Test 1 Flashcards

1
Q

DNA sequence analysis of this structure is widely used in bacterial phylogenetic analysis.

A

Ribosome

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2
Q

Which one of the following is a cell wall component unique to bacteria?

A

Peptidoglycan

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3
Q

Bacteria

A

Prokaryotes (No nucleus) • Complex cell wall • No sterol • Membrane bound organelles are absent • A single circular chromosome (exceptions ?) and no histones • Ribosomes (smaller) 70s • No cytoskeleton • Asexual reproduction (binary fission)

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4
Q

Gram Postive Bacteria

A

Thick peptidoglycan

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5
Q

Gram negative bacteria

A

outer membrane, which contains lipopolysacciride - has a Lipid A(endotoxin) component

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6
Q

Mycobacteria

A

has mycolic acid in the membrane, which is why it stains positive in the acid-fast stain

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7
Q

Gram Staining

A

-based on peptioglycan thickness • Crystal violet- Primary stain • Gram’s Iodine- Mordant • Decoloriser-Acid Alcohol • Safranin-Counter stain • Gram Positive stain violet/blue( retains Crystal violet) • Gram negative stains Pink(safranin)

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8
Q

What is the cause of many clincial signs of Gram negative bacteria?

A

Lipid A or endotoxin( a component of the cell wall) Endotoxin binds to macrophage receptors and stimulates an inflammotory cascade

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9
Q

Test for Endotoxin

A

Limulus Amebocyte Lysate(LAL); everything has to be checked for endotoxin

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10
Q

Which are the bacteria that does not contain peptidoglycan

A

Mycoplasmia and Chlomydia

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11
Q

Flagella

A

Locomotion / Motility Number and arrangement can be used for identification

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12
Q

Endoflagella

A

Flagella inside the cell Endoflagella /axial filaments in the periplasmic space eg. spirochetes

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13
Q

Pili/ fimbriae

A

• Pili/ fimbriae: Small thread like structures • Facilitate adherence to the host tissue • Contribute to antigenicity Eg: Bordetella bronchiseptica, E.coli

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14
Q

K88

A

Neonatal piglets-Fimbrial antigens in E.coli

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15
Q

K99

A

Neonatal calves-Fimbrial antigens in E.coli

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16
Q

Capsule

A

Polysaccharide outer coating of the bacteria - Helps organisms to evade phagocytosis

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17
Q

Which bacterial species has a non-polysaccharide capsule?

A

Bacillus anthracis, thus staining for this capsule is how we ID this bacteria

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18
Q

Endospores

A

Produced when essential nutrients are depleted in a bacteria - or under BAD conditions as the spores are very virulent to poor conditions Organic acid called Dipicolinic acid protects the endospore from damage Eg: Clostridium, Bacillus THESE AID IN BACTERIAL SURVIVAL

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19
Q

aerobic, microaerophilic, capnophilic

A

Oxygen required for growth

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20
Q

obligate anaerobe, aerotolerant anaerobe

A

Oxygen not required or utilized for growth

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21
Q

facultative anaerobe

A

Oxygen not required but can be utilized for growth

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22
Q

Bacterial Virulence Factors

A

properties or traits found in isolates that cause disease but which are not found in isolates of the same species that lack ability to cause disease

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23
Q

Damage caused by bacteria

A

Damage caused by bacteria Using the host’s nutrients Direct damage to the host cell (Toxins) Hypersensitivity reactions (Type IV Hypersensitivity- Tuberculosis)

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24
Q

Pathogenicity

A

Pathogenicity is the ability of a pathogen to produce a disease by overcoming the defense mechanisms of the host.

