Glossary of veterinary gram negative bacteriology

Start Studying! Add Cards ↓

Family of >20 genera of gram-negative rods.
• Enterics: natural habitat includes intestinal tract.
– Grow in presence of bile salts, on MacConkey agar.
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.
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
F: E. coli are natural inhabitants of the GI tract but are more numberous in carnivores and omnivores than in herbivors
Enteric infection: enteritis, diarrhea, scours.
– Urinary tract infection (UTI).
– Opportunistic infections: wounds, respiratory tract,
mastitis, arthritis, etc.
– Bacteremia, septicemia, septic shock (colisepticemia).
Escherichia coli
How are Diarrheagenic types of E. coli. classified
Classification based on toxin production and pattern of
intestinal colonization.
– Most factors encoded by mobile genetic elements:
plasmids, phages, transposons, pathogenicity islands.
• O =
• H =
• K =
• F (P) =
• O = somatic, side-chains of LPS.
• H = flagellar antigen.
• K = capsular antigen.
• F (P) = fimbria or pilus antigen.
Enterotoxigenic E. coli
Enteropathogenic E. coli
Shiga toxigenic E. coli
Enterohemorrhagic E. coli
Diffusely adhering E. coli
Enteroaggregative E. coli
Necrotoxigenic E. coli
Enteroinvasive E. coli
Most important diarrheagenic E. coli
Enterotoxigenic E. coli (ETEC)
• 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.
Enterotoxigenic E. coli (ETEC)
How do Enterotoxigenic E. coli Enterotoxins act
Enterotoxigenic E. coli
• Enterotoxins act
locally, attaching to
– Heat-labile (LT)
enterotoxin affects the
adenylate cyclase
system leading to
massive fluid
– Heat-stable (STa and
STb) enterotoxins
cause fluid secretion in
mice and piglets.
• Fluid secretion leads to diarrhea, dehydration,
hypovolemic shock, death.
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
Enteropathogenic E. coli (EPEC)
• 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
Shiga toxigenic E. coli (STEC) (Verotoxigenic)
• Enterohemorrhagic
E. coli (EHEC)
– AEEC and produces
Shiga toxins.
– Cause nonbloody
diarrhea or
hemorrhagic colitis
in humans and
hemolytic uremic
– Frequently, but
irregularly s
E. Coli O157:H7
– F18 fimbriae-positive and produces Shiga toxin variant
2 (Stx2e).
– Toxin is absorbed; cytotoxic for endothelial cells.
– Edema disease of pigs.
• Porcine Shiga toxigenic E. coli (STEC)
• Attachment, epithelial
cell penetration, lysis
of endocytic vacuole,
extension into adjacent
Enteroinvasive E. coli (EIEC)
Recent reports (2004) suggest that __% of pig
diarrhea isolates are genetic hybrid strains of
known diarrheagenic types.
Recent reports (2004) suggest that ~20% of pig
diarrhea isolates are genetic hybrid strains of
known diarrheagenic types.
• 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], antiphag
Uropathogenic E. coli (UPEC)
Septicemic E. coli infections
• 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.
• Approaches to diagnosis of E. coli associated
• Approaches to diagnosis of E. coli associated
– 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.
– Gram-negative rod, coliform.
– Produces abundant capsule: mucoid colonies.
Klebsiella pneumoniae
– Habitat: intestinal tract of animals and humans, soil and
– Associated with a variety of pyogenic infections.
• Pneumonia in foals and dogs.
• Urinary tract infections in dogs.
• Coliform mastitis in cattle
Klebsiella pneumoniae
• Enterobacteriaceae similar to Klebsiella.
– Enterobacter sp., Citrobacter sp., Serratia sp.
– 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.
Proteus spp.
– Easily recognized by “swarming” on blood agar plates.
Proteus spp.
organisms closely related to:Proteus spp.
– Providencia spp.
– Morganella spp.
Enterobacteriacea Antimicrobial selections
• Predictable susceptibility
– High frequency of R-factors = unpredictable.
– Quinolones, aminoglycosides, cephalosporins,
trimethoprim/sulfas, chloramphenicol.
• Resistance issues
– Most have a β−lactamase, either plasmid or
– Frequent resistance to tetracyclines, sulfonamides.
– Innately resistant to macrolides and lincosamides.
• 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 coldblood
Describe Salmonellosis
• 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.
