Veterinary Gram Negative Bacteriology

Front 1

Family of >20 genera of gram-negative rods.
• Enterics: natural habitat includes intestinal tract.
– Grow in presence of bile salts, on MacConkey agar.

Back 1

Enterobacteriaceae

Front 2

subset of enterics that ferment lactose.
– E. coli - like organisms. Includes Klebsiella and
Enterobacter species.
– Indicators of fecal pollution: potential for presence of
enteric pathogens such as Salmonella, viruses, etc.

Back 2

Coliforms

Front 3

T/F: Escherichia coli are natural inhabitants of the large and lower small intestine of all mammals, and are in larger numbers in herbivors than omnivores and carnivores

Back 3

F: E. coli are natural inhabitants of the GI tract but are more numberous in carnivores and omnivores than in herbivors

Front 4

Enteric infection: enteritis, diarrhea, scours.
– Urinary tract infection (UTI).
– Opportunistic infections: wounds, respiratory tract,
mastitis, arthritis, etc.
– Bacteremia, septicemia, septic shock (colisepticemia).

Back 4

Escherichia coli

Front 5

How are Diarrheagenic types of E. coli. classified

Back 5

Classification based on toxin production and pattern of
intestinal colonization.
– Most factors encoded by mobile genetic elements:
plasmids, phages, transposons, pathogenicity islands.

Front 6

Enterobacteriaceae
serotypes.
• O =
• H =
• K =
• F (P) =

Back 6

• O = somatic, side-chains of LPS.
• H = flagellar antigen.
• K = capsular antigen.
• F (P) = fimbria or pilus antigen.

Front 7

ETEC

Back 7

Enterotoxigenic E. coli

Front 8

EPEC

Back 8

Enteropathogenic E. coli

Front 9

STEC

Back 9

Shiga toxigenic E. coli

Front 10

EHEC

Back 10

Enterohemorrhagic E. coli

Front 11

DAEC

Back 11

Diffusely adhering E. coli

Front 12

EaggEC

Back 12

Enteroaggregative E. coli

Front 13

NTEC

Back 13

Necrotoxigenic E. coli

Front 14

EIEC

Back 14

Enteroinvasive E. coli

Front 15

Most important diarrheagenic E. coli

Back 15

Enterotoxigenic E. coli (ETEC)

Front 16

• Use fimbria as protein adhesins to colonize small
intestine, attaching to glycoproteins on cells.
– K88 (F4), K99 (F5), 987P (F6), F18, F41, etc.
• Receptors for K88 are inherited in pigs as a dominant trait.

Back 16

Enterotoxigenic E. coli (ETEC)

Front 17

How do Enterotoxigenic E. coli Enterotoxins act

Back 17

Enterotoxigenic E. coli
• Enterotoxins act
locally, attaching to
epithelium.
– Heat-labile (LT)
enterotoxin affects the
adenylate cyclase
system leading to
massive fluid
secretion.
– Heat-stable (STa and
STb) enterotoxins
cause fluid secretion in
mice and piglets.
• Fluid secretion leads to diarrhea, dehydration,
hypovolemic shock, death.

Front 18

Diarrheagenic E. coli
• Attaching and effacing E. coli
(AEEC) = EAE factor (intimin).
– Colonize small and large intestine.
– Epithelial cell degeneration,
infiltration of PMN’s.
- Rabbits pigs and dogs (not a common problem in animals/ is a problem in humans)

Back 18

Enteropathogenic E. coli (EPEC)

Front 19

• Enterohemorrhagic E. coli (EHEC)
– AEEC (EAE factor) and produces Shiga toxins 1 and 2
(Stx1 and 2) [Verotoxin].
– Toxin causes hemorrhage and edema in colon,
cytotoxic for endothelial cells.
– Natural disease in calves: nonbloody diarrhea or
hemorrhagic colitis.
– Serotypes other than O157.

Back 19

Shiga toxigenic E. coli (STEC) (Verotoxigenic)

Front 20

• Enterohemorrhagic
E. coli (EHEC)
– AEEC and produces
Shiga toxins.
– Cause nonbloody
diarrhea or
hemorrhagic colitis
in humans and
hemolytic uremic
syndrome.
– Frequently, but
irregularly shed by
cattle and other
animals.

Back 20

E. Coli O157:H7

Front 21

– F18 fimbriae-positive and produces Shiga toxin variant
2 (Stx2e).
– Toxin is absorbed; cytotoxic for endothelial cells.
– Edema disease of pigs.

Back 21

• Porcine Shiga toxigenic E. coli (STEC)

Front 22

• Attachment, epithelial
cell penetration, lysis
of endocytic vacuole,
intracellular
multiplication,
extension into adjacent
cells.

Back 22

Enteroinvasive E. coli (EIEC)

Front 23

Recent reports (2004) suggest that __% of pig
diarrhea isolates are genetic hybrid strains of
known diarrheagenic types.

Back 23

Recent reports (2004) suggest that ~20% of pig
diarrhea isolates are genetic hybrid strains of
known diarrheagenic types.

Front 24

• Reservoir: Intestinal colonization and intracellular
bacterial communities in uroepithelium.
• Specialized virulence factors:
– Adhesins: P fimbria, S fimbria, Type 1 fimbria ….
– Capsule [K-antigen, sialic acid], antiphagocytic.
– LPS: inflammatory, blocks complement activation.
– Toxins: hemolysin, cytotoxic necrotizing factor (CNF) …
– Proteases: outer membrane protease T ….
– Iron acquisition (siderophores): aerobactin,
yersiniabactin ….
– Phenotypic switch for establishment of intracellular
bacterial communities.

Back 24

Uropathogenic E. coli (UPEC)

Front 25

Septicemic E. coli infections

Back 25

• Express similar virulence factors as UPEC, except
different adhesins.
• Associated with septicemia (colisepticemia),
toxemia in coliform mastitis, endotoxemia, etc.
• Lipopolysaccharide (LPS) from the gram-negative
cell wall is known as endotoxin.

Front 26

• Approaches to diagnosis of E. coli associated
disease:

Back 26

• Approaches to diagnosis of E. coli associated
disease:
– Opportunistic infections: isolate E. coli in almost pure
culture from carefully taken samples.
• Tissue swabs, milk, urine, etc.
– Diarrheagenic E. coli identification.
• Identify toxigenic capacity of strain: usually gene probes.
• Presence of colonizing factor: serotyping or gene probes.
• Serotyping O, H, and K antigens [E. coli O157:H7 ].
– Antimicrobial susceptibility testing.