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25
Virulence
the degree of pathogenicity
26
Exotoxins
released from the cell; made in the cell
27
3 types of Endotoxins
1. A-B toxins 2. Membrane disrupting toxins (Leukocidins kill white blood cells (phagocytes), Hemolysins destroy erythrocytes) 3. Superantigens
28
A-B Toxins
Most exotoxins(i.e. tetanus) are A-B toxin • A-B toxins consist of two polypeptides. • The A polypeptide is the active enzyme and the B polypeptide is a binding component • B binds to the cell, the complete toxin is taken into the cell, the two subunits separate, and the A subunit enzymatically kills the cell.
29
What are superantigens?
Cause non-specific activation of T-cells • result in polyclonal T cell activation and massive cytokine release. • Produced by pathogenic microbes (including viruses, mycoplasma, and bacteria) • Indiscriminate binding to MHC class II molecule on the antigen presenting cell and and T helper cell receptor • 1/1000(Superantigens) vs. 1/5 cells by an antigen • Nausea, vomiting, fever\> shock
30
Example of a superantigen
Toxic shock syndrome in humans is caused by a superantigen
31
Main source of virulence factors in bacteria
Plasmids are smaller circular DNA present in Bacteria Bacteriophages are virus particles which attack Plasmids and bacteriophages may carry genes for antibiotic resistance, toxins, capsules and fimbriae and can mediate transfer. Plasmid genes; Tetanus neurotoxin Staphylococcus enterotoxin(superantigens) Bacteriophage genes; Corynebacterium diphtheria (Diphtheria toxin), Clostridium botulinum (Botulinum toxin), E. coli O157 H7( Shiga toxin)
32
Conjugation
is the process by which one bacterium( Bacterium with a fertility factor) transfers genetic material to another through direct contact.
33
Transformation
is the genetic alteration of a cell resulting from the direct uptake and incorporation of exogenous genetic material from its surroundings and taken up through the cell membrane(s)
34
Transduction
is the process by which DNA is transferred from one bacterium to another by a virus
35
Biofilm
virulence factor Microbes come together in masses cling to surfaces, produce extracellular substances and take in nutrients and forms a biofilm Eg. Dental Plaque Pseudomonas aeruginosa biofilms in cystic fibrosis patients
36
Quorum sensing
1. the bacteria appear relatively innocuous as they quietly grow in number 2. When their population reaches a certain level, instant changes occur in their behavior, appearance, and metabolism. 3. These changes culminate in an infection that can ambush and overwhelm our immune system defenses.
37
Opportunistic pathogens
organisms those do not cause disease in a healthy host, with a healthy immune system
38
True pathogens
equipped with virulence genes for adherence, invasion, evasion from the immune system and toxins
39
Nosocomial Infections
Hospital acquired infections Eg. Methicillin resistant Staphylococcus aureus Clostridium difficile
40
Generally bacteria are
extracellular pathogens
41
Obligate intracellular pathogen
Eg. Rickettsia, Chlamydia
42
Facultative intracellular pathogen
(can survive extracellular or intracellular) Eg. Mycobacterium
43
Cell wall component unique to gram negative bacteria
lipopolysaccharide
44
Gram positive staining in some bacteria is due to the presence of a:
Thick Peptiodoglycan
45
Acid fast staining in Mycobacteria is due to the presence of:
Mycolic Acid
46
Gram positive bacteria retains the color of the primary stain and Gram negative bacteria picks up the color of the counterstain. T/F
TRUE
47
Which one of the following process is a least likely virulence mechanism in a bacteria? a. bacterial movement using flagella b.bacterial attachment using fimbriae c. biofilm production and attachement to surfaces d. bacterial protein production by ribosomes
Bacterial protein production by ribosomes
48
Translation
Production of protein
49
DNA sequence coding. Which of these organelles is used for bacterial phylogentic analystis?
Ribosomes
50
Is mitochondria present in bacteria?
NOPE
51
What are antimicrobials?
Drugs that destroy microbes, prevent their multiplication or growth or prevent their pathogenic effect • Differ in their physical, chemical and pharmacological properties • Differ in their antibacterial spectrum of activity • Differ in their mechanism THESE DO HAVE TO KILL THE MICROBE, THEY CAN JUST PREVENT ITS GROWTH
52
• When do you use antimicrobials?
When the patient have a treatable microbial infection
53
Antimicrobial vs antibotic
Antibotics- produced by living organism, Antimicobrial is a broader term
54
What should you know to proceed with treatment with antimicrobials?
location of the infections, likely pathogens involved, which antimicrobials are likely effective against a particular pathogen at a particular site
55
What are the other factors to consider in antimicrobial therapy?
Cost, (type, dose and duration), safety, ease of use, and possible emergence of resistance
56
Antibiotic
chemical substance produced by a microorganism that inhibits the growth of or kills other microorganisms.
57
Antimicrobial agent
a chemical substance derived from a biological source or produced by chemical synthesis that kills or inhibits the growth of microorganisms.
58
Natural (true antibiotics)
produced by bacteria or fungus (Streptomycin, penicillin, tetracycline)
59
Semi-synthetic
chemically-altered natural compound (ampicillin, amikacin)
60
Synthetic
chemically designed in the lab (sulfonamide, enrofloxacin, marbofloxacin)
61
Classification of Antimicrobial agents
A. Chemicalfamilystructure B. Mode of action C. Type of antimicrobial activity D. Spectrum of antibacterial activity
62
What do you need to know to treat with antimicrobial agents?
•Know the drugs •Know the microbiology •Know the patient
63
Mode of action of antimicrobial
inhibitors of cell wall synthesis inhibitors of protein synthesis inhibitors of membrane function inhibitors of nucleic acid synthesis (anti-metabolites)
64
Antibacterial Susceptibility Testing
Done to figure out which antimicrbioals are the best to treat certain infections
65
2 types of Antibacterial Suscpetibility Testing
1. Dilution (broth/agar) 2. Diffusion (disk)- aka Kirby Bauer Test
66
What is a Susceptibility break point?
A drug concentration above which an organism is considered resistant and at or below this value organism is susceptible to that drug. Three Break point values are set at Susceptible, Intermediate, or Resistant IMPORTANT FOR LABS DOING THIS TEST
67
What is Minimum inhibitory concentration (MIC)?
Minimum amount of drug required to inhibit bacterial growth Drugs with lower MIC values are better choices
68
Disk Diffusion
Disk Diffusion (‘Kirby Bauer’) * Must use a bacterial isolate in pure culture * Standardized bacterial inoculum spread on an agar plate * Single-concentration antimicrobial disks are used * Growth inhibition zone diameter measured * Published reference breakpoints (zone size) to interpret results * Different drugs will have different zone sizes based on the published data
69
Broth Dilution
• multiple dilutions of antimicrobial agents (usually 2-fold serial dilutions) Use published reference breakpoints to interpret • Measure AND report growth inhibition endpoint (MIC) (MIC reported in micrograms per milliliter)
70
You always want to keep a dose (below or above) the MIC in the body?
above MIC in the body
71
Gradient diffusion test - E-Test
Measures MIC
72
Bactericidal
kills
73
Bacteriostatic
inhibits
74
Broad spectrum antibiotic
active against a wide variety of bacteria Eg. Tetracycline
75
Narrow spectrum antibiotic
affect only a narrow range of bacteria Eg. Penicillin
76
When do you use antimicrobial combinations?
* Mixed infections * Prevention of antimicrobial resistance * To increase effectiveness in treating some infections Synergistic ( sequential action at different sites, enhanced uptake- beta lactam and aminoglycosides, interference with resistance mechanism, Drugs metabolized to active metabolites (Enrofloxcin to Ciprofloxacin)
77
Innate resistance
preexisting genomic property i.e. Mycoplasa does not have a cell wall, Therefore, you can't use beta lactones
78
Acquired resistance
new genetically encoded trait not representative of the species (acquired by mutation or horizontal gene transfer) Processes that bacteria can aquire virulence factors: -conjugation
79
Mechanisms of Resistance
* Enzymatic destruction or inactivation of drug * Prevention of penetration to target sites within microbe * Alteration of drugs target site * Rapid efflux of antibiotics
80
Strategies to Reduce Antimicrobial Resistance
• Prudent drug use - maximize efficacy of therapeutic regimens - restrict extra-label use to high risk patients - observe withdrawal period - use antimicrobials of limited human health concern - use alternative therapies • Pathogen control - animal waste management - reduce contamination in slaughter and processing - maintain herd health and infection control • Policy - control of drug use in food animals - national antimicrobial resistance monitoring system - educational efforts
81
What antimicrobial should you NOT use?
Vancomycin Vancomycin resistant Enterococcus (VRE)
82
Antimicrobials are used in agriculture for?
Growth Promotion
83
What is one of the main problems with use of antimicrobials in vet med?
Extra Label Use
84
Which will be the least likely scientific factor to be considered regarding antimicrobial therapy? A. know the drugs B. know the microbes C. Know the pt D. Know the Client
D. Know the Client
85
T/F In general drugs with lower MIC values are better choices for treatment.
TRUE; because you can use a lower dose, but remember that MIC is not the only factor(microbe, site of infection etc)
86
Pure Culture of a bacteria is critical for obtaining accurate antimicrobial susceptibility pattern T/F
True- you MUST have a pure culture
87
Which of the following statements is incorrect? A. MIC is the lowest concentration of antimicrobial agent which can inhibit the growth of bacteria B. Published break points are required for interpretation of AST results C. MIC can be measured in E-test D. MIC can be accurately measured in Disk Diffusion test(Kirby Bauer test)
D. Kirby Bauer DOES NOT measured MIC accurately
88
Methods for IDing the agent
1. Direct detection of the agent (simple/ differential staining, antibody staining) 2. Isolation and identification 3. Direct detection of antigens, toxins (Immunology techniques such as ELISA0 4. Nucleic acid detection(PCR)
89
2. Identification of the host immune response
Antibodies(Eg,Brucella infection), Cell mediated immune response(eg.TB)---- very rare and only available for certain conditions
90
Ideal test has
Ideal test has high sensitivity and high specificity
91
Sensitivity
percentage of true positives in a sample population that are correctly identified as positive by a test.
92
Specificity
percentage of true negatives in a sample population that are correctly identified as negative by a test.
93
Positive predictive value
percentage of all positive test results that are true positives.
94
Negative predictive value
percentage of all negative test results that are true negatives.
95
Predictive values associated with individual test results vary
Predictive values associated with individual test results vary with disease prevalence
96
In a high prevalence herd, you will have a
more accurate results.
97
Specimen collection
* Collect from actual site of infection * Minimise contamination * Collect early in the stage of disease process * Use appropriate transportation * Collect before the initiation of antimicrobial therapy
98
Can you submit a swab for a bx?
better to submit the material itself
99
What happens if you submit a fecal sample in a serum tube?
the bacteria will produce lots gas
100
Gram Staining
Gram Positive Purple(Crystal violet) Eg: Streptococcus pyogenes Stapylococcus aureus Gram Negative- Pink (Safranin) Escherichia coli Pasteurella multocida Gram stain -Gram Positive = Thick Peptidoglycan
101
Acid Fast Staining (Kinyon’s stain)
Acid fast positive organism stains: Pink Acid fast negative organism stains: Blue Acid fast stain –Acid fast + =mycolic acid