Salmonellosis Attachment and penetration
Attachment, epithelial cell penetration, survival in
phagosome, intracellular multiplication, extension
into adjacent cells.
• Invasion and septicemia
– 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.
• Salmonella Prevention and Control = Biosecurity
• 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
• Endotoxemia
• 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
– Untreated, the sepsis syndrome may progress to
multiorgan failure and death.
How does LPS cause endotoxemia?
• 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
• LPS receptors found on many cells, especially
– Prostaglandins, thromboxanes, leukotrienes, platelet
activating factor, etc.
– In addition to perfusion collapse, may also lead to
disseminated intravascular coagulation (DIC).
• Anti-endotoxin immunization.
– Antibodies to O-antigens do not neutralize activity.
– Antibody to core antigen neutralizes and cross protects
among various serotypes.
Enteric flora
• Normal enteric microflora is a complex and diverse
population of over 400 species of bacteria.
• The majority of organisms are obligate anaerobes.
• Enterobacteriaceae organisms are present,
usually less than 1 / 1,000,000.
• Role of bacteria flora.
– Digest complex nutrients.
– Reservoir of potential enteric pathogens.
– Genetic reservoir of resistance and virulence factors.
– Immunological adjuvant to strengthen immune function.
– Provide colonization resistance against new organisms.
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
live microbial supplements that exert
a beneficial effect on health and are nonpathogenic.
• Probiotics
•What are the supected actions of Probiotics?
– 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
Probiotic clinical results -- INCONSISTENT
• 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.
Potential applications of probiotics
• Upper respiratory tract infection.
• Prevention of dental carries.
• Lower cholesterol.
• Metabolize carcinogens and carcinogenic
Are probiotics regulated drugs?
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”
– Non-digestable by host (inulin, oligofructose), pass to
large intestinal flora.
• 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).
Yersinia pestis
– Transmission primarily by fleas.
• Colonizes proventriculus, blocks, regurgitated by feeding flea.
– Oral acquisition by predation, cannibalism, scavenging.
– Airborne aerosols, especially from pneumonic cases.
Yersinia pestis
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.
Yersinia pestis
• Clinical presentations:
Bubonic, pneumonic, septicemic.
• Agent: Yersinia pestis
• Infective aerosol dose:
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.
Plague Incubation period:
2-3 days (1-6 days).
• Clinical features:
– 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.
• ______and ________ are very susceptible.
• _Cats_ and _humans_ are very susceptible.
Plague Antimicrobial selections
– Streptomycin, gentamicin.
– Doxycycline, ciprofloxacin, chloramphenicol.
• 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
– Increased resistance
Pseudomonas aeruginosa
• Causes pyogenic infections.
– Wound, ear, eye, urinary and genital infections,
• Causes necrosis and liquefaction by hemolysins,
phosphatase, etc.
Pseudomonas aeruginosa
– 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
Pseudomonas aeruginosa
• 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.
Pseudomonas aeruginosa
Pseudomonas aeruginosa Antimicrobial selections
• 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
• 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 frog
Aeromonas hydrophila
Hemorrhagic septicemia, motile aeromonad
septicemia, red pest, redsore, fin rot,red leg in frogs
Aeromonas hydrophila
• Aerobic, small, gram-negative coccobacillus.
• Parasites of ciliated epithelium of respiratory tracts.
Bordetella bronchiseptica
• Common infections by B. bronchiseptica
– Infectious tracheobronchits (canine kennel cough).
– Porcine atrophic rhinitis.
– Bronchopneumonia in many species.
rhinotracheitis in turkeys.
Bordetella avium
Bordetella bronchiseptica
• Reservoir
– 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.
Bordetella bronchiseptica • Transmission
– Primarily aerosolized microdroplets, some dog-to-dog
direct spread (high density).
Bordetella bronchiseptica
• Pathogenesis
– 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.
• Canine infectious tracheobronchitis
– Tenacious mucoid to mucopurulent exudate.
– Acute, contagious respiratory infection; sudden onset,
paroxysmal cough, variable expectoration and nasoocular
Bordetella bronchiseptica
Bordetella bronchiseptica Antimicrobial selections
• Predictable susceptibility
– Quinolones, aminoglycosides, tetracyclines,
chloramphenicol, trimethoprim/sulfas.
• Resistance issues
– Innately resistant to penicillin, macrolides, lincosamides.