Front 27

– Gram-negative rod, coliform.
– Produces abundant capsule: mucoid colonies.

Back 27

Klebsiella pneumoniae

Front 28

– Habitat: intestinal tract of animals and humans, soil and
woodchips.
– Associated with a variety of pyogenic infections.
• Pneumonia in foals and dogs.
• Urinary tract infections in dogs.
• Coliform mastitis in cattle
• Cervicitis and metritis in mares.

Back 28

Klebsiella pneumoniae

Front 29

• Enterobacteriaceae similar to Klebsiella.

Back 29

– Enterobacter sp., Citrobacter sp., Serratia sp.

Front 30

– Gram-negative rod inhabiting the intestinal tract of
animals and the environment.
• Much more common in carnivores.
– Associated with external otitis and urinary tract
infections in dogs.

Back 30

Proteus spp.

Front 31

– Easily recognized by “swarming” on blood agar plates.

Back 31

Proteus spp.

Front 32

organisms closely related to:Proteus spp.

Back 32

– Providencia spp.
– Morganella spp.

Front 33

Enterobacteriacea Antimicrobial selections

Back 33

• Predictable susceptibility
– High frequency of R-factors = unpredictable.
– Quinolones, aminoglycosides, cephalosporins,
trimethoprim/sulfas, chloramphenicol.
• Resistance issues
– Most have a β−lactamase, either plasmid or
chromosomal.
– Frequent resistance to tetracyclines, sulfonamides.
– Innately resistant to macrolides and lincosamides.

Front 34

• Genus consists of two species, and over 2400 serotypes
based on O and H antigens.
– Arranged in serogroups: B, C1, C2, D1, E1, etc.
– Most are named as if species:
• Inhabit the intestinal tract of warm-blooded and coldblooded
animals.
– Survive for 9 months or more in fecal contaminated moist soil,
animal feeds (blood-and-bone and fish meals).
– Fecal-oral transmission via food and water; Transovarian in eggs.
• Broad range of host susceptibility to infection, with some
serotypes exhibiting host adaptation.

Back 34

Salmonella

Front 35

Describe Salmonellosis

Back 35

• Colonize distal small intestine and colon.
– Inhibited by volatile organic acids produced by normal
flora and access to attachment sites blocked.
• Disruption of flora by antibiotics, diet changes, etc. increase
susceptibility to colonization and disease.
• Some strains produce enteritis and diarrhea.
– Adhere, produce toxins, invade epithelial cells.
– May cause death and sloughing of cells leading to
abdominal discomfort and diarrhea with blood and
inflammatory debris.
• Invasion and septicemia.
– Attachment, epithelial cell penetration, survival in
phagosome, intracellular multiplication, extension into
adjacent cells.

Front 36

Salmonellosis Attachment and penetration

Back 36

Attachment, epithelial cell penetration, survival in
phagosome, intracellular multiplication, extension
into adjacent cells.

Front 37

Salmonellosis
• Invasion and septicemia

Back 37

– Attachment, epithelial cell penetration, survival in
phagosome, intracellular multiplication, extension into
adjacent cells.
– Strains with serum resistance become bacteremic.
– Multiply within macrophages of the liver and spleen and
escape destruction.
– Multiplication can lead to severe endotoxemia.

Front 38

• Salmonella Prevention and Control = Biosecurity

Back 38

• Acquired immunity (vaccines).
– Bacterins: abundant serovar specific antibodies, weak
cellular immunity, risk of LPS adverse reactions.
– Live mutant strains: oral delivery stimulates mucosal
immunity and cell-mediated activation of phagocytes.
• Potential as vaccine vectors.
• Salmonella antimicrobial selections.
– Predictable susceptibility.
• Quinolones, aminoglycosides, trimethoprim/sulfas.
– Resistance issues.
• Most carry transmissible resistance factors.
• Ampicillin, tetracyclines, chloramphenicol.
• Cephalosporins not clinically effective despite laboratory
susceptibility.

Front 39

• Endotoxemia

Back 39

• Endotoxemia, a form of septicemia.
– A clinical syndrome characterized by a systemic
physiologic response, including organ hypoperfusion
and dysfunction, mediated by endogenous modulators
whose activity may be initiated by a wide variety of
stimuli.
– Untreated, the sepsis syndrome may progress to
multiorgan failure and death.

Front 40

How does LPS cause endotoxemia?

Back 40

• LBP binds LPS,
aggregates with CD14,
interacts with TLR and
IRAK, cascading
production of
inflammatory mediators.
• LPS induces secretion
of TNF-α, IL-6, and IL-1
by monocytes.
LBP = LPS binding protein
TLR = Toll-like receptor
IRAK = IL-1 receptor-associated kinase
IRAK
Endotoxemia
• LPS receptors found on many cells, especially
macrophages.
– Prostaglandins, thromboxanes, leukotrienes, platelet
activating factor, etc.
– In addition to perfusion collapse, may also lead to
disseminated intravascular coagulation (DIC).

Front 41

Endotoxemia
• Anti-endotoxin immunization.

Back 41

– Antibodies to O-antigens do not neutralize activity.
– Antibody to core antigen neutralizes and cross protects
among various serotypes.

Front 42

Salmonella antimicrobial selections

Back 42

• Predictable susceptibility
– Quinolones, aminoglycosides, trimethoprim/sulfas.
• Resistance issues
– Most carry transmissible resistance factors.
– Ampicillin, tetracyclines, chloramphenicol.
– Cephalosporins not clinically effective despite laboratory
susceptibility.

Front 43

•What are the supected actions of Probiotics?

Back 43

– Establishment of inoculated organisms as residents.
• Scientific documentation lacking.
– Alter concentration of other members of microflora.
• Counteract disturbances.
– Interfere with adhesion by pathogens.
– Produce antimicrobial substances.
– Adjuvant-like effects on intestinal and systemic
immunity.

Front 44

Probiotic clinical results -- INCONSISTENT

Back 44

• Improved general health.
• More efficient food utilization.
• Faster growth rates.
• Increased milk and egg production.
• Reduced frequency and duration of rotavirus
infection in children.
• Prevention of enterotoxigenic diarrhea in travelers.
• Prevention of UTI in women.
• Prevention of antibiotic-associated diarrhea.
• Benefit non-breast fed children.