102
Largest Problem with direct staining
Sensitivity is very poor ## Footnote Blood • CSF • Mycoplsama, spirochetes( can not be stained)
103
Urine
Collection, • Cystocentesis preferred over catheterization • Urethral contamination occurs in free catch and catheterized samples • \<105/ml- probable contamination( • Gram staining(2 bacteria/ oil immersion) • Capped syringe, sterile container • Refrigerate if cannot be cultured if cannot be cultured immediatly • May use Urine preservation tubes
104
Transudates and exudates
* Syringe * Remove air * Anaerobic transport medium •Lavages or washes use a buffered solution •Saline vs. lactated ringer’s solution
105
Feces
* 2-3 gms * Leak proof container * Repeated culture needed in shedding/chronic infections
106
Blood
* Several specimens over a period of time, onset of fever, * 3- 4 in first 1.5 -3 hours
107
Tissue samples
* Portion of a tissue * Multiple specimens * Collect first during necropsy * Sealed leak proof container * Refrigerate if delivery delayed
108
Interpretation
Normal flora Vs. Pathogens Correlate with clinical signs and the organism Quantitation- light, moderate, heavy (Isolation of four or more organism; Most likely contamination)
109
False negative results
May be due to sampling, transport, storage issues, antimicrobial therapy, Fastidious organisms or when specific procedures needed Consult with clinical microbiologist
110
The most dangerous pathogens are classified as
BSL-4
111
Principle of Secondary Containment
transport in secondary container that is leakproof, puncture proof and contains liquid absorbent
112
Rare bacteria are
Gram Negative cocci
113
Polymerase Chain Reaction
• Non culture based from clinical samples • For identification of isolates. * Conventional PCR * Real Time PCR * What is the limitation for PCR identification? You have to know what you are dealing with
114
Antigen detection
(EIA, agglutination, FA, etc.) | (tests use antibody reagents to detect antigens in serum, feces, urine, tissue.)
115
Chemical detection
(HPLC, GLC, MALDI-TOF- MS) (analysis of total cell fatty acids/proteins; limited use on clinical specimens)
116
Biological detection
(Limulus amoebocyte assay) (test for LPS, adapted from clotting mechanism of horseshoe crab)
117
Detection of Specific Immune Response to a bacteria or fungus
• Humoral (antibody) Response Eg: Agglutination, precipitation, ELISA • Cell mediated immune response Eg: Tuberculin reaction, Interferon gamma test Generation of an immune response requires time and immune response may persist
118
False positives for immune tests can mean
prior antigen exposure, vaccination, cross-reactions
119
False negatives for immune tests can mean...
anergy, immunosuppression
120
Beta Lactam(b-Lactam) antimicrobials
All have a b-Lactam Ring Members of the group Penicillins,( Ampicillin, Amoxicillin, Ticarcillin) Cephalosporins(1st, 2nd,3rd, 4th Generations) Carbapenems (Imipenem) Monobactams (Aztreonam) Mechanism of action Inhibit Cell wall synthesis(transpeptidation step) in the peptidoglycan synthesis, Stimulate autolysins which degrade peptidoglycan b-Lactam antimicrobials differ in their spectrum of activities Some are effective against both Gram Negatives and Gram positives Some are effective against only Gram Negatives than Gram positives or vice versa Vary in their absorption, toxicity, and their ability to penetrate tissues or blood brain barrier Bactericidal antimicrobials- KILL THE BACTERIA Excretion through kidneys Time Dependant killing- you have to have a concentration over a period of time
121
Mechanism of action of Beta Lactam antimicrobials
Mechanism of action Inhibit Cell wall synthesis(transpeptidation step) in the peptidoglycan synthesis, Stimulate autolysins which degrade peptidoglycan
122
Resistance mechanisms of b-Lactamase
Resistance mechanisms; • b-Lactamase(enzyme which cleaves b lactam ring) production • Extended Spectrum b lactamase • Alteration in penicillin binding proteins
123
cell wall synthesis inhibitors
* Glycopeptides(Vancomycin, daptomycin) * Last resort antimicrobial in S. aureus, and Enterococcus • Fosfomycin, bacitracin
124
Gram positive cocci
Staphylococcus Streptococcus Enterococcus Micrococcus
125
Staphylococcus
Facultative anaerobic catalase positive cocci Exceptions: Anaerobic species;S.sacharolyticus, S.aureus subsp.anaerobius Classic opportunistic pathogens Natural habitat is skin and mucous membranes May be a part of resident or transient flora
126
Staph in a dog is is almost always...
S. pseudintermedius
127
What is Coagulase?
Enzyme which Convert fibrinogen to Fibrin
128
Staph causes
Suppurative conditions • Superficial: skin and soft tissue infections pyoderma, folliculitis, furunculosis, wound infections • Deep infections Abscess, cellulitis, mastitis, pyomyositis, Necrotizing fasciitis and myositis * Infections of other body systems * Empyema, osteomyelitis, arthritis, endocarditis, pneumonia,otitis,sinusitis, meningitis • Invasive bacteremia
129
pyogranulomatous
Chronic persistent relapsing infections in staph infections
130
Toxin Mediated Diseases from Staph
* Toxin mediated diseases: * Staphylococcal toxic shock syndrome(TSST-1) * Staphylococcal food poisoning(Staphylococcal enterotoxin) •Staphylococcal scalded skin syndrome (Exfoliative toxins) All of these are superantigens!
131
Superantigen
Causes indiscriminate binding to MHC Class II receptor and releasing lots of cytokines and T cells
132
Virulence factors of Staph
* Protein A: Bind to FC portion of IgG- prevents phagocytosis * Hemolysins: lyse RBC and other body cells * Proteases: Destroy tissues * Hyaluronidase: destroy connective tissue * Lipases * Alpha toxins: membrane damaging toxin * Leukocidin (role in necrotizing fasciitis and pneumonia in dogs) * Exfoliative toxins * Biofilm formation
133
Staph in Dogs
Wound infections, surgical site infections, septic arthritis, osteomyelitis, Urinary tract infections, endocarditis, peritonitis, ocular infections, ear infections * Necrotizing fasciitis and necrotizing pneumonia * Bacterial folliculitis and furunculosis
134
Why do dogs get staph so easily?
“Epidermal barriers are less well developed” ??? Thin stratum corneum Lack of Follicular Plug
135
Diagnosis of Staph
Direct examination of the specimen Gram positive cocci in clusters are indicative Evidence of inflammation with abundance of neutrophils is highly suggestive Culture (infection or contamination especially when CoNS is isolated) Semiquantitative culture is useful (heavy, moderate, few) PCR (What are the issues associated with PCR in diagnosing Staphylococcal skin infections?- There is LOTS OF CONTAMINATION)
136
What kind of culture do you use with Staph
anerobic
137
Greasy Pig Disease
Exudative epidermitis caused by S. hyicus
138
Cattle: S. aureus • Sub-acute chronic or acute **mastitis** • Per-acute mastitis (Gangrenous mastitis)
139
Ulcerative Pododermatitis (S. aureus)
140
BIRDS Bumble foot; S. aureus
141
Botryomycosis
Botryomycosis- Rodents, Human, Horses Chronic pyogranulomatous inflammation Most common isolate : S. aureus
142
Treatment of staph
Antimicrobial susceptibility testing is a critical component Variability in susceptibility pattern Emergence of multidrug resistant Staphylococci Make sure that the labs follow appropriate guidelines CLSI or EUCAST Inducible Clindamycin resistance in macrolide resistant Staphylococcus **Nothing will substitute culture and AST** Therapy depends on Infection site and severity Species variation and geographic variations, 1st generation Cephalosporins (Cephalexin) are the first line of treatment choice Quinolones Not the first line of choice(resistance efficacy not well documented, and due to rapid development of resistance
143
All staphylococcus isolates which are macrolide(erythromycin) resistant should be
All staphylococcus isolates which are macrolide(erythromycin) resistant should be considered Clindamycin resistant unless otherwise confirmed by a D-test
144
Antimicrobial resistance in Staph bacteria
b lactamase -mediated resistance common Methicillin resistance becoming problematic (MRSA & MRSP) Mediated by mecA gene resulting in altered penicillin binding protein(PB2a) **Multidrug** resistance (macrolide, aminoglycoside, tetracycline, potentiated sulfas)
145
How would you determine whether staphylococcus sp. isolated from the owner and pet are the same?
Pulse Field Gel Ectrophoreisis
146
What is the best treatment for a mature staphylococcal abscess?
open, flush and use local treatment- YOU DON"T NEED AN ANTIMICROBIAL!
147
T/F A disease can be diagnosed by identifying the infectious agent and the host immune response to that agent.
TRUE-
148
Humoral immune response is measured by screening for:
Antibodies
149
Cell- mediated immunity measures
T Cells
150
Ability of a test to accuratley ID an infected agent as postive is known as
Sensitivity
151
Ability of a test to accurately ID a non-infected animal as negative is known as
Specificity
152
An ELISA was used to screen two cattle herds for the presnce of Johne's Disease. Herd A has a prevalence of 80% and Herd B has a prevalence of 15%. The positive predicitive value of this test is much higher in which herd?
Herd A The higher the prevalence of a disease, the higher the predicitive value
153
Which of the following is not an appropraite practice in sample collection and transport? A. Urine collected by free catch shipped overnight in ice B. urine collected by catherization C. Urine collected by cystocentesis D. Urine collected and shipped to the lab in a syringe with a needle attached to it
D. Urine collected and shipped to the lab in a syringe with a needle attached to it
154
Streptococcus
Gram-positive cocci in pairs or chains * Facultative anaerobe (aerobic and anaerobic) * Catalase negative * Many species can be pathogenic * Commensal of oral cavity, nasopharynx, skin, GI and Genital tracts • Hemolytic activity used for classification (a, b, g)
155
Streptococcal Diseases
Acute suppurative – local to systemic Immunologic post-streptococcal diseases (mostly human) Subacute (vegetative) endocarditis Chronic mastitis Streptococcal toxic shock syndrome (STSS) Necrotizing fasciitis and myositis(NFM)
156
Lancefield classification
used for Strep ## Footnote based on cell wall carbohydrates (A,B,C, D,E, F, G,H)
157
Streptococcus Cell-Associated Virulence Factors
Capsules Peptidoglycan Teichoic/lipoteichoic acid M protein- VERY IMPORTANT IN STRANGLES Ig binding proteins Streptokinase, Streptococcal pyrogenic exotoxins (superantigens)
158
S. pyogenes
Scarlet fever in humans
159
S. canis
Group G streptococcus infections in dogs and cats * S. canis * Commensal of skin and mucous membrane Kittens and puppies Infection from vagina or Umbilical vein\>Peritoneal cavity, liver\>bacteremia Septicemia and embolic lesions in heart and lung Skin ulceration and chronic respiratory infection necrotizing sinusitis and meningitis, necrotizing fasciitis with skin ulceration to toxic shock-like syndrome, sepsis, and death. Flesh eating bacteria
160
Streptococcus suis
Pathogenic or commensal organism usually associated with pigs. At least 35 serotypes of S. suis Type 2 is usually isolated most often from clinical cases in pigs, and is the predominant isolate from humans. Weanlings and growing pigs, Septicemia, serositis, meningitis, polyarthritis, pneumonia, abortions, abscesses and endocarditis.
161
What is the strains of Strep that is highly zoonotic?
Streptococcus suis and streptococcus iniae
162
Streptococcus iniae
Acute fulminating septicemia in fish chronic form limited to the central nervous system. **meningoencephalitis**, perineuritis, polyserositis, epicarditis, myocarditis, and cellulitis.
163
This is caused by....
Streptococcus porcinus Jowl Abscess in pigs
164
Viridans group of Streptococcus
* Do not react with Lancefield grouping sera. * Definitive species identification is difficult. * These bacteria can be found in the mouth, gastrointestinal tract and vagina of healthy humans, as well as in animals, dairy products and other sources. * Human infections
165
Streptococcus pneumoniae
* Streptococcus pneumoniae: pneumococcal pneumonia, septicemia and meningitis in humans * Pneumonia in guinea pigs and rodents • Domestic pets can act as carriers