– Very inconsistent data regarding susceptibility to other
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
Bordetella bronchiseptica
• Porcine atrophic rhinitis
– Dermonecrotoxin impairs osteoclast function.
– Transient and self-limiting unless combined with
toxigenic Pasteurella multocida.
Bordetella bronchiseptica
• Bordetellosis of turkeys (Rhinotracheitis)
– Economically significant disease.
– Coryza -- catarrhal or suppurative rhinitis, sinusitis,
tracheitis, bronchopneumonia, aerosacculitis.
Bordetella avium
• Aerobic, small, gram-negative rods or coccobacilli.
• Most are commensals on the mucous membranes
of the upper respirenrichment for
– Poor survival in environment.
– Spread by direct contact with carriers, colon
Mannheimia, Pasteurella, Actinobacillus
• 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) .
– Mos
Mannheimia, Pasteurella, Actinobacillus
• Bronchopneumonia, shipping fever complex.
• Cattle, sheep, goats
Mannheimia haemolytica
Mannheimia haemolytica • Pathogenesis
– 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.
– Bronchopneumonia
• Nearly all species of animals (cattle, swine, cats, dogs, rabbits,
– Atrophic rhinitis in swine.
• Severe, progressive disease.
• Type D toxigenic strains.
Pasteurella multocida
– Fowl cholera
• Septicemia in poultry.
– The most common pyogenic agent in cats.
– Animal bite wounds (humans and cats).
Pasteurella multocida
• Aerobic, gram-negative, pleomorphic rods.
• Related to Pasteurella and Haemophilus.
• Commensals on mucous membranes.
– Fastidious, requiring blood or serum enrichment for
– Poor survival in environment.
• 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.
– Wooden tongue in cattle.
– Sporadic, chronic fibrosing granulomatous infection.
Actinobacillus lignieresii
– Sleepy foal disease.
– Septicemia via umbilical or placental entry.
– Also causing pneumonia, arthritis.
Actinobacillus equuli
– Acute, severe fibrinous pleuropneumonia in swine.
– 15 serotypes, 4 toxin types.
– Exogenous infection, contagious.
Actinobacillus pleuropneumoniae
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.
• 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
• Glasser’s disease: polyserositis, polyarthritis and
• Acute pneumonia without polyserositis,
septicemia, DIC, acute fasciitis and myositis.
• A major cause of pig nursery mortality.
Haemophilus parasuis
• Commensal of nasopharynx of swine.
• VF: Capsule, fimbria, LPS, neuraminidase, et al.
• Multiple serovars: commercial and autogenous
• PCR diagnostic tests.
Haemophilus parasuis
– Infectious thromboembolic meningoencepthalitis
• Septicemic, vasculitis, thrombosis and infarcts in brain.
– Pneumonia, genital infections, abortion, arthritis.
– Primarily a pathogen of cattle, pyogenic in sheep.
Histophilus somni (Haemophilus somnus)
Antimicrobial selections for Mannheimia,
Pasteurella, Actinobacillus, and Haemophilus
• Predictable susceptibility
– Penicillin/ampicillin, tetracyclines, cephalosporins
(cefitiofur), sulfonamides, quinolones, florfenicol,
• Resistance issues
– Lincosamides.
– Variable susceptibility to macrolides and
– Food animal isolates are acquiring R-factors for
penicillin-ampicillin, tetracyclines, sulfonamides.
• Contagious disease
• Abortion, retained placenta, orchitis, epididymitis,
• Inapparent, chronic infection -- rarely clinical signs
outside reproductive tract in natural host
Brucellosis (Bang’s disease)
• Laboratory diagnosis is essential.
– Difficult to isolate, use serology for diagnosis.
• Antimicrobial treatment is unreliable.
• Zoonotic infection -- undulant fever of humans.
Brucellosis (Bang’s disease)
• Small, gram-negative rods.
• Slow growth, requiring 3-5 days / up to 3 weeks for isolation.
• Obligate parasites, each species has a natural
– Predilection for ungulate placentas, testes of bulls,
rams, boars and
Brucellosis (Bang’s disease)
• 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 indire
Brucellosis (Bang’s disease)
• Pathogenesis
– 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
• Second week onwards
– Intracellular localization in cells of target organs.
• Uterus, placenta, and fetus.
• Seminal vesicles, testes, epididymus.