Front 45

Potential applications of probiotics

Back 45

• Upper respiratory tract infection.
• Prevention of dental carries.
• Lower cholesterol.
• Metabolize carcinogens and carcinogenic
enzymes.

Front 46

Are probiotics regulated drugs?

Back 46

Nutrients – not regulated drugs.
• No evidence that inoculated organisms
successfully colonize.
– Daily intake of probiotics is probably required for
maximal efficacy.
• Prebiotics
– Nutrients that stimulate growth of “probiotic-type”
microbes.
– Non-digestable by host (inulin, oligofructose), pass to
large intestinal flora.

Front 47

• Cause of plague, a rodent based zoonosis.
• Reservoir is primarily tolerant rodents (Sylvatic
plague) in endemic areas.
– Western US (>70% of US cases in NM, CO, AZ, CA).

Back 47

Yersinia pestis

Front 48

– Transmission primarily by fleas.
• Colonizes proventriculus, blocks, regurgitated by feeding flea.
– Oral acquisition by predation, cannibalism, scavenging.
– Airborne aerosols, especially from pneumonic cases.

Back 48

Yersinia pestis

Front 49

Gram negative which stains in a bipolar arrangement in blood
• Resists phagocytosis and grows in macrophages.
– Exotoxins and LPS contribute to tissue damage.
– Elicit hemorrhagic inflammatory lesions in lymph nodes.

Back 49

Yersinia pestis

Front 50

Plague
• Clinical presentations:

Back 50

Bubonic, pneumonic, septicemic.

Front 51

Plague
• Agent: Yersinia pestis
• Infective aerosol dose:

Back 51

100-500 organisms.
– 50 kg aerosol over a city of 5 million: 150,000
pneumonic plague cases, 36,000 deaths.
– Viable 1 hour in aerosol, travel up to 10 km.

Front 52

Plague Incubation period:

Back 52

2-3 days (1-6 days).

Front 53

Plague
• Clinical features:

Back 53

– Fever, cough, shortness of breath,
hemoptysis, and chest pain. Nausea,
vomiting, abdominal pain, diarrhea.
– Almost always fatal if treatment is not
initiated with 24 hours of onset of
symptoms. Deaths at 2-6 days.
– Contagious.

Front 54

Plague
• ______and ________ are very susceptible.

Back 54

Plague
• _Cats_ and _humans_ are very susceptible.

Front 55

Plague Antimicrobial selections

Back 55

– Streptomycin, gentamicin.
– Doxycycline, ciprofloxacin, chloramphenicol.

Front 56

• Gram-negative, aerobic rod.
– Motile by one or several polar flagella.
– Natural habitat is water, soil, and decaying vegetation.
– Thrives in wet, poorly aerated environments within
hospitals.
– Increased resistance to some disinfectants.

Back 56

Pseudomonas aeruginosa

Front 57

• Causes pyogenic infections.
– Wound, ear, eye, urinary and genital infections,
abscesses.
• Causes necrosis and liquefaction by hemolysins,
phosphatase, etc.

Back 57

Pseudomonas aeruginosa

Front 58

– Possess pili, facilitate adherence to epithelial cells when
fibronectin coat is disrupted.
– Can colonize deep tissue as well when exposed by
burns and trauma.
– Capsule and LPS protect against phagocytic destruction
– Produces numerous extracellular toxins and enzymes,
pyocyanin and fluorescein pigments.

Back 58

Pseudomonas aeruginosa

Front 59

• Opportunist in weakened tissues, wounds,
debilitated patients.
• Frequent contaminant in disease processes;
isolation alone is not necessarily significant.
• Unique “fruity” odor on agar and in wounds.

Back 59

Pseudomonas aeruginosa

Front 60

Pseudomonas aeruginosa Antimicrobial selections

Back 60

• Predictable susceptibility
– Aminoglycosides (amikacin > gentamicin), quinolones,
carbenicillin, third generation cephalosporins.
• Resistance issues
– β−lactams, tetracyclines, chloramphenicol, macrolides,
lincosamides can not penetrate cell wall unless present
in very high concentrations.
– Most sulfonamides not effective.
-expensive to treat
-resistance issues a big problem

Front 61

• Gram-negative, oxidase-positive rods.
• Widely distributed in fresh water, sewage, soil and
on marine animals, especially fish.
• Primarily a pathogen of fish, reptiles, amphibians.
– Septicemia, e.g. Red leg disease in frogs.
– Furunculosis in salmonid fishes.
– Necrotic stomatitis, septicemia in reptiles.
• Rarely opportunistic pathogen in terrestrial and
marine mammals.
– Implicated in cellulitis, diarrhea, septicemia, UTI,
osteomyelitis, peritonitis, otitis, endocarditis,
pneumonia.
• Hemorrhagic septicemia, motile aeromonad
septicemia, red pest, redsore, fin rot

Back 61

Aeromonas hydrophila

Front 62

Hemorrhagic septicemia, motile aeromonad
septicemia, red pest, redsore, fin rot,red leg in frogs

Back 62

Aeromonas hydrophila

Front 63

• Aerobic, small, gram-negative coccobacillus.
• Parasites of ciliated epithelium of respiratory tracts.

Back 63

Bordetella bronchiseptica

Front 64

• Common infections by B. bronchiseptica

Back 64

– Infectious tracheobronchits (canine kennel cough).
– Porcine atrophic rhinitis.
– Bronchopneumonia in many species.

Front 65

rhinotracheitis in turkeys.

Back 65

Bordetella avium

Front 66

Bordetella bronchiseptica
• Reservoir

Back 66

– Many species (dogs, swine, rabbits, rodents, guinea
pigs, cats, horses, etc.).
– Found in nasopharynx of healthy animals.
– Not considered part of normal, resident flora.
– Shedding up to 3 months or longer.

Front 67

Bordetella bronchiseptica • Transmission

Back 67

– Primarily aerosolized microdroplets, some dog-to-dog
direct spread (high density).

Front 68

Bordetella bronchiseptica
• Pathogenesis

Back 68

– Attachment to epithelium using adhesins.
• FHA, pertactin, pili.
– Bacterial proliferation and ciliostasis.
• Tracheal cytotoxin.
– Inflammation initiated by LPS, etc.
– Adenylate cyclase may interfere with phagocytosis and
intracellular killing.
• Depresses respiratory clearance mechanisms
facilitating secondary infection.

