1 First Case Phil’s Friendly Filly: Philena Quarter horse One-year-old Owner’s complaint: Yucky yellow-green stuff running out if its nose…………. (aka nasal discharge) Not eating well Acting “sick” Philena the Philly Physical exam: Fever Nasal discharge Swelling behind the mandible: right side Tip: This is abnormal 24 hour BAP culture Some Help? Gram’s stain of exudate What’s Your Diagnosis? Diagnosis? (disease common name) A. Strangles B. Lymphadenitis C. Mastitis D. Runny nose
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Philena the Philly Some Help?people.upei.ca/bdespres/Streptococcus_PEI-10_handout-color.pdf · Staph. aureus (dbl zone) Synergistic hemolysis What’s Your Diagnosis? Mastitis Streptococcus
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First Case Phil’s Friendly Filly: Philena
Quarter horse
One-year-old
Owner’s complaint: Yucky yellow-green
stuff running out if its nose…………. (aka nasal discharge)
Not eating well
Acting “sick”
Philena the Philly
Physical exam: Fever
Nasal discharge
Swelling behind the mandible: right side
Tip: This is abnormal 24 hour BAP culture
Some Help?
Gram’s stain of exudate
What’s Your Diagnosis? Diagnosis? (disease common name)
A. Strangles
B. Lymphadenitis
C. Mastitis
D. Runny nose
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What is the cause?
A. Streptococcus suis
B. Streptococcus agalactiae
C. Streptococcus equi
D. None of the above
What is the most probable source of the infection?
A. Soil
B. Feed
C. Normal bacterial flora in the nose
D. Another infected horse
Which of the following are important to the pathogenesis?
A. M protein on Strep. equi
B. Age of the horse
C. Acute inflammatory response: PMNs
D. Localization in regional lymph nodes
E. All of the above
Source = infected horse; another foal or adult carrierExposure history, e.g.. horse showHost immunologically vulnerable; age / naïveCritical time between end of passive immunity and beginning of active immunity
Inhalation or ingestion: infection starts at tonsilsInvasion – inflammation (PMN) – dissemination S. equi factors:resists phagocytosis: M proteinkills phagocytes: leukotoxinimpairs host attempt to wall off: fibrinolysinDNAase: thin runny pus
Source = infected horse; another foal or adult carrierExposure history, e.g.. horse showHost immunologically vulnerable; age / naïveCritical time between end of passive immunity and beginning of active immunity
Inhalation or ingestion: infection starts at tonsilsInvasion – inflammation (PMN) – dissemination S. equi factors:resists phagocytosis: M proteinkills phagocytes: leukotoxinimpairs host attempt to wall off: fibrinolysinDNAase: thin runny pus
Key Elements of the Story
More Key Story Elements
Swelling = pain, abscessation = dead PMNs
Dissemination = bastard strangles
Antibiotic resistance not a problem: penicillin
To treat or not to treat………THAT is the question
Diagnosis by culture
Prevention by vaccination
Lymph node infection – more inflammation
Swelling = pain, abscessation = dead PMNs
Dissemination = bastard strangles
Antibiotic resistance not a problem: penicillin
To treat or not to treat………THAT is the question
Diagnosis by culture
Prevention by vaccination
Lymph node infection – more inflammation
Human version of the story
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What if The Foal Was Vaccinated?
Strep equi vaccine
IM
2 doses
2 weeks apart
Vaccines Sometime Fail..why?
Dratt!
Vaccines Sometime Fail..why?
D ose; too low, not often enough or inactive (dashboard)
R oute; antibodies not at site of infection
A gent wrong; by genus, species or strain (antigenic type)what else causes strangles?
A ge; too young or too old
T iming; too soon before challenge or too long ago
T ype; killed – shorter immunity, live – longer immunity
Next Case
Marvin’s MistakeI expanded my herd by 200 cows last month. Now I’ve got some serious cases of mastitis.
Millie's Mammary
Holstein
4 years-old
Ten days post-calving
One quarter hot and inflamed
Don’t you DARE touch me!
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Milk abnormal -High somatic cell count (SCC)
Clotted, stringy, cellular
Additional information
BAP at 24 hours
Gram stain
CAMP Test
Strep unknown
Staph. aureus (dbl zone)
Synergistic hemolysis
What’s Your Diagnosis?
MastitisStreptococcus agalactiae
(a Group B Streptococcus)
What was the primary source of infection?
A. Infected purchased cattle
B. Skin of the milker’s hands
C. Cow’s environment
D. Normal microflora of the udder
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Source = infected cowOBLIGATE pathogenCan be eradicated from herd
Prevention by pre-purchase testingSpreads at milking - - HYGIENEAscending infectionAcute inflammation; neutrophilsAntibiotic resistance not a problemDiagnosis: culture, cow or bulk tankCAMP test = definitive
Source = infected cowOBLIGATE pathogenCan be eradicated from herd
Prevention by pre-purchase testingSpreads at milking - - HYGIENEAscending infectionAcute inflammation; neutrophilsAntibiotic resistance not a problemDiagnosis: culture, cow or bulk tankCAMP test = definitive
Key Elements of the Story Culture, treat, and follow-up when eradicating Strep ag
1. Culture ALL cows – not just high SCC.
2. Use commercial intramammary drugs. Use aseptic good technique when treating
3. Recheck all treated cows 10 days later.
4. Cull cows that did not cure.
What is an SCC?How do you measure the SCC?What is an SCC?How do you measure the SCC?
Mastitis Measures SCC = somatic (animal) cell
count; primarily inflammatory cells (PMNs) most common measure of milk quality; farmers paid a premium for milk with lower SCC.
DHI labs –automated cell counters.
Cow-side – CMTCalifornia Mastitis Test rough estimate of SCC.
Strains of Strep. can be distinguished based on cell wall carbohydrates, known as Lancefield antigens. Commercial agglutination tests allow for rapid identification of Strep. GROUPS.
Story - continuedSuperantigen Binding Site Outside Typical Receptor
Activates only“primed” T-cells
Activation ofALL T-cells
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Flesh Eating BacteriaA well-deserved name
Summary: Strep Virulence Factorsnot all factors are present in all species or strains of Strep.
M-proteins Block phagocytosis Bind fibronectin to covers C’ binding sites Adherence to host cells
Capsule Low immunogenicity
Hyaluronic acid (like host tissue) Polysaccharide
Hydrophilic Impairs phagocytosis
Blocks complement (C’) activation by covering C’ binding sites
Other cell wall proteins Bind Fc portion of antibodies covering
Strep cell with host IgG decreasing C’binding and phagocytosis
Lipoteichoic acid Host cell binding
C5a peptidase Cleaves C5a (chemotaxin) preventing
recruitment of PMNs.
Exoenzymes Streptolysin S
β hemolysin; creates pores in cell membrane Fibrinolysin - fibrin lysis enhances spread of Strep
into deeper tissues
Hyaluronidase DNAases
Superantigens Toxic shock-like toxins
Immunomodulatory; triggers nonspecifc T cell stimulation and cytokine release serious negative affects on multiple organ systems leading to shock and death.
Leukocidin Kills leukocytes
Cell-associated Secreted
Multiple redundant virulence factors make streptococci very common and successful pathogens.
Multiple redundant virulence factors make streptococci very common and successful pathogens.
Immune-Mediated Sequelae Rheumatic fever – after Strep pharyngitis