• Parenchymous organs, mammary gland.
Intracellular bacteria – in endoplasmic reticulum
Transmission of brucellosis in cattle -most likey methods
Infected cow
•fetal membranes
•aborted fetus
Method of
Direct contact
animals: sexual mature cow or bull
• 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
• Immunological responses
– Antibody titers can be detected within 3-4 weeks postinfection
in adults.
– Elimination of infection depends upon cell-mediated
– Presence of antibody titer does not prevent infection,
abortion or bacteremia.
Brucella Vaccination
• Vaccination tends to prevent abortion and
increase resistance, but does NOT prevent
• Smooth (S) and rough (R) serogroups.
– B. abortus, B. suis, B. melitensis are smooth.
– Naturally infects cattle, bison, water buffalo resulting in
– Aberrant infection in horses, humans, dogs, etc.
– Test and slaughter eradication program in the USA.
– Vaccination of heifers.
• Strain 19 -- li
Brucella abortus
Why do you vaccinate cattle for Brucella abortus is a rough strain?
So you do not get a false positive on blood test
– Naturally infects goats, sheep, cattle resulting in
– Not found in USA (?), Canada, Australia, New Zealand.
Brucella melitensis
– Naturally infects pigs resulting in abortion, orchitis,
arthritis, infertility.
– Also infects reindeer and caribou in the Arctic Circle.
– Test and slaughter eradication, no vaccine.
Brucella suis
– 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
Brucella ovis
– 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.
Brucella canis
– 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, abor
Brucella canis
– 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, seri
Brucella canis
Transmission of canine brucellosis- most likely methods
Infected male dog
Sources:feces, urine
Method of
animals:All ages are susceptible
Human brucellosis agents:
Brucella melitensis, B. suis, B. abortus
Human brucellosis
• Infective aerosol dose:
• Incubation period:
• Clinical features:
control and treatment
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).
• Like a “hangover with a fever.”
• Profound depression.
• Orchitis – testicles swollen 4x.
Human brucellosis
Brucellosis issues.
• New Brucella isolates from marine
mammals are emerging.
• Yellowstone National Park - infected
bison (20-50%).
• Elk on feeding grounds in Wyoming
• Feral swine as potential reservoir.
• Canine brucellosis.
• 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: sp
Taylorella equigenitalis
• 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 v
Taylorella equigenitalis
– Temporary infertility and abortion within the first 60 days
of pregnancy.
• Mare carries organism in clitoral sinuses and fossa
for long periods.
Taylorella equigenitalis
• Thin, curved, gramnegative,
motile rods.
– S-shaped, seagull-shaped,
long spiral forms.
• 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 nonpat
• 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).
Campylobacter jejuni
• 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
Campylobacter jejuni
hazard of healthy living; bottled water and salad vegetables as risk factors for_________ __________
Campylobacter jejuni
– 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
Campylobacter fetus ssp. fetus
– 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 bu
Campylobacter fetus ssp. venerealis
GIT → local invasion → enteritis
GIT → bacteremia → abortion
GIT → bacteremia → abortion
Repro tract → Venereal → infertility
C. jejuni
GIT → local invasion → enteritis
GIT → bacteremia → abortion
C. fetus ssp. fetus
GIT → bacteremia → abortion
C. fetus ssp. venerealis
Repro tract → Venereal → infertility
Antimicrobial selections Campylobacter
• 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
• Resistance issues
– Quinolone resistance emerging in
food-borne strains following use
of quinolones in poultry.
• Helically coiled, motile, gram-negative bacteria.
– Many tight, fine spirals, hooked end.
– 6-20 μm long, 0.1-0.2 μm diameter.
• Leptospira
– 6-14 regular spirals with 1 μm amplitude.
– 5-20 μm long, 0.1-0.5 μm diameter.
• Brachyspira (Serpulina, Treponema)
– 4-8 loose spirals with 3 μm amplitude.
– 3-20 μm long, 0.2-0.5 μm diameter.
• Borrelia
• 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
Brachyspira hyodysenteriae
Several species of Brachyspira of varying virulence.
– __________________ is strongly hemolytic and anaerobic.
Several species of Brachyspira of varying virulence.
– B. hyodysenteriae is strongly hemolytic and anaerobic.
• Spirochetes highly adapted to arthropod
transmission. Ticks are the main reservoir.