Front 69

• Canine infectious tracheobronchitis
– Tenacious mucoid to mucopurulent exudate.
– Acute, contagious respiratory infection; sudden onset,
paroxysmal cough, variable expectoration and nasoocular
discharge.

Back 69

Bordetella bronchiseptica

Front 70

Bordetella bronchiseptica Antimicrobial selections

Back 70

• Predictable susceptibility
– Quinolones, aminoglycosides, tetracyclines,
chloramphenicol, trimethoprim/sulfas.
• Resistance issues
– Innately resistant to penicillin, macrolides, lincosamides.
– Very inconsistent data regarding susceptibility to other
β−lactams.

Front 71

in many species.
– Predispose to secondary infections.
• Bacteria can persist and be shed for several
months following infection.
• Local antibody prevents colonization in dogs.
– Highly resistant following recovery from infection for 6
months.
– Parenteral and intranasal vaccines used.

Back 71

Bordetella bronchiseptica

Front 72

• Porcine atrophic rhinitis
– Dermonecrotoxin impairs osteoclast function.
– Transient and self-limiting unless combined with
toxigenic Pasteurella multocida.

Back 72

Bordetella bronchiseptica

Front 73

• Bordetellosis of turkeys (Rhinotracheitis)
– Economically significant disease.
– Coryza -- catarrhal or suppurative rhinitis, sinusitis,
tracheitis, bronchopneumonia, aerosacculitis.

Back 73

Bordetella avium

Front 74

• Aerobic, small, gram-negative rods or coccobacilli.
• Most are commensals on the mucous membranes
of the upper respirenrichment for
growth.
– Poor survival in environment.
– Spread by direct contact with carriers, colonized
animals.

Back 74

Mannheimia, Pasteurella, Actinobacillus

Front 75

• Many species; new species and taxonomic
changes are expected.
– Several biotypes and serotypes in each species.
• Biotypes: Metabolic pathways, host adaptations, etc.
• Serotypes: Capsular and LPS (O antigens) .
– Most species/biotypes have host specificity.
– Endogenous or exogenous infections.
• Carried as normal flora, opportunistic.
• Carrier animals, contagious diseases.
– Pyogenic, endotoxic diseases.

Back 75

Mannheimia, Pasteurella, Actinobacillus

Front 76

• Bronchopneumonia, shipping fever complex.
• Cattle, sheep, goats

Back 76

Mannheimia haemolytica

Front 77

Mannheimia haemolytica • Pathogenesis

Back 77

– Colonization, compromised clearance.
• Overwhelming inoculum into airways and lungs.
– Leukotoxin kills ruminant leukocytes.
– LPS stimulates inflammatory response.
• Leukotoxin neutralizing antibody response
required for resistance to disease.
• Plasmid-mediated antibiotic resistance.
• P. haemolytica biotype T (P. trehalosi)
– Septicemia in lambs.

Front 78

– Bronchopneumonia
• Nearly all species of animals (cattle, swine, cats, dogs, rabbits,
etc.)
– Atrophic rhinitis in swine.
• Severe, progressive disease.
• Type D toxigenic strains.

Back 78

Pasteurella multocida

Front 79

– Fowl cholera
• Septicemia in poultry.
– The most common pyogenic agent in cats.
– Animal bite wounds (humans and cats).

Back 79

Pasteurella multocida

Front 80

• Aerobic, gram-negative, pleomorphic rods.
• Related to Pasteurella and Haemophilus.
• Commensals on mucous membranes.
– Fastidious, requiring blood or serum enrichment for
growth.
– Poor survival in environment.
– Spread by direct contact with carriers, colonized
animals.
– More likely carried in intestinal tract than Pasteurella
and Haemophilus sp.

Back 80

Actinobacillus

Front 81

• Several biotypes and serotypes in each species.
• Most species/biotypes have host specificity.
• Endogenous or exogenous infections.
– Carried as normal flora, opportunistic.
– Carrier animals, contagious diseases.
• Pyogenic, endotoxic diseases.
• Some cause chronic pyogranulomatous lesions.

Back 81

Actinobacillus

Front 82

– Wooden tongue in cattle.
– Sporadic, chronic fibrosing granulomatous infection.

Back 82

Actinobacillus lignieresii

Front 83

– Sleepy foal disease.
– Septicemia via umbilical or placental entry.
– Also causing pneumonia, arthritis.

Back 83

Actinobacillus equuli

Front 84

– Acute, severe fibrinous pleuropneumonia in swine.
– 15 serotypes, 4 toxin types.
– Exogenous infection, contagious.

Back 84

Actinobacillus pleuropneumoniae

Front 85

Small, gram-negative rods, require growth factors.
• X-factor: iron porphyrin, hemin (chocolate blood).
• V-factor: nicotinamide adenine dinucleotide (NAD) (yeast
extract, Staph nurse colonies) - satellitism.

Back 85

Haemophilus

Front 86

• Commensals of upper digestive, respiratory and
genital tracts.
– Very limited survival in the environment off animals.
• Transmission: airborne or close contact.
– Both endogenous and exogenous infections.
• Virulence factors: capsules and LPS.
• Lesions of lungs, body cavities and joints are
serofibrinous and/or suppurative.

Back 86

Haemophilus

Front 87

• Glasser’s disease: polyserositis, polyarthritis and
meningitis.
• Acute pneumonia without polyserositis,
septicemia, DIC, acute fasciitis and myositis.
• A major cause of pig nursery mortality.

Back 87

Haemophilus parasuis

Front 88

• Commensal of nasopharynx of swine.
• VF: Capsule, fimbria, LPS, neuraminidase, et al.
• Multiple serovars: commercial and autogenous
bacterins.
• PCR diagnostic tests.

Back 88

Haemophilus parasuis

Front 89

– Infectious thromboembolic meningoencepthalitis
(TEM).
• Septicemic, vasculitis, thrombosis and infarcts in brain.
– Pneumonia, genital infections, abortion, arthritis.
– Primarily a pathogen of cattle, pyogenic in sheep.
– Bacterins: limited antigenic diversity.