166
S. equi
* Beta hemolytic, Group C Streptococcus * Usually has marked mucoid appearance due to abundant hyaluronic acid capsule • Must be distinguished from other equine group C S. zooepidemicus and S. equisimilis, by sugar fermentation tests or nucleic acid-based testing Equids are the only known hosts All ages are susceptible, average age \<2 yr Weaned foals, yearlings most susceptible \<4 mo usually protected by maternal antibodies Worldwide distribution, prevalence varies morbidity can be high, mortality is usually low
167
What causes Strangles in horses?
S. equi ## Footnote Abscessation of regional lymph nodes in the intermandibular area usually caused by infection with S. equi
168
S. equi: virulence factors
• Cellular - hyaluronic acid capsule - M protein - IgG Fc binding proteins - peptidoglycan/teichoic acid •Extracellular -streptokinase, hyaluronidase Streptolysin S, DNAase Streptococcal Pyrogenic Exotoxins
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S. equi: Transmission
Direct: contact with horse shedding bacterium Indirect: contact with contaminated environments (buckets, feed, walls, floor, grass, flies, water troughs)
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S. equi: Clinical Signs
(Signs appear 3-14 days after exposure) • - fever (39-39.5) (appears first) - purulent nasal discharge - depression, anorexia, dysphagia - moist cough - lymph node abscessation (submandibular, retropharyngeal) (within 2 weeks of initial signs)
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S. equi: Potential Complications
* Disseminated infection (bastard strangles)---- CAN SPREAD TO ALL OF THE LYMPHNODES * Purpura hemorrhagica (immune complex mediated vasculitis)
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Guttural Pouch Empyema
(accumulation of purulent material in guttural pouch) Usually 2° to an upper respiratory infection Streptococcus equi – most common Spread from retropharyngeal lymph nodes into guttural pouches through lymphatic drainage & rupture into pouch
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Chondroids
Guttural Pouch Chondroids * Chondroids = accumulation of soft or hard concretions in one or both guttural pouches * Associated with chronic empyema
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S. equi: Carriers
• Incubatory (nasal shedding begins 4-7 days after exposure with or without clinically evident nasal discharge) • Clinical (shedding from affected sites; nasal, pharynx, lymph nodes, guttural pouch) • Convalescent (nasal shedding for up to 6 weeks after recovery) • Long term (5-7 months or more, mostly from guttural pouch)
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S. equi: Recovery and Immunity
* Infected animals usually recover after abscesses mature and rupture * Most (\>75%) animals have strong immunity following recovery
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S. equi: Diagnostic Tests
• Culture: swab, lavage fluid (nasal, pharynx, LN, GP) - 3 negatives at weekly intervals sufficient to release from quarantine (convalescent carriers) - test Guttural Pouch \> 30 days after recovery (for long-term carriers) • Serology: ELISA for antibodies to M protein • PCR: M protein gene target used to detect asymptomatic carriers; must confirm positive PCR by culture (detects live and dead bacteria)
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S. equi: Vaccines
Killed, IM S. equi vaccines (M protein enriched) used in pregnant mares and foals to maintain high levels of anti M protein opsonizing antibodies Live, IN S. equi vaccine used similarly to stimulate mucosal immunity as well as serum opsonizing antibodies (can complicate culture-based screening)
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Enterococcus
* Inhabit GI tract * Survive in environment * Nosocomial infections(systemic infections) • Persistent UTI • Vancomycin resistance pathogenicity island • In vivo resistance
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Gram Positive rods
* Listeria * Erysipelothrix * Bacillus * Corynebacterium * Rhodococcus * Nocardia * Actinomyces, Trueperella, Actinobaculum, Dermatophilus • Anaerobes(Clostridium) * Mycobacterium
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Listeria
**FOOD SAFETY PATHOGEN** Small, Gram positive, facultative anaerobic rods Isolated from many species of animals _Capable of growing at a wide range of temperature (4- 44o C)_- SUCH AS THE FRIDGE Ubiquitous in the environment, especially temperate zones Carried in the GI tract of animals Resistant to harsh environmental conditions **Sporadic disease in a variety of animals including man**
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most frequent listeria
Listeria monocytogenes
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Clinical significance of Listeria
Winter-spring disease of feedlot or housed ruminants. **Outbreaks typically occur after feeding poor-quality silage.** Economically important disease with seasonal occurrence (winter months) Ingestion or inhalation \>septicemia, abortion, and latent infection. \>localize in the intestinal wall, medulla oblongata, and placenta \>encephalitis via minute wounds in buccal mucosa. Poultry; septicemic listeriosis
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Pathogenesis of Listeria
• Invasive (bacterial directed invasion of epithelial cells)\>Enters blood stream * Facultative intracellular bacteria: persist in macropahges * Intracellular growth leads to cell death and focal microabscesses
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Disease presentations of Listeria
Encephalitis: Most common presentation in ruminants(cattle, sheep, goat) Bacteria invade through oral mucosa travels along trigeminal nerve and have affinity for brainstem Abortion: Hematogenous spread to gravid uterus, organisms penetrate the placenta and spread to fetal liver resulting in focal hepatic necrosis Septicemia; common in monogastrics, Intracellular replication in macrophages, multifocal miliary abscess in spleen. Liver. Mainly occurs in neonates as a continuation of the fetal infection
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Virulence factors of Listeria
* Internalin: adhesion, entry, phagocytosis * Listeriolysin O) (Hemolysin): required for intracellular multiplication Facilitate bacterial release from phagosomes • Act A: intracellular movement
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If you are doing a necropsy and you suspect Listeria, what tissue do you want to send off for testing?
brain stem
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Which listeria uses uses host actin filaments to travel between cells
L. monocytogenes, THUS THEY CAN GET AWAY FROM THE IMMUNE SYSTEM
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Diseases from Listeria
* Neurologic symptoms: Dullness, turning or twisting of head to one side, walking in circles (circling disease) * Unilateral facial nerve paralysis with drooping of eyelid and ear, drooling due to pharyngeal paralysis, Strabismus, nystagmus, hemiparesis, head pressing, decreased rumen motility * Purulent endophthalmitis, usually unilateral
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Circling Disease is from
Listeria there is also Unilateral signs of trigeminal and facial paralysis
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Lesions of Listeria
Microabscesses and glial nodules infiltrated by neutrophils and gitter cells that may contain bacteria Acute vascular fibrinoid necrosis secondary to drainage into Virchow-Robin space Leptomeningitis and densely cellular perivascular cuffs composed of lymphocytes and histiocytes with fewer neutrophils and eosinophils Neuronal necrosis Cranial nerves may have intrafascicular and perineural accumulations of inflammatory cells (lymphocytes, macrophages, plasma cells and neutrophils)
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Diagnosis of Listeria
CNS disease Ante-mortem: Presumptive diagnosis from symptoms Post-Mortem: No gross lesions, Histopathology, Culture of Brain stem Listeria enrichment culture Gram stained CSF sediment short intracellular and extracellular Gram positive bacteria Immunohistochemical staining Septicemia culture of liver and spleen
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Post Mortem for Listeria
* Few gross lesions except for some congestion of meninges. * Microscopic lesions are confined primarily to the pons, medulla oblongata, and anterior spinal cord • In septicemic listeriosis, in calves that die when \<3 wk old, • Focal hepatic necrosis, and hemorrhagic gastroenteritis
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Listeria
194
Therapy for Listeria
* L monocytogenes is susceptible to penicillin (the drug of choice), ceftiofur, erythromycin, and trimethoprim/sulfonamide. * High doses are required because of the difficulty in achieving minimum bactericidal concentrations in the brain.
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Control of Listeria
No vaccines; cell-mediated immunity important Avoid high risk foods poor quality silage, pH\>5.5 unpasteurized dairy products processed meats uncooked vegetables Minimize aerosol exposure Precautions for pregnant and immunosupressed animals
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Erysipelothrix spp
Small, non-sporeforming, Gram-positive rods A Gram-positive, non spore-forming, facultative anaerobic bacillus 26 serotypes identified and isolated from many species of wild and domestic mammals, birds, reptiles, amphibians, and from the surface slime of fish Swine are the most important reservoir of the organism. 30-50% of healthy swine harbor the organism in their tonsils or other lymphoid tissue, and occasionally shed the organisms in their feces **Swine from 3 months to 1 year of age and pregnant sows are most susceptible** Disease manifestations include: Septicemia, polyarthritis, and endocarditis
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Disease Outcome
* Number of organisms exposed to •Route of exposure * Virulence of strain * Immune status of host going to be an exam question
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Erysipelothrix rheusiopathiae
Erysipelothrix rheusiopathiae – most frequent Most common in pigs and birds but also seen in many other species including man. (serotypes 1a, 1b and 2 common in pigs)
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Erysipelothrix tonsillarum
Erysipelothrix tonsillarum – less common Not virulent for pigs. Has been associated with disease in dogs.
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Transmission and virulence factors for Erysipelothrix
• Transmission is primarily oral, with infection of palatine tonsils or GALT, * Organism may enter through skin abrasions * Neuraminidase; Adherence to endothelial cells * Heat labile capsule resists phagocytosis by neutrophils
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Erysipelothrix rhomboid lesions
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Diseases of Erysipelothrix
• Acute - septicemia, common (pigs, birds, others) - abortion, rare (pigs) - cutaneous cellulitis/urticaria, occasional (pigs, birds, man) • Subacute - vegetative (valvular) endocarditis, occasional (pigs, birds, man, others) • Chronic - arthritis , common (pigs, birds)
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common in Erysipelothrix
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Diagnosis, Treatment, Control of Erysipelothrix
* Diagnosis: culture * Treatment: antimicrobial treatment of acute infections (penicillin, tetracycline) • Control: treat and isolate infected animals cull chronically affected animals good hygiene practices vaccination (pigs, turkeys) (live attenuated + bacterin) (surface proteins, eg. 60 kd, Spa, 19kd thought to be important protective antigens)
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The most common Staphylococcus isolates from dogs belongs to the species..
Staphylococcus pseudintermedius