• Infections tend to have blood-borne phases and
can become localized and generalized.
lameness involving several
joints. (Lyme disease in humans).
Borrelia burgdorferi
• Canine borreliosis
• Reservoir and transmission: interaction of Bacteria, Ixodes ticks, and tick hosts: mice &
– Spirochete resides in midgut of tick.
– Stimulated by blood-meal (1-2 days feeding) to move to
salivary glands of tick.
Borrelia burgdorferi
• 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.
• T
Borrelia burgdorferi
– Deer clear infection with no persistence
or disease.
vectored by ticks
Borrelia burgdorferi
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.
OspA antibody used in vaccine for Borrelia burgdorferi
􀂄 Losses in livestock:
􀂄 Abortions, stillbirths, birth of weak neonates,
animal deaths, loss of milk production, costs of
treatments, vaccines.
􀂄 Significance in companion animals:
􀂄 Animal suffering, high risk of tra
􀂄 Human leptospirosis: issues
􀂄 Medical care costs and loss of work time.
􀂄 Occupational and recreational risks.
Leptospirosis key issues of today
􀂄 Classification and nomenclature as related to
molecular diagnostics and serology.
􀂄 Unique host-pathogen relationships:
maintenance host or incidental host.
􀂄 Emergence of different serovars.
Leptospira classification
􀂄 >284 serovars of Leptospira.
􀂄 Clinically and epidemiologically distinct serovars.
􀂄 Serology used for diagnosis because they are very
difficult to isolate.
􀂄 Serovars are reported as if species.
􀂄 L. pomona, L. canicola, L. hardjo, etc.
􀂄 Serogroups (n=31) contain closely related
􀂄 Overlapping antigens between different serovars.
􀂄 Diagnostic serology differentiates serogroups, not
Leptospira Genotypic classification
􀂄 17 genomospecies, >284 serovars.
􀂄 Pathogens found in 8 genomospecies.
􀂄 Serogroups are not used in genetic classification.
􀂄 Most serovars are genetically distinguishable.
Leptospira Environmental survival
􀂄 Pathogenic leptospires do NOT multiply
outside the host.
􀂄 Survival favored by moisture, moderately
warm temperatures, stagnant waters.
􀂄 Highly susceptible to drying.
􀂄 Tolerate pH range of 6-8. Alkaline, wet soils.
􀂄 Temperature range 10-36°C.
􀂄 Outbreaks associated with flooding, rainy seasons,
run off in low lying areas, marshy fields and
muddy areas.
􀂄leptospira Invasion:
Leptospira Invasion: Entry via mucous membranes
(mouth, conjunctiva, genital tract) or small
skin abrasions.
Leptospira Pathogenesis – Acute stage
􀂄 Incubation 2-20 days.
􀂄 Leptospiremia: Survival, growth, spread
(blood, CSF, urine).
􀂄 Exponential growth, limited tissue inflammation,
endothelial damage: hemorrhage, plasma leakage,
􀂄 Hematogenous spread with localization and
proliferation in parenchymous organs (liver,
kidney, lungs, brain, genital tract).
􀂄 Leptospiremia 4-11 days.
Leptospirosis Clinical signs
􀂄 Fever, transitory anemia due to hemolysis,
iceterus, leukocytosis, hemoglobinuria,
albuminuria, etc.
􀂄 Hardjo: mastitis, abortion, infertility.
􀂄 Pomona: hemolytic disease in calves.
Leptospira Pathogenesis – Convalescence
􀂄 Production of agglutinating antibodies
coincides with clearance of leptospires from
blood and most organs.
􀂄 Leptospires remain in sequestered sites:
lumen of renal tubules, the eye, and genital
Leptospira Delayed pathogenesis
􀂄 Penetration and multiplication in fetus,
leading to fetal death, abortion, stillbirth or
weak offspring.
􀂄 Development of persistent infection in lumen
of ____________ ________results in shedding for
weeks, months or years.
proximal tubules
􀂄 Vasculitis, endothelial
damage, inflammatory
􀂄 Petechial hemorrhages.
􀂄 Liver, kidney, heart and
􀂄 Uveitis.
Leptospira Maintenance hosts
􀂄 Efficient transmission between animals.
􀂄 Direct contact with infected urine, placental
fluids or milk. Transplacental, venereal.
􀂄 High incidence (30-50%).
􀂄 Chronic, persistent infection.