Back 89

Histophilus somni (Haemophilus somnus)

Front 90

Antimicrobial selections for Mannheimia,
Pasteurella, Actinobacillus, and Haemophilus

Back 90

• Predictable susceptibility
– Penicillin/ampicillin, tetracyclines, cephalosporins
(cefitiofur), sulfonamides, quinolones, florfenicol,
tilmicosin.
• Resistance issues
– Lincosamides.
– Variable susceptibility to macrolides and
aminoglycosides.
– Food animal isolates are acquiring R-factors for
penicillin-ampicillin, tetracyclines, sulfonamides.

Front 91

• Contagious disease
• Abortion, retained placenta, orchitis, epididymitis,
infertility.
• Inapparent, chronic infection -- rarely clinical signs
outside reproductive tract in natural host

Back 91

Brucellosis (Bang’s disease)

Front 92

• Laboratory diagnosis is essential.
– Difficult to isolate, use serology for diagnosis.
• Antimicrobial treatment is unreliable.
• Zoonotic infection -- undulant fever of humans.

Back 92

Brucellosis (Bang’s disease)

Front 93

• Small, gram-negative rods.
• Slow growth, requiring 3-5 days / up to 3 weeks for isolation.
• Obligate parasites, each species has a natural
host.
– Predilection for ungulate placentas, testes of bulls,
rams, boars and dogs.

Back 93

Brucellosis (Bang’s disease)

Front 94

• Excreted in body fluids, aborted tissues.
• Remain viable, surviving off host in milk, water,
damp soil for weeks to a few months, no growth.
– Survive freeze/thaw, killed by pasteurization.
• Transmitted by direct or indirect contact with
infected excretors.

Back 94

Brucellosis (Bang’s disease)

Front 95

Brucella
• Pathogenesis

Back 95

– Route of infection primarily by ingestion; also venereal,
via conjunctiva, by inhalation, congenital.
• First week
– Entry across skin or mucosa, phagocytized and begins
intracellular multiplication in local or regional lymph
nodes.
• Second week onwards
– Intracellular localization in cells of target organs.
• Uterus, placenta, and fetus.
• Seminal vesicles, testes, epididymus.
• Parenchymous organs, mammary gland.

Front 96

Intracellular bacteria – in endoplasmic reticulum

Back 96

brucellosis

Front 97

Transmission of brucellosis in cattle -most likey methods

Back 97

Infected cow
Sources
•fetal membranes
•aborted fetus
Method of
infection:
Ingestion
Direct contact
Susceptible
animals: sexual mature cow or bull

Front 98

• Infection of the sexually mature.
– Erythritol (present in the placenta and male genital tract
of ungulates) stimulates growth.
• Persistent infection with variable bacteremia.
• Females usually abort only once, but remain
infected and shed large numbers of organism at
subsequent parturitions.
• Permanent infertility may occur in rams and male
dogs.

Back 98

Brucella

Front 99

Brucella
• Immunological responses

Back 99

– Antibody titers can be detected within 3-4 weeks postinfection
in adults.
– Elimination of infection depends upon cell-mediated
immunity.
– Presence of antibody titer does not prevent infection,
abortion or bacteremia.

Front 100

Brucella Vaccination

Back 100

• Vaccination tends to prevent abortion and
increase resistance, but does NOT prevent
infection.
• Smooth (S) and rough (R) serogroups.
– B. abortus, B. suis, B. melitensis are smooth.

Front 101

– Naturally infects cattle, bison, water buffalo resulting in
abortion.
– Aberrant infection in horses, humans, dogs, etc.
– Test and slaughter eradication program in the USA.
– Vaccination of heifers.
• Strain 19 -- live, attenuated for cattle, nontransmissible, smooth
strain, persistent infection in males and sexually mature.
• RB 51 -- live, rough strain, replacing S19 as preferred vaccine.

Back 101

Brucella abortus

Front 102

Why do you vaccinate cattle for Brucella abortus is a rough strain?

Back 102

So you do not get a false positive on blood test

Front 103

– Naturally infects goats, sheep, cattle resulting in
abortion.
– Not found in USA (?), Canada, Australia, New Zealand.

Back 103

Brucella melitensis

Front 104

– Naturally infects pigs resulting in abortion, orchitis,
arthritis, infertility.
– Also infects reindeer and caribou in the Arctic Circle.
– Test and slaughter eradication, no vaccine.

Back 104

Brucella suis

Front 105

– Naturally infects sheep causing ram epididymitis, rarely
abortion in ewes.
– Sexually transmitted, reduced fertility.
– Not known to infect other species or humans.
– Rough organism - doesn’t cross react serologically with
S strains.

Back 105

Brucella ovis

Front 106

– Dogs are the definitive host, transmission to humans is
rare (most recorded cases were laboratory accidents).
– Rapidly contagious disease among closely confined
dogs; abortion in kenneled dogs.

Back 106

Brucella canis

Front 107

– Transmission by ingestion of contaminated materials,
sometimes venereal.
– Bacteremia persists 18-24 months (6-64), no fever.
• Semen abnormalities 5 weeks post-infection; autoimmune
mechanisms, epididymitis, prostatitis, abortion.
– Localize and persist in non-reproductive tissues:
• Diskospondylitis, uveitis, meningoencephalitis.

Back 107

Brucella canis

Front 108

– Despite tissue persistence, when bacteremia is no
longer detected, serum antibody titers decrease.
– No vaccine available.
– Treatment is not practical, uncertain outcome.
– Kennels: isolate and eliminate infected dogs, serial
testing, disinfect facilities.
– Pets: minimally, neuter and treat to reduce risk of
zoonotic infection.

Back 108

Brucella canis

Front 109

Transmission of canine brucellosis- most likely methods

Back 109

Infected male dog
Sources:feces, urine
Method of
infection:Coitus
Susceptible
animals:All ages are susceptible

Front 110

Human brucellosis agents:

Back 110

Brucella melitensis, B. suis, B. abortus

Front 111

Human brucellosis
• Infective aerosol dose:
• Incubation period:
• Clinical features:
control and treatment

Back 111

Human brucellosis
• Agent: Brucella melitensis, B. suis, B. abortus
• Infective aerosol dose: 10-100 organisms
– Most infections occur by ingestion or contact with
mucosal surface, broken skin.
• Incubation period: 5-60 days (months)
• Clinical features:
– Generalized infection of the reticuloendothelial system.
– Systemic symptoms may last for weeks or months.
– Fatalities in less than 5% of untreated patients.
• Pasteurization of dairy products recommended.
• Doxycycline, trimethoprim/sufla, rifampin, aminoglycosides
(usually some combination of these).