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Blackie, a 5 year old female dog was presented to the vet clinic with unresolving skin lesions. Purulent and bloody secretions were oozing out of some of the lesions. What staphyloccus species is most likely involved?
Staph pseduintermedius
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Streptococcus- chain of cocci
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Staphylococcus
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Staphylococcal enterotoxin exerts its pathogenic effect by: A. Binding indiscriminately to the T cell receptor and class II MHC Molecule B. Binding to receptor using the B unit and activation of an enzyme using the A unit C. Binding to the CD14 receptor and activating macrophages to release TNF alpha
A. Binding indiscriminately to the T cell receptor and class II MHC Molecule because it's a superantigen; when it binds it releases lots of cytokines
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Bacillus spp
Large Gram-positive rods Endospore-forming * Thick peptidoglycan layer * Teichoic and lipo-teichoic acids * No outer membrane * Rapidly growing bacteria * (On Gram+ selective and non-selective media) * No growth on MacConkey’s agar (MacConkey agar is selective for Gram negatives) • Aerobic or facultative anaerobes • Variation in hemolytic activity • Saprophytes identified only to Genus level
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Pathogenic Bacillus spp.
* Bacillus anthracis – obligate mammalian pathogen * Bacillus cereus – rare cause of opportunistic infections and food poisoning in mammals * Few Insect pathogens eg. Bacillus thuringiensis Most species are soil saprophytes
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Bacillus anthracis
Koch’s postulates were developed using Anthrax bacilli Aerobic, non-motile, large, square-end Gm+ rods in chains Non-hemolytic (rough/ground glass/Medusa head colonies) Mature endospores do not bulge from cell
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Medusa head colonies as seen in Bacillus antracis
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Virulence Factors for bacillus anthracis
Cell associated **Capsule (Polymers of D glutamic acid)** Extracellular Anthrax toxin (3 proteins: edema factor, lethal factor and protective antigen) Both virulence factors encoded by plasmids Both are required for virulence
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Bacillus anthracis capsules
• produced only in vivo (capsule biosynthesis operon)- **ONLY IN THE BODY OF THE ANIMAL** transcriptionally upregulated by CO2/bicarbonate signal) * polymers of D-glutamic acid * encoded on a plasmid • anti-phagocytic
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McFadyean Reaction
Bacillus anthracis Capsule stain as a pink shadow with Polychromatic methylene Blue
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Anthrax toxin
(three separate(Tripartite toxin), proteins encoded on one plasmid) Edema factor – calmodulin-dependent adenylate cyclase (inhibits neutrophil function) Lethal factor – zinc metalloprotease (cell death, hypoxia-induced tissue injury/shock) Protective antigen – cell binding factor (translocation into cell) Together the components of anthrax toxin cause increased vascular permeability and cell necrosis
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Habitat of Bacillus anthracis
• Dependent on susceptible animals for replication (limited period of growth: bacterium kills host or host kills bacterium) • Dependent on endospores for survival in soil (exposure of carcass to oxygen increases sporulation) • Ecological cycles of infection (sporulation and germination have specific requirements)
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Predisposing factors that increase exposure of animals to anthrax spores in soil
* History: site (general) of previous anthrax deaths * Flooding: soil rearrangement brings endospores to surface, endospore concentration is increased in standing surface water as it recedes • Soil conditions: Alkaline (pH\>6), rich in calcium (calcareous) and nitrogen (decaying vegetation, etc.): favors endospore survival • Warm temperature (\>60-80 degree daily low temp): during drought conditions animals forage closer to the ground increasing chances of soil ingestion and mechanical injury to GI mucosa
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Disease Pathogenesis of Bacillus anthracis
Exposure to endospores: Most common Endospores germinate within phagolysosomes of macrophage Intracellular survival factors allow growth initiation and a phospholipase mediates escape from the phagocytic cell Capsule and edema factor inhibit phagocytosis of vegetative cells Vegetative cells grow rapidly in the body Complete anthrax toxin causes cell death and affects vascular permeability
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Forms of Anthrax
* Per acute septicemia – ruminants (cattle Sheep) •Acute septicemia – horses * Pulmonary – man (wool sorter’s disease) •Pharyngeal – pigs, dogs •Intestinal – man, pigs, horse •Cutaneous – man (malignant carbuncle)
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Antemortem signs of anthrax
rapidly fatal disease high fever, bleeding from orifices, shock, respiratory distress
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Postmortem signs of anthrax
Dark, unclotted blood, Incomplete rigor mortis Splenomegaly: large, “current-jelly” spleen, widespread edema bacteremia(80% of bacteria in blood at time of death)
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Anthrax
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Diagnosis, Treatment, Control of Anthrax
Blood smear examination: for presumptive diagnosis Aerobic Culture and PCR from Blood Fluorescent antibody staining DO NOT conduct a Field Necropsy if you have Anthrax in your DD list Call the state/ Federal officials
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If you did a necropsy on an animal with anthrax, what would you see?
Hypertrophy of the spleen
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Diagnosis of Anthrax
Sample Collection Blood and aqueous humor for culture, Spleen If you happened to open up the carcass and observe splenomegaly Blood and organ smears stained with Polychromatic Methylene Blue (McFadyean’s methylene blue) Blue staining organisms with a pink capsule Chains of encapsulated, gram positive, non- spore forming rods, non-motile, roughly rectangular rods with square ends in Gram stains
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Treatment of anthrax
Treatment: (vegetative cells only) antimicrobials effective if given early localized forms may resolve without treatment penicillin, tetracycline, doxycycline, ciprofloxacin Control: vaccinate healthy animals (endemic/high risk areas only)
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Response to anthrax in range/pastured cattle
Quarantine herd (for at least 30 days following last death) Use personal protective equipment when handling animals and contaminated materials (eg. gloves, coveralls, etc) Treat all animals in herd with long-acting antimicrobials (eg. Oxytetracycline ) Move herd from field/pasture/range Examine animals daily (treat those with increased temp.) Vaccinate8-12daysafterantibiotictreatment Properly dispose of carcasses Disinfect contaminated materials
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How do you dispose of anthrax animals that have died?
incineration or deep burial (\>6.5 ft) under layer of quicklime (anhydrous calcium oxide)
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Anthrax and Humans
Cutaneous anthrax Complications include subcutaneous edema and septicemia The case fatality rate is 10-20% Gastrointestinal anthrax: Follows consumption of contaminated meat Pharyngeal lesions, sore throat and dysphagia, Regional lymphadenopathy, Inappetence, nausea, vomiting blood and bloody diarrhea , Massive septicemia and toxemia, Fatality rate 25-60% Pulmonary or inhalation anthrax Produce pulmonary edema, hemorrhagic pneumonia, and sometimes meningitis Mortality approaches 100%, Sudden onset of acute symptoms, Hypotension, edema and fatal shockLength of incubation period inversely related to dose Spores may remain dormant until engulfed by pulmonary alveolar macrophages
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A bacteria which uses host actin filaments to travel between cells....
Listeria monocytogenes
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What are the intercellualar pathogens?
Listeria
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Which of the following is incorrect about listeriosis in ruminants? A. Outbreaks occurs after feeding solied silage B. encephaltitis and neurological signs occurs after the organism enters through the wounds in buccal mucosa C. Generally disease occurs in the winter months D. Hepatic necrosis is the main lesion in adult animals
D. Hepatic necrosis is in YOUNG ANIMALS and monogastric animals
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Toxin and capsule are required for the virulence of bacillus anthracis T/F
TRUE
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Capsule of anthrax bacilli is composed of a polysaccharide T/F
FALSE- the capsule is polylucemic acid
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McFayden staining reaction is used for detecting....
capsule of anthrax bacilli
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In avirulent forms of Bacillus anthracis presence of toxin is essential for protective immune response.
TRUE
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T/F Anthrax is a contagious disease
FALSE- Anthrax is an infectious disease-- this is why there are sporative outbreaks
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Corynebacterium spp.
Gram-positive, pleomorphic non-spore forming, non-motile, rods Facultative anaerobe, catalase positive Diverse genus, many species found in soil and other environmental sources Animal associated species are commensals on skin and mucous membranes Environmental survival of lipophilic species may be prolonged Lipophilic spp.: Facultative Intracellular bacteria Pyogranulomatous C. pseudotuberculosis, C. urealyticum Non-lipophilic spp pyogenic, toxic C. renale group C. diphtheria Most species recovered from animals are not considered pathogenic **HAS MYCLOIC ACID**
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Contagious Bovine PyelonephritiS
Corynebacterium renale Group (C. renale, C. cystiditis, C. pilosum) Disease of adult cows Reservoir: clinically normal carrier cows Risk factors: trauma to bladder and urethra during parturition Transmission: contaminated bedding, venereal transmission non-sterile OB instruments
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Antemortem signs of Contagious Bovine Pyelonephritis
Persistent temperature increase (39.5) Loss of appetite and weight loss Painful urination and increased frequency **Ammoniac odor of urine** Acute abdominal pain (colic) Decreased rumen contractions Decreased milk production
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Postmortem findings of contagious bovine pyelonephritis
Multifocal abscesses in renal cortex, medulla, pelvis Enlarged renal lymph nodes Uremia Diagnosis: culture (urine or renal tissues)
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Diseases from Corynebacterium
Caseous lymphadenitis in sheep and goats * Corynebacterium pseudotuberculosis * C. pseudotuberculosis is a gram-positive, facultative, intracellular coccobacillus. • The disease is characterized by abscess formation in or near major peripheral lymph nodes (external form- goats) or within internal organs and lymph nodes (internal form- Sheep). Pigeon fever in horses(Colorado strangles”, “dry-land distemper”) Nitrate-reducing biotype of C. pseudotuberculosis Ulcerative lymphangitis of lower extremities Cattle can also get infected Abscesses in the pectoral region ventral abdomen Western and Midwestern states Enter through skin abrasions arthropod vectors such as stable flies, horn flies, and house flies, or contaminated fomites or soil.
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Virulence factors and pathogenesis of Corynebacterium