􀂄 Shed for months to years in urine.
􀂄 Relatively low antibody response, not able to
eliminate carrier status.
Leptospira Incidental Hosts
􀂄 Sporadic transmission.
􀂄 Indirect contact with areas
contaminated with urine of
maintenance host.
􀂄 Low susceptibility.
􀂄 High pathogenicity, acute
􀂄 Short renal carrier phase –
few days to weeks.
􀂄 Marked antibody response.
Leptospira Emergence
􀂄 Confinement systems for swine reduce the
incidence of incidental infections from
rodents, wildlife and cattle.
􀂄 Maintenance-host infections remain a problem.
􀂄 Incidence in dogs shifting from Canicola and
Icterohemorrhagiae to Pomona,
Grippotyphosa and Bratislava.
􀂄 Increasing contact between suburban dogs and
skunks, raccoons, and opossums?
􀂄 Widespread use of vaccines?
Leptosiprosis Changing patterns
􀂄 The prevalent serovars vary by geographic
region (ecological system), and therefore
efforts to diagnose and control leptospirosis
within an area must be based on a thorough
understanding of the serovars present and
their maintenance hosts.
􀂄 Introduction of a new serovar?
􀂄 Changing host behaviors?
􀂄 Increasing recognition?
Leptosipra Laboratory diagnosis
􀂄 Direct detection of leptospires.
􀂄 Microscopic examination of urine.
􀂄 Culture.
􀂄 Antigen detection by FA, IHC.
􀂄 Serology.
􀂄 Molecular detection of nucleic acid.
Leptospirosis Antimicrobial treatment
􀂄 Predictable susceptibility
􀂄 Penicillin, quinolones, tetracyclines,
chloramphenicol, aminoglycosides, erythromycin.
􀂄 Doxycycline, penicillins, some cephalosporins.
􀂄 Rapidly reduce bacteremia and eliminate
carrier state.
􀂄 Decrease risk of transmission.
Leptospira Vaccination
􀂄 Serovar-specific vaccination generally
prevents disease.
􀂄 Does not prevent infection, may decrease
frequency or severity of infection.
􀂄 Does not prevent shedding, may decrease
duration of shedding.
􀂄 No change in shedding by carrier animal.
􀂄 Duration of immunity?
Urinary Tract Infections:natural Defenses
• Flow of urine, its direction, diluting effect, and
frequent periodic removal, discourage
• Epithelial desquamation and prompt neutrophilic
response aid in clearing bacteria from the bladder
• Urine has some antimicrobial properties:
– High osmolality.
– pH ranges may be bacteriostatic, but not bactericidal.
– Urea is bacteriostatic. Methionine, hippuric acid and
ascorbic acid produce antibacterial effects by acidifying
UTI: Routes of infection
• Ascending via the urethra. Abundance of the
common agents near the urethral orifice.
– Resident flora of external genitalia: nonspore-forming
anaerobes, α-Streptococcus, β-Streptococcus,
Mycoplasma, Haemophilus, Corynebacterium,
Propionibacterium, Lactobacillus, coag-neg
– Transients from rectum and perineum: E.coli,
Enterococcus, Staph. intermedius, Proteus, Klebsiella,
• Hematogenous infection of the urinary tract
secondarily to bacteremia – primarily affects the
– Renal cortical abscesses in neonates.
– Leptospirosis.
UTI: Etiologic agents in dogs
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.
UTI pathogenesis
• Agent factors:
– Adhesins (fimbria), hemolysins, etc.
UTI pathogenesis
• Host factors:
UTI pathogenesis
• Host factors:
– Interference with free flow of urine.
• Tumors, polyps, calculi, anatomic anomalies, and neural
• Vesico-ureteral reflux.
– Endocrine disturbances.
– Long-term use of corticosteroids.
UTI pathogensis
• Colonization of the urethral orofice, extension
along epithelial surface, inflammation (transitional
cells of bladder secrete IL-8), PMN response.
UTI: Collection of samples
• Clean midstream catch.
– Invariably leads to some
• Catheterization.
– Less contamination, but also
introduces contaminants into
bladder, causes irritation and
• Antepubic cystocentesis (bladder
– Any bacteria in sample should have
originated from bladder.
UTI: Direct Microscopic Examination
• Pyuria:
– >3 WBCs/high power field in cystocentesis samples.