Front 112

• Like a “hangover with a fever.”
• Profound depression.
• Orchitis – testicles swollen 4x.

Back 112

Human brucellosis

Front 113

Brucellosis issues.

Back 113

• New Brucella isolates from marine
mammals are emerging.
• Yellowstone National Park - infected
bison (20-50%).
• Elk on feeding grounds in Wyoming
(31%).
• Feral swine as potential reservoir.
• Canine brucellosis.

Front 114

• Gram-negative, microaerophilic, coccobacillus
– Fastidious, slow growing (chocolate agar, CO2).
– Exclusively a parasite in the equine genital tract.
• Contagious equine metritis (CEM)
– Limited geographic distribution: spread from Europe to
Japan, Australia and USA (KY 1978, MO 1979).

Back 114

Taylorella equigenitalis

Front 115

• Transmission: venereal and on fomites.
• Stallion: no clinical signs of infection, found on
surface of penis, in preputial smegma and in
urethral fossa
• Mare: infection limited to mucosal surfaces of
uterus, cervix and vagina.
– Copious mucopurulent uterine discharge a few days
following breeding.

Back 115

Taylorella equigenitalis

Front 116

– Temporary infertility and abortion within the first 60 days
of pregnancy.
• Mare carries organism in clitoral sinuses and fossa
for long periods.

Back 116

Taylorella equigenitalis

Front 117

• Thin, curved, gramnegative,
motile rods.
– S-shaped, seagull-shaped,
long spiral forms.

Back 117

Campylobacter

Front 118

• Difficult to isolate in laboratory.
• Commensals on the mucosa of the oral cavity and
intestinal tract; one found in genital tract of cattle.
• Little is known about pathogenic mechanisms.
– Many commensal species are nonpathogenic.
• Transmission is primarily fecal-oral route.
– Exception is venereal transmission in cattle.

Back 118

Campylobacter

Front 119

• Inhabits the intestinal tract of most species of
domestic and wild animals and birds (poultry).
– Fecal contamination of food and water.
– Survives 10 days in refrigerated foods (poultry).

Back 119

Campylobacter jejuni

Front 120

• Causes enteritis with diarrhea in humans,
occasionally dogs, cats, and many other species.
• One of the most important bacterial foodborne
pathogens of humans.
• Some strains invade mucosa, become bacteremic,
localize in pregnant uterus of sheep and goats,
leading to outbreaks of abortion in latter stages.

Back 120

Campylobacter jejuni

Front 121

hazard of healthy living; bottled water and salad vegetables as risk factors for_________ __________

Back 121

Campylobacter jejuni

Front 122

– Colonizes intestinal tract, fecal-oral transmission.
– Invades mucosa, becomes bacteremic, localizes in
pregnant uterus of sheep and goats, leading to
outbreaks of abortion in latter stages.
liver lesions

Back 122

Campylobacter fetus ssp. fetus

Front 123

– Colonizes preputial crypts of the bull and vaginal
mucosa of cows.
– Transmitted venereally.
– Causes post-breeding endometritis and infertility.
– Heifers and cows usually eliminate infection after a few
months, but bulls remain long term carriers.

Back 123

Campylobacter fetus ssp. venerealis

Front 124

________________
GIT → local invasion → enteritis
GIT → bacteremia → abortion
_____________________
GIT → bacteremia → abortion
_____________________
Repro tract → Venereal → infertility

Back 124

C. jejuni
GIT → local invasion → enteritis
GIT → bacteremia → abortion
C. fetus ssp. fetus
GIT → bacteremia → abortion
C. fetus ssp. venerealis
Repro tract → Venereal → infertility

Front 125

Antimicrobial selections Campylobacter

Back 125

• Predictable susceptibility
– Erythromycin is treatment of
choice for enteritis. Also
tetracyclines and quinolones.
– Tetracyclines may control
abortion in small ruminants.
– Aminoglycosides have been used
to eliminate venereal
campylobacters.
• Resistance issues
– Quinolone resistance emerging in
food-borne strains following use
of quinolones in poultry.

Front 126

• Helically coiled, motile, gram-negative bacteria.

Back 126

Spirochetes

Front 127

– Many tight, fine spirals, hooked end.
– 6-20 μm long, 0.1-0.2 μm diameter.

Back 127

• Leptospira

Front 128

– 6-14 regular spirals with 1 μm amplitude.
– 5-20 μm long, 0.1-0.5 μm diameter.

Back 128

• Brachyspira (Serpulina, Treponema)

Front 129

– 4-8 loose spirals with 3 μm amplitude.
– 3-20 μm long, 0.2-0.5 μm diameter.

Back 129

• Borrelia

Front 130

• Former names: Serpulina hyodysenteriae,
Treponema hyodysenteriae
Swine dysentery
• Found in the intestinal tract of pigs; convalescent
carriers can shed in feces >3 months.
– Survival in soil and environment limited to 1-2 days.
– Infection by fecal-oral route.
• Invades colonic
mucosa, causes
necrosis and erosion of
epithelium.
– Diarrhea with mucus,
blood, necrotic debris =
swine dysentery.

Back 130

Brachyspira hyodysenteriae

Front 131

Several species of Brachyspira of varying virulence.
– __________________ is strongly hemolytic and anaerobic.

Back 131

Several species of Brachyspira of varying virulence.
– B. hyodysenteriae is strongly hemolytic and anaerobic.

Front 132

• Spirochetes highly adapted to arthropod
transmission. Ticks are the main reservoir.
• Infections tend to have blood-borne phases and
can become localized and generalized.

Back 132

Borrelia

Front 133

lameness involving several
joints. (Lyme disease in humans).

Back 133

Borrelia burgdorferi
• Canine borreliosis

Front 134

• Reservoir and transmission: interaction of Bacteria, Ixodes ticks, and tick hosts: mice &
deer.
– Spirochete resides in midgut of tick.
– Stimulated by blood-meal (1-2 days feeding) to move to
salivary glands of tick.
– Injected into skin of host animal.
• Pathogenesis of lesions poorly understood.
– Considered to be immunologically mediated.

