/potassium iodide IV (70 mg/kg of
10-20% solution) or in local lesions
effectively stop the acute signs of the
disease within two days-discouraged if
going to slaughter
– Antibiotics-streptomycin is considered the
treatment of choice, tetracyclines and
tilmicosin are also effective
– Prevent feeding of coarse feedstuffs

Question 53

A. suis
* Primarily resides on swine mucosal surfaces
– will grow on McConkey agar
* sticky and adherent
– hemolytic

Question 54

Diseases caused by A. suis
– Most important infection is bacteremia in piglets
1-8 weeks old
– Endocarditis, pericarditis, edema, and petechiae
throughout organs may occur
– Febrile, respiratory distress,
neurologic symptoms, death

Question 55

Question 56

Question 57

Question 58

In older pigs, lesions are more localized (e.g.
arthritis, pneumonia, and abscesses)
– Infections in older pigs are associated with
stress
* Source of infection is likely the upper respiratory
tract, with dissemination resulting in vascular
hemorrhage and necrosis

Question 59

Virulence Properties of A. suis
* RTX toxin
– cross-reactive with RTX toxins of A.
pleuropneumoniae
* Capsule
* LPS
* Adhesions

Question 60

Transmission and Compromising Factors
* Transmission
– The bacteria are carried in the respiratory tract
and tonsils of healthy and infected pigs
– Transmission is via the respiratory tract when pigs
are very young
* In older animals, stress and previous infection
predispose them to infection

Question 61

Immunity
* Passive protection of piglets from colostrum
* Antibodies to RTX toxins

Question 62

Vaccination and treatment
* Use of vaccines not common
* Live, attenuated vaccines should work best
(immunize sows?), but are not available
* Ceftiofur, gentamycin, and
trimethoprim/sulfadiazine are effective in
treating the disease if diagnosis is made early
enough
* confirm with susceptibility test

Question 63

Diagnosis
* Any of these organisms need to be isolated in pure
culture or predominance because they can be
normal flora
* A. pleuropneumoniae
– Most require V factor for growth
– chocolate agar, or blood and staph streak required
* A. lignieresii
– requires blood and CO 2 for growth
– granules may be present
* A. equuli and A. suis
– can also isolate on MacConkey agar

Question 64

SUMMARY-clinical diseases
* A. lignieresii
– wooden tongue – granulomatous lesions, granules
* A. pleuropneumoniae
– pleuropneumonia – hemorrhagic lesions
* A. suis
– swine neonatal septicemia; petechiae and edema;
pneumonia in adults
* A. equuli
– foal septicemia; aneurysms, systemic infections