veterinary gram negative bacteriology
Terms
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-
Family of >20 genera of gram-negative rods.
• Enterics: natural habitat includes intestinal tract.
– Grow in presence of bile salts, on MacConkey agar. - Enterobacteriaceae
-
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. - Coliforms
- 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. -
Enterobacteriaceae
serotypes.
⬢ O =
⬢ H =
⬢ K =
⬢ F (P) = -
⬢ O = somatic, side-chains of LPS.
⬢ H = flagellar antigen.
⬢ K = capsular antigen.
⬢ F (P) = fimbria or pilus antigen. - ETEC
- Enterotoxigenic E. coli
- EPEC
- Enteropathogenic E. coli
- STEC
- Shiga toxigenic E. coli
- EHEC
- Enterohemorrhagic E. coli
- DAEC
- Diffusely adhering E. coli
- EaggEC
- Enteroaggregative E. coli
- NTEC
- Necrotoxigenic E. coli
- EIEC
- 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
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. -
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
syndrome.
– 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,
intracellular
multiplication,
extension into adjacent
cells. - 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
disease: -
• 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. -
– Gram-negative rod, coliform.
– Produces abundant capsule: mucoid colonies. - Klebsiella pneumoniae
-
– 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 - 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
chromosomal.
– 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 - Salmonella
- 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. -
Salmonellosis
⬢ 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
susceptibility. - ⬢ 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
stimuli.
– 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
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). -
Endotoxemia
⬢ 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
susceptibility. -
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
immunity. - 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
enzymes. - 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-typeâ€
microbes.
– 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
-
Plague
⬢ Clinical presentations: - Bubonic, pneumonic, septicemic.
-
Plague
⬢ 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).
-
Plague
⬢ 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. -
Plague
⬢ ______and ________ are very susceptible. -
Plague
⬢ _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
hospitals.
– Increased resistance - Pseudomonas aeruginosa
-
• Causes pyogenic infections.
– Wound, ear, eye, urinary and genital infections,
abscesses.
• 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
discharge. - 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
β−lactams. -
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
growth.
– 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,
etc.)
– 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
growth.
– Poor survival in environment.
- Actinobacillus
-
• 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.
†- Actinobacillus
-
– 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. - Haemophilus
-
• 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 - Haemophilus
-
• Glasser’s disease: polyserositis, polyarthritis and
meningitis.
• 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
bacterins.
⬢ PCR diagnostic tests. - Haemophilus parasuis
-
– Infectious thromboembolic meningoencepthalitis
(TEM).
• 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,
tilmicosin.
• Resistance issues
– Lincosamides.
– Variable susceptibility to macrolides and
aminoglycosides.
– Food animal isolates are acquiring R-factors for
penicillin-ampicillin, tetracyclines, sulfonamides. -
⬢ Contagious disease
⬢ Abortion, retained placenta, orchitis, epididymitis,
infertility.
⬢ 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
host.
– 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)
-
Brucella
⬢ 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
nodes.
• 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
- brucellosis
- Transmission of brucellosis in cattle -most likey methods
-
Infected cow
Sources
⬢fetal membranes
⬢aborted fetus
Method of
infection:
Ingestion
Direct contact
Susceptible
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 - Brucella
-
Brucella
⬢ Immunological responses -
– 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. - Brucella Vaccination
-
• 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. -
– 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 -- 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
abortion.
– 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
infection:Coitus
Susceptible
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.â€
• 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
(31%).
⬢ 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. - Campylobacter
-
• 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 - Campylobacter
-
• 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
campylobacters.
• Resistance issues
– Quinolone resistance emerging in
food-borne strains following use
of quinolones in poultry. - ⬢ Helically coiled, motile, gram-negative bacteria.
- Spirochetes
-
– 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. - Borrelia
-
lameness involving several
joints. (Lyme disease in humans). -
Borrelia burgdorferi
⬢ Canine borreliosis -
• 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.
- 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 - Leptospirosis
- 􀂄 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
serovars.
􀂄 Overlapping antigens between different serovars.
􀂄 Diagnostic serology differentiates serogroups, not
serovars! - 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,
hypoxia.
􀂄 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
tract. - Leptospira Delayed pathogenesis
-
􀂄 Penetration and multiplication in fetus,
leading to fetal death, abortion, stillbirth or
weak offspring. -
Leptospiruria
􀂄 Development of persistent infection in lumen
of ____________ ________results in shedding for
weeks, months or years. - proximal tubules
-
LESIONS
􀂄 Vasculitis, endothelial
damage, inflammatory
infiltrates.
􀂄 Petechial hemorrhages.
􀂄 Liver, kidney, heart and
lungs.
􀂄 Uveitis. - Leptospira
- 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
disease.
􀂄 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
colonization.
• Epithelial desquamation and prompt neutrophilic
response aid in clearing bacteria from the bladder
wall.
• 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
urine. - 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
Staphylococcus.
– Transients from rectum and perineum: E.coli,
Enterococcus, Staph. intermedius, Proteus, Klebsiella,
etc.
• Hematogenous infection of the urinary tract
secondarily to bacteremia – primarily affects the
kidneys.
– 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
defects.
• 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
contamination.
• Catheterization.
– Less contamination, but also
introduces contaminants into
bladder, causes irritation and
trauma.
• Antepubic cystocentesis (bladder
tap).
– 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
Enterococcus
St. intermedius
Proteus - – 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
ingestion.
– 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
-
Tularemia
⬢ 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
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) -
Tularemia
⬢ 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 -
Tularemia
⬢ 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
mammals.
â - Bartonella
-
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
anorexia - 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,
hepatosplenomegaly,
glomerulonephritis,
pneumonia, relapsing
bacteremia, osteomyelitis,
etc. -
Causes bacillary angiomatosis in
immunocompromised patients. (proliferative vascular
lesion) - 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. -
Family:___________
⬢ 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
mineralization.
• Most are obligate anaerobes or capnophilic.
• Some produce L-forms in tissue. - Actinomycosis
-
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),
tetracyclines.
– 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
-
Calves:
New born diarrhea (0-1 wk)
E. Coli: ETEC
adhesins:___________
Toxins:_____________ -
Adhesins: F5(K99), F41
Toxins: STa -
Calves Hemorragic dysenteria (1-6 wk)
EHEC
Adhesins:_________
Toxins: _________ -
adhesins: EAE
Toxins: STx1 -
Piglets
Newborn diarrhea (0-1 wk)
Young pig diarrhea (2-4 wk)
Hemorrhagic gastroenteritis (1-8 wk)
ETEC
Adhesins:_________
Toxins:__________ -
Adhesins: F4(K88), F5(K99), F6(987P), F41
Toxins: STa, STb, LT -
Piglets:
post weaning diarrhea (4-8 wk)
ETEC
Adhesins:________
Toxins:__________ -
Adhesins: F4, F18
Toxins:STa, STb, LT -
Piglets:
post weaning diarrhea (4-8 wk)
EPEC
Adhesins:________
Toxins:__________ -
Adhesins: EAE
Toxins:? -
Piglets:
Edema disease(4-8 wk)
STEC
Adhesins:________
Toxins:__________ -
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
- Salmonella