Back 134

Borrelia burgdorferi

Front 135

• Large % of seropositive dogs and horses do not
show clinical signs.
– Arthritis develops 2-5 months after tick exposure.
– PCR-negative glomerulonephritis associated with
infection in Labrador and golden retrievers.
• Tubular necrosis.

Back 135

Borrelia burgdorferi

Front 136

– Deer clear infection with no persistence
or disease.
vectored by ticks

Back 136

Borrelia burgdorferi

Front 137

antibody in midgut of tick, NOT expressed in
salivary glands or mammalian host.
– Antibody in blood meal agglutinates, immobilizes,
lyses(?) bacteria; prevents move to salivary gland.

Back 137

OspA antibody used in vaccine for Borrelia burgdorferi

Front 138

Leptospiruria

Back 138

proximal tubules

Front 139

UTI: Etiologic agents in dogs

Back 139

E. coli: 42-46
Enterococcus 11-14
St. intermedius 12
Proteus 6-12
Klebsiella 8-12
Enterobacter <5
Pseudomonas <5
• Others:
– β-Streptococcus, Mycoplasma, Providencia,
Citrobacter, Pasteurella, Candida, etc.

Front 140

UTI: Etiologic agents in dogs
Four organisms account for 75-90% of UTIs.

Back 140

E. coli
Enterococcus
St. intermedius
Proteus

Front 141

• Zoonotic, small, gram-negative rod.
– septicemia that affects >250 species of wild
– Infected rodents (beavers, muskrats).
• Transmission by surface water contamination in fall and winter.
and domestic mammals, birds, reptiles, fish, humans.
• Reservoirs in the Northern hemisphere.
– Infected lagomorphs (rabbits, hares).
• Most transmission by arthropods in summer and fall.

Back 141

Francisella tularensis

Front 142

transmitted by aerosol, direct contact, and
ingestion.
– Pneumonic form; ulceroglandular, oculoglandular,
oropharyngeal (local lesion with regional lymphadenitis)
form; septicemia.

Back 142

Francisella tularensis

Front 143

• Highly invasive, after bacteremia, localizes in
lymph nodes and parenchymous organs.
– Characteristic gross lesions in rabbits and other wild
animals are small necrotic granulomatous foci in spleen,
liver and lymph nodes.

Back 143

Francisella tularensis

Front 144

• Clinical manifestations in domestic animals:
– Septicemia in sheep.
– Cats: fever, anorexia, lymphadenopathy, oral ulcers,
hepatomegaly, icterus.
– Greater than 55% of cases in MO, AR, OK.

Back 144

Francisella tularensis

Front 145

Tularemia pneumonic form

Back 145

ulceroglandular, oculoglandular, oropharyngeal (local lesion with regional lympadenitits form; spepticemia

Front 146

Tularemia
• Requires special ________ ______ to isolate:
Consult with reference laboratory.

Back 146

enrichment media

Front 147

Tularemia treatment

Back 147

• Doxycycline, quinolones, aminoglycosides.
• Contained casualties.
– Streptomycin or Gentamicin.
– Doxycycline, Chloramphenicol, Ciprofloxacin.
• Mass casualties and prophylaxis.
– Doxycycline or Ciprofloxacin.
• Vaccine no longer available.

Front 148

• Infective aerosol dose: 10-50
organisms
– 50 kg aerosol over a city of 5 million:
250,000 incapacitating casualties, 19,000
deaths.
– Organism persists for months in moist soil.
• Incubation period: 3-5 days (1-21).
• Primary disease presentations:
– Pneumonic, ulceroglandular, ocular,
oropharyngeal, septic.

Back 148

Tularemia
• Agent: Francisella tularensis

Front 149

• Clinical features:
– Fever, prostration, pharyngitis, bronchiolitis,
pneumonitis, pleuritis, hilar lymphadenitis.
– Duration of illness up to 2 weeks, relapses weeks to
months later.
– Case-fatality rate is approximately 35% in untreated
patients.

Back 149

Tularemia
• Agent: Francisella tularensis

Front 150

• Gram-negative, short, plump, coccobacillus.
• Infectious bovine keratoconjunctivitis.
• Commonly called ‘pinkeye’ in calves.
• Also causes keratoconjunctivitis in goats and sheep.

Back 150

Moraxella bovis

Front 151

• Commensals of the conjunctiva and nasopharynx
of asymptomatic cattle.
• Very susceptible to desiccation.
• Transmission by direct contact or flying insects.
• Highly contagious.
• Risk factors implicated include UV irradiation, flies,
dust, tall vegetation, facial pigment.

Back 151

Moraxella bovis

Front 152

Moraxella bovis
• Pathogenesis

Back 152

– Pili mediate attachment to conjunctiva.
– Hemolysin, cytotoxin, LPS, collagenase, hyaluronidase.
– Invasion of conjunctiva and cornea resulting in ulcer.
– Corneal opacity and edema surround the ulcer.
– Mild epiphora and vascularization.
– Deeper ulceration may lead to increased
vascularization, and rupture leading to uveal prolapse
and panophthalmitis.

Front 153

Moraxella bovis treatment

Back 153

• Healing requires several weeks, central scarring
may persist for months.
• Susceptible to nearly all antibiotics.
• Successful immunization requires surface
immunity to block colonization and invasion.

Front 154

• Curved or spiral-shaped organisms.
• Isolated from cases of chronic gastritis
including gastric ulcers.

Back 154

Helicobacter spp.

Front 155

• Prolific producers of urease, provides alkaline
environment to colonize acidic stomach.
• Many species (> 22 named):
– Some proven as gastric pathogens.
– Some appear to be nonpathogens in stomach.
– Some associated with hepatic tumors in mice.
– Some associated with colitis in immunocompromised
humans.

Back 155

Helicobacter spp.

Front 156

Helicobacter spp. Diagnosis and treatment

Back 156

• Diagnosis: Endoscopic gastric mucosal biopsy.
• Antimicrobial treatment:
– Amoxicillin, tetracyclines, metronidazole, clarithromycin.

Front 157

Helicobacter infection in animals

Back 157

• Dogs and cats:
– Patchy colonization of gastric fundus and cardia.
– Mild to moderate mononuclear cell inflammation.
• Treatment to remove bacteria did not change histology.
– Dogs: H. bizzozeroni, H. heilmannii, H. felis, H. canis.
– Cats: H. heilmannii, H. felis

Front 158

Family:___________
• Filamentous, branching, gram-positive rods.