– >8 WBCs/high power field in other urine samples.
• Bacteria:
– Rod-shaped bacteria may be seen in unstained
preparations when >10,000 per ml.
– Cocci are reliably detected in unstained preparations
when >100,000 per ml.
– Observation of more than 1 gram-stained organism in
every 10 oil immersion fields suggests >100,000 cfu/ml.
UTI: Etiologic agents in dogs
Four organisms account for 75-90% of UTIs.
E. coli
St. intermedius
– Minimum Inhibitory Concentration (MIC)
= the lowest
concentration of drug that visibly inhibits grow of
bacteria following 18-22 hour incubation.
– Disk-diffusion susceptibility test (K-B)
= Diameter of
zone of inhibition correlates inversely with MIC.
• 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, rep
Francisella tularensis
transmitted by aerosol, direct contact, and
– Pneumonic form; ulceroglandular, oculoglandular,
oropharyngeal (local lesion with regional lymphadenitis)
form; septicemia.
Francisella tularensis
• 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.
Francisella tularensis
• 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.
Francisella tularensis
Tularemia pneumonic form
ulceroglandular, oculoglandular, oropharyngeal (local lesion with regional lympadenitits form; spepticemia
• Requires special ________ ______ to isolate:
Consult with reference laboratory.
enrichment media
Tularemia treatment
• Doxycycline, quinolones, aminoglycosides.
• Contained casualties.
– Streptomycin or Gentamicin.
– Doxycycline, Chloramphenicol, Ciprofloxacin.
• Mass casualties and prophylaxis.
– Doxycycline or Ciprofloxacin.
• Vaccine no longer available.
• Infective aerosol dose: 10-50
– 50 kg aerosol over a city of 5 million:
250,000 incapacitating casualties, 19,000
– Organism persists for months in moist soil.
• Incubation period: 3-5 days (1-21)
• Agent: Francisella tularensis
• 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 approximatel
• Agent: Francisella tularensis
• Gram-negative, short, plump, coccobacillus.
• Infectious bovine keratoconjunctivitis.
• Commonly called ‘pinkeye’ in calves.
• Also causes keratoconjunctivitis in goats and sheep.
Moraxella bovis
• 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 ir
Moraxella bovis
Moraxella bovis
• Pathogenesis
– 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.
Moraxella bovis treatment
• 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.
• Curved or spiral-shaped organisms.
• Isolated from cases of chronic gastritis
including gastric ulcers.
Helicobacter spp.
• 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 associate
Helicobacter spp.
Helicobacter spp. Diagnosis and treatment
• Diagnosis: Endoscopic gastric mucosal biopsy.
• Antimicrobial treatment:
– Amoxicillin, tetracyclines, metronidazole, clarithromycin.
Helicobacter infection in animals
• 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
• Fastidious, gram-negative coccobacillary or
curved intraerythrocytic rods (hemotropic). Slow
growing, up to 45 days. Most identification based
on PCR assays.
– Identified in a wide range of domestic and wild
Causes cat scratch disease
(CSD) in immunocompetent humans.
• Bartonella henselae:
– Up to 40% of cats are asymptomatic, bacteremic
carriers. 4-90% of cats have antibodies.
– Transmission by cat fleas & cat contact: in flea feces.
– Fever, lethargy, lymphadenopathy, gingivitis,
neurological diseases, repro
Bartonella henselae
Cat Scratch Disease
Typical symptoms:
• Papule at inoculation
site in 3 to 10 days
• Unilateral regional
lymphadenopathy within
2 weeks
• Fever
• Malaise, headache and
Cat Scratch disease human cases/year
Cat Scratch disease
• 22,000 human cases/year
• Mostly in children
• Usually mild and selflimiting
Cat Scratch disease
• Atypical manifestations (5
to 15%):
– Oculoglandular syndrome,
encephalitis, endocarditis,
hemolytic anemia,
pneumonia, relapsing
bacteremia, osteomyelitis,
Causes bacillary angiomatosis in
immunocompromised patients. (proliferative vascular
Bartonella henselae:
Bartonella henselae:• Antimicrobial susceptibility:
• Antimicrobial susceptibility:
– Doxycycline, tetracycline, erythromycin, amoxicillinclavulanate,
or enrofloxacin can limit bacteremia but
does not cure infection in all cats.
• Filamentous, branching, gram-positive rods.