Exotoxin phospholipase D damaging endothelial cells and increasing vascular permeability. External lipid coat that provides protection from hydrolytic enzymes in host phagocytes. Entry through skin and mucous membrane\>Travel to lymphnodes and Viscera\>Replication of bacteria occurs in the phagocytes\>process of bacterial replication, and inflammation\>formation of abscesses distinctive lamellated "onion skin" appearance. Disease severity increases with age
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Corynebacterium tuberulosis- ## Footnote **THIS IS CONTAGIOUS**
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Caseous Lymphadenitis (C.pseudotuberculosis)
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Caseous necrosis
Caseous necrosis of lymph nodes is the predominant feature. The initial lymph node lesion begins as lymphadenitis with the formation of multiple microscopic abscesses in the cortex; eosinophils may predominate initially. Microabscesses rapidly coalesce, forming areas of caseation. Abscesses become rapidly encapsulated by fibrous connective tissue, and the lymph node enlarges.
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Diagnosis of Corynebacterium
Culture of purulent materials
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Diagnosis by Serology of corynebacterium tuberoslosis
A synergistic hemolysin inhibition (SHI) test that detects antibodies to the phospholipase D exotoxin Positive titers indicate past resolved infections, recent exposure, recent vaccination, or active lesions Interpretation of titers??? False-negative results early in the infection and with chronic, walled- off abscesses. Colostral antibodies in young animals
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If you see antibodies from an ELISA test for Corynebacterium psuedotuberolosis what can that mean?
1. could have the infection now 2. exposure 3. previous infection YOU CAN NOT TAKE A POSITIVE RESPONSE AS A POSITIVE TEST RESULT.
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Treatment and control of corynebacterium psuedotuber
Owner education Not considered a “curable” disease. Animals with genetic or emotional value are treated Treatment options have included lancing and draining, surgical excision, formalin injection of lesions, systemic antibiotics, and intralesional antibiotics. (Extra label use) Penicillin, Rifampin, Tulathromycin,
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Control of corynebacterium
* Biosecurity practices * Culling of infected animals * Hygiene and management practices * Vaccines are available but strictly adhere to the label • Purchase animals from negative herds
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Corynebacterium kutscheri
Murine pseudotuberculosis Lung: Suppurative pneumonia Kidney, liver, heart: Similar nodular lesions Joints: arthritic lesions of pedal extremities subcuticular abscesses Lymph nodes: Lymphoid hyperplasia of regional nodes
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Corynebacterium bovis
Dermatitis, Hyperkeratosis in mice
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Virulence Factors of R. equi
Capsule **virulence associated proteins (VAPs)** (encoded on large plasmids) (promotes survival in non-activated macrophage) Mycolic acid, teichoic acid/peptidoglycan cholesterol oxidase (equi factor) phospholipase C
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Rhodococcus equi (Foal pneumonia)
(rhodo, “rose” or red-colored) Gram-positive rods or coccobacilli, non-spore forming Weakly acid-fast (modified stain) Aerobic, catalase-positive, non-motile Growth in 48-72 hrs on blood agar No growth on MacConkey’s agar Facultative intracellular pathogen Unique lipid-rich cell envelope structures rich in mycolic acid Promotes intra-macrophage survival and granuloma formation One of the main cause of Foal Pneumonia
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Enviornment of Rohodococcus Equi
Habitat is soil; however, it appears that **virulence is maintained in horses**. Over a long period of time, soil isolates may lose the virulence associated plasmids Non-pathogenic strains of R. equi and other species of Rhodococcus are soil saprophytes Found infrequently as an opportunistic pathogen in other animals (isolates from non-equine hosts usually lack virulence associated proteins)
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Rhodococcus equi
Rhodococcus equi is the most serious cause of pneumonia in foals 1–4 month old. Significant economic consequences because of mortality, prolonged treatment, surveillance programs for early detection, and relatively expensive prophylactic strategies. Clinical disease is rare in horses \>8 mo old. pulmonary infection probably originates within the first week of life.
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Things found in a necropsy for R. equi
Lung: Multiple 1-100 mm diameter, coalescing, firm, caseonecrotic foci predominately in the crainioventral lung lobes Gastrointestinal tract: Ulcerative enterocolitis often based over Peyer’s patches in the ileum and irregular well defined ulcers in the large intestine occur in more than 50% of foals with pneumonia. Bronchial and mesenteric lymph nodes: Swollen and edematous often with pyogranulomatous lymphadenitis Bone: Osteomyelitis
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Rhodococcus equi in other species
Cattle: Metritis, lymphadenitis and pneumonia in calves Sheep: Caseous bronchial lymphadenitis Goats: Pyogranulomatous lesions in the liver and lungs; osteomyelitis of the vertebra and skull; fibrinous enterocolitis Pigs: Tuberculosis-like lesions in submaxillary and cervical lymph nodes Cats: Pyogranulomatous skin lesions Humans: Zoonotic in immunocompromised individuals
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R. equi ddx: could also be herpes
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Diagnosis: screening tests for R. equi
Evaluate the entire premise (needs for each farm will vary) Screen for early detection of disease or infection elevated plasma fibrinogen visual inspection (clinical signs often absent early) (increased respiratory effort, lethargy, polyarthritis) rectal temp. 2x/day physical exam 2x /week CBC (increased WBC) thoracic radiographs/ultrasound (foals 1-3 months-old) Serology tests are available but are not reliable for screening or diagnosis
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Diagnosis: diagnostic tests for R. equi
Definitive diagnosis = Culture or PCR (for VAP A/B) on transtracheal aspirate (or specimen from other lesions) PLUS cytologic evidence of sepsis Culture of feces not reliable for diagnosis of granulomatous enterocolitis (However, organisms may be shed f virulent organisms) Serology not reliable
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Treatment for R. equi
Treatment prolonged (7 days to \>3 weeks) **because it's an intercelluar pathogen**, expensive, may have adverse effects and is variably successful Standard empirical treatment = Combination of macrolide (erythromycin or clarithromycin) and rifampin (they exhibit synergy in vitro) • Resistance to macrolides has been reported • Hyperimmune plasma and NSAID use is variable
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Prevention of R. equi
Young foals (\<2weeks) are more susceptible; it is hypothesized that exposure may occur very early in life Hyperimmune plasma can prevent pneumonia (given on 1st or 2nd, 3rd and 4th day of life) (protective components unknown – cellular immunity important) Course of azithromycin chemoprophylaxis treatment given shortly after birth also has promise Vaccination of mares or colostrum from immunized mares have not been effective A combination of early detection, treatment and environmental management is needed Untreated or uncontrolled disease can have negative effects on an individual animal’s future performance and a farm’s reputation
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Nocardia
* Nocardia: pleomorphic, gram-positive, facultative intracellular bacterium, nonmotile and non-spore-forming * In Gram stained smears, it appears as rods, cocci, or cocobacilli forms with characteristic long or branching filaments and a tendency to fragment into rods and cocci. * Pathogenic Nocardia spp are strictly aerobic, growing over a wide temperature range * Ubiquitous in the soil and water Nocardiosis is more common in dogs than in cats.
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N. asteroide
the most commonly isolated species in dogs and cats Nocardiosis is an opportunistic, noncontagious, pyogranulomatous to suppurative disease of domestic animals, wildlife, and people. Mastitis, pneumonia, abscesses, and cutaneous/subcutaneous lesions Livestock and companion animals.
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Cutaneous nocardiosis
Cutaneous nocardiosis in cattle, called “bovine farcy”, is caused by N. asteroides (formerly called N. farcinica); lesions are typically associated with lymphangitis and lymphadenitis
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Nocardia asteroides
has been associated with abortion in horses, cattle, sheep, and swine, often with no other signs in the dam. Causes granulomatous mastitis in cattle and small ruminants
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In horses, N. asteroides and N. braziliensis can cause
n horses, N. asteroides and N. braziliensis can cause fibrinopurulent pneumonia and pyothorax with sulfur granules
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In humans, most patients with N.asteroides infections have
In humans, most patients with N.asteroides infections have defects with T- cell mediated immunity, often associated with prolonged steroid use, HIV infection, or diabetes mellitus
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Disease for Norcarida
Not usually pathogenic for immunocompetent individuals • Causes pyogranulomatous infections (thorax, skin, mammary gland, systemic) Feline pyothorax
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Malitof
mass spec is what we use
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Nocardia mastitis
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Diagnosis, Treatment, Control for Norcarida
* Diagnosis: culture, acid-fast stain, ID can predict susceptibility * Treatment: susceptibility varies with species Best empirical choice for systemic, life-threatening infection is a combination of an aminoglycoside (eg. amikacin) and a carbapenem (eg. imipenem). Single treatment with trimethoprim/sulfa is effective for many species. •Control: difficult (Disease is sporadic)
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Casoeus lymphadenitis in sheep is caused by:
Corynebacterium psuedotuberculosis
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Casoeus lymphadenitis is a contagious disease T/F
TRUE
279
Positive antibody titers to phospholipase D extoxin of c. Pseduotuberculosis is diagnostic for Caseous lymphadentitis. T/f
FALSE- one titer is not diagnostic; it can be positive due to exposure or previously having the disease
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Rhodococcus equi is an olbigate intracellular pathogen T/F
FALSE- It is NOT obligate- it can be extracelluar as well as intracellular
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Toxin and capsule are required for the virulence of bacillus anthracis. T/F
TRUE
282
Antibiotics from Actinomycets
Amphotericin Chloramphenicol Tetracycline Erythromycin Neomycin Streptomycin Gentamicin
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actinomycets
Many actinomycetes are soil dwelling environmental saprophytes; Many genera produce cell fragments that resemble fungal spores (can be released into the air causing allergic respiratory diseases **NO MYCOLIC ACID** **Gram positive non-sporeforming rod May show filamentous branching Non-acid fast** **Virulence factors are not well-described** **Habitat of pathogenic species is mucosa of the oropharynx (some** **species host restricted)** **Facultative anaerobic & anaerobic spp. some are capnophilic** **Most are catalase negative** **Colonies vary, usually small slow-growing** **“molar tooth-like”**