Back 158

Family: Actinomycetes
• Filamentous, branching, gram-positive rods.

Front 159

• Present on mucous membranes, often in oral
cavity and nasopharynx.
• Endogenous infections causing pyogenic or
pyogranulomatous reactions.
– Chronic infections, may have multiple draining tracts.

Back 159

Actinomyces spp.

Front 160

• May form ‘sulfur
granules’ in tissues
and exudate.
– Bacterial colonies
surrounded by
calcium phosphate
mineralization.
• Most are obligate anaerobes or capnophilic.
• Some produce L-forms in tissue.

Back 160

Actinomycosis

Front 161

causes lumpy jaw.
– Chronic progressive infection, principally of cattle, with
development of granulomatous, suppurative lesions
involving bone and soft tissue.

Back 161

Actinomyces bovis

Front 162

• Filamentous, branching, gram-positive rods.
– Cutaneous pyogranulomas, pyothorax, osteomyelitis.

Back 162

Actinomyces viscosus

Front 163

• Filamentous, branching, gram-positive rods.
– Cutaneous pyogranulomas, pyothorax, osteomyelitis
often associated with tissue migrating foxtail awns.

Back 163

Actinomyces hordeovulnaris

Front 164

Actinomyces AB treatment

Back 164

• Trimethoprim/sulfa, penicillin/ampicillin (not for Lforms),
tetracyclines.
– Not aminoglycosides or quinolones.

Front 165

Dermatophilus congolensis AB treatment

Back 165

• Penicillins, tetracyclines.
associated with poor hygene

Front 166

most common pyogenic agent of cattle

Back 166

Arcanobacterium pyogenes

Front 167

most common pyogenic agent in cats

Back 167

Pasteurella multocida

Front 168

AB slections for gram neg enteric pathogens

Back 168

AB that kill gram negatives but not anaerobes
Aminoglycosides Fluoroquinolones

Front 169

Infectious coryza of chickens: an acute respiratory disease of growing and laying chickens
Marked drop in egg production
Multiple serovars: limited cross-protection with vaccines

Back 169

Haemophilus paragallinarum

Front 170

Cattle respritory infections primary cause and 2nd bacteria infections

Back 170

primary cause: viral/stress
2nd bacteria infections:
1.Mannheimia haemolytica
2.Pasteurella multocida
3.Histophilus somni

Front 171

Horse respritory infections primary cause and 2nd bacteria infections

Back 171

primary cause: viral
secondary bacterial infections:
1.Actinobacillus equi
2.Streptococcus equi spp. zooepidemicus

Front 172

Canine respritory infections primary cause and 2nd bacteria infections

Back 172

Primary cause: Bordetella bronchiseptica
Secodary bacterial infections:
1.Pasteurella multocida
2.Staphylococcus intermedius
3.Beta Streptococcus

Front 173

Feline respritory infections primary cause and 2nd bacteria infections

Back 173

Primary cause: viral
sencondary bacterial infections:
1.Pasteurella multocida
2.Yersinia pestis

Front 174

cephalosporins not clinically effective despite laboratory susceptibility

Back 174

Salmonella

Front 175

Septicemia in weaned lambs

Back 175

Bieberseinia trehelosi

Front 176

Most common pyogenic agent of cats

Back 176

Pasturella mulocida type A

Front 177

Bronchopneumonia in nearly all species

Back 177

Pasturella multocida type a

Front 178

Porcine atrophic rhinitis

Back 178

bordetella bronchiseptica +/- pasturella multocida

Front 179

increases osteoclast activity while decreasing osteoblast activity

Back 179

type D Pasturella multocida

Front 180

Wooden tongue in cattle

Back 180

Actinobacillus lignieressi

Front 181

Sleepy foal disease

Back 181

Actinobacillus equuli

Front 182

Contageous pneumonia in swine

Back 182

Actinobacillus pleuropneumoniae

Front 183

Glassers disease

Back 183

Haemophilus parasuis

Front 184

Pig nursery mortality

Back 184

Haemophilus parasuis

Front 185

Polyserositis, septicemia, DIC in pigs

Back 185

Haemophilus parasuis

Front 186

Thromnoembolitic meningoencephalities of sheep and cattle

Back 186

Histophilus somni

Front 187

Tyzzers disease

Back 187

Clostridium piliforme

Front 188

Contageous foot rot in sheep

Back 188

Dichelobacter nodosus

Front 189

Scours

Back 189

E. coli

Front 190

Most important E.coli of humans

Back 190

ETEC

Front 191

Coliform mastitis in cattle

Back 191

Klebsiella pneumoniae

Front 192

UTI in dogs, mastitis in cattle, pneumonia in foals, veneral transmission

Back 192

Klebsiella pneumoniae

Front 193

Leptorspirosis hosts/spp

Back 193

Dogs: CANICOLA, Bratislava, Gippotyphosa, Icterohaemorrhagia, Pomona
Cattle: POMONA, HARDGO, Grippotyphosa
Sheep/goats: Pomona HARDJO
Horse: Pomona, Bratislava, Grippotyphossa

Front 194

Causes neccrosis and erosion of intestinal epithelium in pigs

Back 194

Brachyspira hyodysenteriae

Front 195

Blunting of microvillia, fecal oral, GIT of pigs

Back 195

Brachyspira hyodysenteriae

Front 196

Glander's disease

Back 196

Burkholderia mallei

Front 197

Furunculosis in salmon

Back 197

Aeromonas hydrophila

Front 198

Near drowning dogs

Back 198

Aeromonas hydrophila

Front 199

Septicemia in weaned lambs

Back 199

Bibersteinia trehelosi

Front 200

Glasser's disease caused by...

Back 200

Haemophilus parasuis

Front 201

Polyserositis, polyarthrisit, meningitis

Back 201

Glasser's disease from haemophilus parasuis

Front 202

Pig nursery mortality

Back 202

Haemophilus parasuis

Front 203

Obligate inhabitant of respiratory and genital mucosa of cows and sheep

Back 203

Hitophilus somni

Front 204

Acute, fatal infection in foals. Focal necrotic hepatitis in foals. Rodent reservoir

Back 204

Tyzzer's disease from Clostridium piliforme

Front 205

Biofilm on teeth, periodontal dz

Back 205

Clostridium piliforme spp. porhyromonas