Family: Actinomycetes
• Filamentous, branching, gram-positive rods.
• Present on mucous membranes, often in oral
cavity and nasopharynx.
• Endogenous infections causing pyogenic or
pyogranulomatous reactions.
– Chronic infections, may have multiple draining tracts.
Actinomyces spp.
• May form ‘sulfur
granules’ in tissues
and exudate.
– Bacterial colonies
surrounded by
calcium phosphate
• Most are obligate anaerobes or capnophilic.
• Some produce L-forms in tissue.
causes lumpy jaw.
– Chronic progressive infection, principally of cattle, with
development of granulomatous, suppurative lesions
involving bone and soft tissue.
Actinomyces bovis
• Filamentous, branching, gram-positive rods.
– Cutaneous pyogranulomas, pyothorax, osteomyelitis.
Actinomyces viscosus
• Filamentous, branching, gram-positive rods.
– Cutaneous pyogranulomas, pyothorax, osteomyelitis
often associated with tissue migrating foxtail awns.
Actinomyces hordeovulnaris
Actinomyces AB treatment
• Trimethoprim/sulfa, penicillin/ampicillin (not for Lforms),
– Not aminoglycosides or quinolones.
– Aerobic, saprophytic soil organisms.
– Partial acidfast staining differs from Actinomyces.
– Cause suppurative and pyogranulomatous reactions in
immunosuppressed hosts or compromised tissues.
– Rarely produce sulfur granules
Nocardia spp.
– Cutaneous granulomas and pyothorax in dogs.
– Mastitis in cattle.
– Pneumonia in SCID foals.
Nocardia asteroides
Nocardia spp AB treatment
Trimethoprim/sulfas, tetracyclines.
NO pens
– Pleomorphic, beaded chains, gram-positive.
• Reside in foci of infection on carrier animals or
within scabs in environment.
• Cause superficial dermatitis with thick crusts, hair
loss in scabs.
Dermatophilus congolensis
• Affects cattle, horses, sheep, goats, etc.
• Many names
– Rain-scald, cutaneous streptothricosis, lumpy wool,
strawberry footrot
Dermatophilus congolensis
Dermatophilus congolensis AB treatment
• Penicillins, tetracyclines.
associated with poor hygene
most common pyogenic agent of horses
Sreptococcus equi spp. zooepidemicus
most common pyogenic agent of dogs
Staphylococcus intermedius
most common pyogenic agent of cattle
Arcanobacterium pyogenes
most common pyogenic agent in cats
Pasteurella multocida
AB slections for gram neg enteric pathogens
AB that kill gram negatives but not anaerobes
Aminoglycosides Fluoroquinolones
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
Haemophilus paragallinarum
New born diarrhea (0-1 wk)
E. Coli: ETEC
Adhesins: F5(K99), F41
Toxins: STa
Calves Hemorragic dysenteria (1-6 wk)
Toxins: _________
adhesins: EAE
Toxins: STx1
Newborn diarrhea (0-1 wk)
Young pig diarrhea (2-4 wk)
Hemorrhagic gastroenteritis (1-8 wk)
Adhesins: F4(K88), F5(K99), F6(987P), F41
Toxins: STa, STb, LT
post weaning diarrhea (4-8 wk)
Adhesins: F4, F18
Toxins:STa, STb, LT
post weaning diarrhea (4-8 wk)
Adhesins: EAE
Edema disease(4-8 wk)
Adhesins: F18
Toxins: STx2e
Cattle respritory infections primary cause and 2nd bacteria infections
primary cause: viral/stress
2nd bacteria infections:
1.Mannheimia haemolytica
2.Pasteurella multocida
3.Histophilus somni
Horse respritory infections primary cause and 2nd bacteria infections
primary cause: viral
secondary bacterial infections:
1.Actinobacillus equi
2.Streptococcus equi spp. zooepidemicus
Canine respritory infections primary cause and 2nd bacteria infections
Primary cause: Bordetella bronchiseptica
Secodary bacterial infections:
1.Pasteurella multocida
2.Staphylococcus intermedius
3.Beta Streptococcus
Feline respritory infections primary cause and 2nd bacteria infections
Primary cause: viral
sencondary bacterial infections:
1.Pasteurella multocida
2.Yersinia pestis
cephalosporins not clinically effective despite laboratory susceptibility

Add Cards

You must Login or Register to add cards