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Actinomyces, Actinobaculum and Trueperella
Frequently associated with pyogenic infections in livestock, Eg. Trueperella pyogenes (formerly Corynebacterium, Actinomyces, and Arcanobacterium pyogenes)
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Disease from actinomycetes
Chronic, progressive, pyogranulomatous disease **Polymicrobial infection** with oropharyngeal flora Initiated by disruption of mucosal barrier, often involving plant material (foreign bodies, grass awns), bite wounds, oral trauma Spread by direct extension (lymphogenous and hematogenous spread also possible) Chronic infections may cause bone lysis Common in active outdoor animals (eg. hunting breeds) • Actinomyces sp. grow as colonies in center of lesion (granule-like consistency) Pyogenic response surrounding colony often forms draining tracts Outer zone of lesion has granulomatous characteristics (chronic infection)
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Actinomyces bovis
Cattle: Actinomyces bovis (lumpy jaw) Pyogranulomatous osteomyelitis Lumpy jaw is a localized, chronic, progressive, granulomatous abscess that most frequently involves the mandible, the maxillae, or other bony tissues in the head. Introduced to underlying soft tissue via penetrating wounds of the oral mucosa from wire or coarse hay or sticks. Involvement of adjacent bone frequently results in facial distortion, loose teeth (making chewing difficult), and dyspnea from swelling into the nasal cavity. A Gram stain of purulent material will reveal gram-positive, club- shaped rods and filaments (sulfur granules).
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Actinomyces hordeovulneris
Foxtail (grass awns)
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Diagnosis, Treatment, Control for Actinomyctes
• Diagnosis: - Culture / microscopic examination of granules Must request aerobic and anaerobic culture( Actinomyces can be aerobic anaerobic or capnophilic) • Treatment: - susceptible to penicillin G, iodides - may require long term treatment (3-12 months) with high dose penicillin - surgical excision of foreign bodies/circumscribed lesions • Control: - minimize risk of mechanical injury, remove foreign bodies
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Dermatophilus congolensis
Filamentous, branching Divides in two planes to give “tram-track” appearance and produce coccoid fragments which become motile zoospores Zoospores have chemotaxis for CO2 Aerobic, catalase positive Habitat is skin of infected animals Dermatophilosis can affect cattle, sheep, goats, horses, and less frequently pigs, dogs, and cats.
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Disease for D. congolensis
Motile zoospores are attracted to moist, damaged skin * Cause epidermal abscesses with hyperkeratosis * Virulence properties include, chemotaxis of zoospore, keratinolytic activity and survival of zoospores in dry scab- like crusts
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D. congolensis
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Rain Scald- D. Congolensis
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D. congolensis or strawberry foot rot in cattle
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Diagnosis, Treatment, Control for D. congolensis
* Diagnosis: * microscopic demonstration of organisms in scabs • Treatment: systemic antibiotic treatment (susceptible to penicillin G and Tetracycline) Control: treat and isolate infected individuals eliminate predisposing factors and vectors dry shelter- tick control, brush removal
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D. congolensis- on cows in St. Kitts
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Trueperella pyogenes
Pleomorphic, facultative anaerobe, non-spore forming, non-motile, non-capsulated, capnophilic Causes suppurative infections in ruminant and swine Diseases prevalence is sporadic and governed by precipitating stress or trauma Found on mucous membranes Most infections are probably endogenous **COMES FROM THE COW'S BODY- COMES OUT WHEN THEIR IS AN IMMUNITY PROBLEM WITH THE COW**
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Trueperella pyogenes in Cattle
nvolved in most purulent infection of traumatic or opportunistic origin May be local, regional, or metastatic Common locations include: The lung, pericardium, endocardium, pleura, peritoneum, liver, joints, uterus, renal cortex, brain, bones, and subcutaneous tissues Causes abortion and mastitis in cattle Summer mastitis is a communicable disease among pastured daily cattle during the dry period
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Trueperella pyogenes
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Actinobaculum suis
Anaerobic bacteria • Commensal diphteroid organism in prepucial mucosa of boars * Sexually transmitted pathogen * Causes cystitis and pyelonephritis 3-4 weeks post-coitus • Death as a consequence of renal failure * Pathogenesis similar as bovine pyelonephritis (C. renale) • UREASE as virulent factor
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Summer mastitis
is a communicable disease among pastured daily cattle during the dry period Trueperella pyogenes in Cattle
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What are the two spore forming bacterias?
Anthrax and Clostridium
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Tyzzers disease
Clostridium piliforme A Gram negative Clostridium which causes Tyzzers disease in laboratory animals
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Clostridium spp.
Large, endospore-forming, Gram-positive rods Except for Clostridium piliforme A Gram negative Clostridium which causes Tyzzers disease in laboratory animals
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Clostridium
3 categories of Clostridium: * Neurotoxic * Histotoxic and invasive •Enteric/ Enterotoxigenic Widespread distribution in soil and intestines of animals Endospore amplification may occur in well-defined geographical locations (requires anaerobic conditions)
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Virulence Factors of Clostridium
All pathogenic Clostridia produce one or more bacterial protein toxins or extracellular enzymes. Growth of Clostridia in the body requires anaerobic conditions: Necrosis is both a common predisposing factor for and host response to clostridial infection Necrosis provides an initial opportunity for Clostridium to grow Necrosis is the host response to many clostridial toxins Necrosis facilitates the rapid spread of infection through the body
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Clostridium tetani
* Anaerobic Gram positive rod * Cause tetanus * Terminal endospores * Widespread in soil and feces * Grow in contaminated wounds * Produce a potent neurotoxin (tetanospasmin) * AB toxin with zinc endopeptidase activity * Wound infection by Clostridium tetani\>Toxin produced in the wounds\>Toxin enters nearest motor nerves by receptor mediated endocytosis \>Retrograde transport along axons of peripheral motor nerves and spinal cord or via blood stream, enters neuromuscular endings of many motor nerves\>Prevents release of neurotransmitters, glycine and GABA \>**Causes spastic paralysis**
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Clostridium tetani; called "wooden horse" in horses
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Diagnosis of C. tetani
* History of recent wound and Clinical signs * Culture often unrewarding * Demonstration of toxin in serum or tissue difficult, often unrewarding, and testing not widely available * Serology not useful
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Treatment of C. tetani
Antitoxin (to neutralize unbound toxin) Anti-tetanus equine serum given IV or IM; anaphylaxis possible Antimicrobial treatment (to stop production of toxin) Surgical debridement of wounds; hyperbaric oxygen (to stop production of toxin) Supportive care – reduce external stimuli, sedatives, muscle relaxants
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Control of C. tetani
Toxoid immunization (man, horses, small ruminants) Post exposure prophylaxis (toxoid booster in man, horses) Prompt wound management (vaccinated and unvaccinated animals) Rational Antimicrobial therapy • Aseptic techniques while surgery, Proper sterilization of surgical instruments
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Clostridium botulinum
* Diverse group of organism (Toxin types A-G) • Toxin type/ Species affinity * Botulism * Botulinum neurotoxin * Food intoxication (food poisoning) * Toxin absorbed and distributed in bloodstream * Occasional toxico-infectious forms – wounds, intestinal • (infant botulism/shaker foal) * Inhibits neurotransmitter release (acetylcholine) Preformed toxins in a variety of sources including decaying vegetable matter (e.g., grass, hay, haylage, grain, spoiled silage), meat and fish, carcasses, invertebrates and contaminated * Carnivores are usually fed the toxins in contaminated meat or fish, or ingest the toxins in carcasses or decaying, high protein garbage. * Cattle in phosphorus-deficient areas may develop pica and chew bones and scraps of attached meat; * “a gram of dried flesh may have enough botulinum toxin to kill a cow”
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Clinical Signs of C. Botulinum
• Symmetrical flaccid paralysis of muscles Early symptoms in humans usually involve cranial nerve functions (double vision, dysphagia, speech dysfunction, etc.) Early symptoms in other mammals usually involve hind limb paralysis, recumbence Skeletal muscle paralysis can lead to respiratory failure
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C. botulinum
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botulism is called _____ in poultry
limberneck
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Diagnosis of C. botulinum
Demonstration of toxin in serum of animal Demonstration of toxin in food/stomach contents (mouse bioassay/neutralization test- gold standard) MALDI TOF
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Treatment of C. botulinum
IV or IM antitoxin (affects unbound toxin only) Only of use if animal is still actively absorbing toxin. Once toxin enters blood stream it is quickly bound to receptors Therapeutic drugs to enhance cholinergic neurotransmitter (acetylcholine) release Supportive care (fluids, respiratory maintenance, feeding/elimination functions)
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Control of C. botulinum
Toxoid immunization in high risk animals • Avoid feeding suspect foodstuff | (farmed mink, susceptible exhibit animals) Occupational protection in man discontinued, 2011 Most animals not routinely vaccinated)
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botulism is very common in\_\_\_\_\_
aquatic birds because they eat maggots
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Histotoxic Clostridia
C. chauvoei C.septicum C. novyi Less potent Toxins Invasive infections Myositis
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Histotoxic Clostridial Diseases
Wounds resulting from mechanical injury or vascular compromise result in anaerobic environments for deposited endospores to germinate and grow Toxins elaborated during growth cause more tissue destruction. Fermentation of muscle glycogen results in gas accumulation (hydrogen/methane). Metabolic end products (organic acids, amines) often have distinctive smells. Mechanically deposited endospores or that leave the intestinal tract may remain dormant in the body for extended periods **endospores stay dorminate** **necrosis and lots of gas production** **racid smell**
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Clostridium species frequently associated with
necrotic myositis **C. chauvoei** C. perfringens C. septicum C. novyi ndospores (widely distributed in soil/GI tract) Rapid growth in anaerobic conditions fermentative/proteolytic activities Exotoxins/extracellular enzymes
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Gas gangrene, Black disease(necrotic hepatitis)
C. novyi (A, B , C)
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Black leg
C. chauvoei Acute, febrile, highly fatal disease of cattle and sheep Emphysematous swelling, commonly affecting heavy muscles. Endogenous infections in cattle well-nourished young cattle Wound infections shearing cuts, docking, crutching, or castration in sheep * 100% fatality * Characteristic edematous and crepitant swellings develop in the hip, shoulder, chest, back, neck * Myocardium and diaphragm are affected
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Malignant edema, Braxy, Necrotic dermatitis (chicken)
C. septicum
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Necrotic hepatitis
C. novyi type B -Black disease – Necrotic hepatitis • Spores in the intestine and reach liver remail dormant in Kupffer cells\> traumatic damage by **liver fluke**\> anaerobic conditions\> germination of spores
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Disease of Clostridium
* Cellulitis, necrotic myositis * Often moves along fascial planes * Lesions appear hemorrhagic (edematous or dry) •May detect crepitus * Sudden death common •Clinical signs may include: fever, anorexia, depression, lameness
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Malignant edema
C. septicum • Fatal toxemia affects all species and ages of animals Dormant spores present in muscle tissues. Risk factors include IM injections in horses; shearing, docking, and lambing in sheep; and traumatic parturition and castration in cattle. Local exotoxins cause excessive inflammation, resulting in severe edema, necrosis, and gangrene. C septicum also causes braxy in sheep, a highly fatal infection characterized by toxemia and inflammation of the abomasal wall.
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Diagnosis, of clostridial necrotic myositis
Diagnosis: Direct Fluorescent antibody staining test (DFA) The most practical and faster option Available for C. chauvoei, C. septicum, C. novyi Anaerobic culture not very rewarding and time consuming
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Treatment, Control of necrotic myositis
Treatment: antimicrobial treatment (penicillin) (only effective if given early) hyperbaric oxygen surgical debridement/amputation • Control: routine vaccination of farm animals with multicomponent bacterin/toxoids
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Enteric Clostridium
* C. perfringens * C. difficile * C. spiroforme necrotic/hemorrhagic enteritis, necrotic hepatitis enterotoxemia
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C. perfringens
Four Major Toxins used for toxin biotyping (Types A-E based on the presence of Alpha, Beta, Iota, Epsilon) Necrotizing haemorrhagic enteritis in multiple species of animals Enterotoxaemia in cattle pigs horse sheep goat Type C in piglets * TYPE D ENTEROTOXEMIA * (Pulpy kidney disease, Overeating disease) http://www.merckvetmanual.com/mvm/generalized\_conditions/ clostridial\_diseases/enterotoxemias.html
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C. perfringens
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C. perfringens Type D enterotoxemia
A fluid-distended intestine with hemorrhagic petechiae on the serosal surface. Edema and malacia can be detected in the basal ganglia and cerebellum of lambs. **(focal encephalomalacia**) Rapid postmortem autolysis of the kidneys (pulpy kidney disease)
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C. perfringens Type D enterotoxemia
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pulpy kidney disease
Rapid postmortem autolysis of the kidneys C. perfringens Type D enterotoxemia
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Diagnosis and treatment for C. perfringens Type D enterotoxemia
Microscopic appearance/relative number Culture (determine toxin genotype of isolates) Toxin detection in intestinal contents Biological assay (mouse neutralization) Serological tests for toxin antigen ( cpe ELISA) * Treatment: * hyperimmune serum may be of value (if available and given early) * antimicrobial therapy not generally effective for GI diseases * Control: routine immunization of farm animals with toxoid/bacterins avoid sudden diet changes or stresses that might alter GI flora or damage GI mucosa
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Clostridium difficile enterocolitis
Affects colon and cecum of man, horse, pig, dog, cat, laboratory rodents, others Risk factors include recent antibiotic use, increased-age, hospitalization Neonates are resistant (may harbor toxigenic strains/toxins) * Endospores widespread (low numbers in normal intestine) * Most disease results from disruption of normal flora, proliferation of C. difficile, and toxin production * Nosocomial transmission has also been suggested
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Actinomyces bovis can be acid fast positive by Kinyoun's staining protcol. T/F
FALSE- it doesn't have mycolic acid
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What type of culture would you request from a lesion like this in a dog?
Aerboic and anerobic culture- absyess submit both!
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Which of the following feature helps in the ID of Dermatophilus congolensis infection in cattle? A scabby lesions B. presence of gram positive coccbacilli in the smear C. tram track appearance of the organism in the stained smears of scabs D. presence of gram variable filamentous bacteria in the smear
C
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Trueperella pyogenes is a common bacterial isolate form pyogenic lesions of internal organs in cattle. T/F
True
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Which of the following agent disease pair is incorrect? A. Actinobaculum suis-pyelonephritis in swine B. Corynebacterium bovis-pyelonephritis in cattle C. Actinomyces bovis- Lumpy jaw in cattle D. Dermatophilius congolensis- rain scald in horses
B Corynebacterium renele causes pyelonepritis in cattle
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Dysbiosis
when the normal flora of the GI tract is disturbed- these cause Pseudomembraneous colitis which causes
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Clostridium difficile toxins
Tox A – enterotoxin - fluid loss - affect G proteins Tox B – cytotoxin (in vitro) - similar mechanism of action - destroys cells more rapidly - acts synergistically with Tox A Most strains produce both toxins A&B A few strains produce Tox B only
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Approaches to diagnosis of Clostridium difficile diarrhea
• Culture Obligate anaerobe Vegetative cells sensitive to handling/treatment Selective media enhances germination of spores • Direct toxin detection Tissue culture assay (tox B) with specific antibody neutralization Toxin antigen detection (ELISA, latex aggn.- tox A or toxA/B)
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Approaches to treatment of C. difficile diarrhea
* Supportive electrolytes and fluids * Stop antibiotics * Clindamycin should not be used in horses * (antimicrobials may be needed in severe cases) * Probiotics (Lactobacillus, Saccharomyces replaces flora) • Avoid anti-diarrheals accumulates toxin) * Toxin adsorbent (adsorbs meds also)
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Clostridium spiroforme and Rabbits
Enterotoxemia an explosive diarrheal disease Primarily of rabbits 4–8 wk old. It Necropsy reveals the typical lesions of enterotoxemia, ie, a fluid-distended intestine with hemorrhagic petechiae on the serosal surface. • The primary causative agent is Clostridium spiroforme (commensal) which produces an **iota toxin.** • lincomycin, clindamycin, and erythromycin induce Clostridium-related (eg, C difficile and C. spiroforme) enterotoxemia due to their selective effect on normal gram- positive bacteria, they are contraindicated in rabbits.
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Tyzzer’s Disease
Clostridium piliforme- Tyzzer’s Disease • Acute, fatal diarrheal disease of lab animals with associated focal liver necrosis • C. piliforme does not grow in cell-free media; seen in bundles in hepatocytes (may also infect myocardium, smooth muscle, enterocytes) • Disease also reported in other mammals (eg. dogs, cats, foals, primates) **ONLY GRAM NEGATIVE CLOSTRIDIUM** **DX POST MORTEM**
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Non-Sporeforming Anaerobes
Gram Positive Cocci: Peptostreptococcus, Sarcina Rods: Propionibacterium, Bifidobacterium, Actinobaculum (Lactobacillus, Actinomyces) • Gram Negative Cocci: Veillonella, Ruminococcus Rods: Fusobacterium, Bacteroides, Dichelobacter Porphyromonas, Prevotella Spirochaetes: Treponema, Brachyspira, unclassified * Commensals on mucous membranes and skin * Many require enriched media with vitamin K, hemin and other growth factors Many grow more slowly than common aerobic and facultative anaerobic bacteria Clinical identification is based on morphology, antimicrobial susceptibility pattern, biochemical tests, products of fermentation, and molecular testing **IN GIT**
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Virulence Factors OF Non-Spore forming Anaerobes
* Not well characterized in all species – adhesins, extracellular enzymes, LPS shown to be important for some example: * Fusobacterium necrophorum – leukotoxin Dichelobacter nodosus – fimbriae, proteases • Catalase and superoxide dismutase Protect some from oxygen toxicity (aerotolerance) • Synergistic activities – tissue damaging factors that establish niche for second organism
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Anaerobic Infections
Most are of endogenous origin Require anaerobic environment/ devitalized tissue for growth Usually localized, often oral/GI tract- associated, spread by direct extension (can cause transient bacteremia & secondary localization, especially on damaged heart valves) Mixed infections (polymicrobial) Synergistic relationships are common
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Signs consistent with anaerobic infection
* Foul smelling discharges * Gas in tissues or discharges * Necrotic tissue, abscesses * Pyogranulomatous lesions with granules * Infections near or on mucous membranes * Infections not responding to aminoglycosides • Disease in the absence of significant growth in aerobic cultures
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Fusobacterium necrophorum
leukotoxin- kills leukocytes
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Anaerobic, Non-sporeforming Gram- negative Rods
Fusobacterium necrophorum (multispecies, rumen) (foot rot, hepatic abscesses, calf diphtheria,) * Dichelobacter nodosus (foot rot in sheep) • Bacteroides fragilis * Porphyromonas spp (most produce black iron porphyrin pigments) • Prevotella spp (some produce black iron porphyrin pigments)
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Fusobacterium necrophorum
Liver abscess Foot Rot extensive necrosis and keratinolysis in severe cases
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Control of Fusobacterium necrophorum
• Control: - keep feet dry, avoid mechanical injury - parasite control, routine immunizations, good nutrition, dental prophylaxis, etc. - vaccines: sheep & cattle (Fusobacterium necrophorum) sheep (Dichelobacter nodosus
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aminoglycosides you don't use in
anerobic infection
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Diagnosis, Treatment, Control of fusobacterium ncrophorum
* Diagnosis: * Culture, (PCR?) • Treatment: - remove necrotic tissue, oxygenate, antiseptic foot baths - antimicrobials - penicillin, metronidazole, clindamycin, chloramphenicol, doxycycline (aminoglycosides, sulfonamides not effective)
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Anaerobe identification
Identification of anaerobes requires specialized methods and is often incomplete • Current methods include: - Biochemical test kits - 16S rRNA gene sequencing - MALDI-TOF-MS • Susceptibility testing specialized and only standardized for a few genera (eg. Bacteroides and Clostridium)