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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
Q

Virulence

A

the degree of pathogenicity

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26
Q

Exotoxins

A

released from the cell; made in the cell

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27
Q

3 types of Endotoxins

A
  1. A-B toxins 2. Membrane disrupting toxins (Leukocidins kill white blood cells (phagocytes), Hemolysins destroy erythrocytes) 3. Superantigens
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28
Q

A-B Toxins

A

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.

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29
Q

What are superantigens?

A

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

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30
Q

Example of a superantigen

A

Toxic shock syndrome in humans is caused by a superantigen

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31
Q

Main source of virulence factors in bacteria

A

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)

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32
Q

Conjugation

A

is the process by which one bacterium( Bacterium with a fertility factor) transfers genetic material to another through direct contact.

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33
Q

Transformation

A

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)

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34
Q

Transduction

A

is the process by which DNA is transferred from one bacterium to another by a virus

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35
Q

Biofilm

A

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

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36
Q

Quorum sensing

A
  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.
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37
Q

Opportunistic pathogens

A

organisms those do not cause disease in a healthy host, with a healthy immune system

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38
Q

True pathogens

A

equipped with virulence genes for adherence, invasion, evasion from the immune system and toxins

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39
Q

Nosocomial Infections

A

Hospital acquired infections Eg. Methicillin resistant Staphylococcus aureus Clostridium difficile

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40
Q

Generally bacteria are

A

extracellular pathogens

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41
Q

Obligate intracellular pathogen

A

Eg. Rickettsia, Chlamydia

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42
Q

Facultative intracellular pathogen

A

(can survive extracellular or intracellular) Eg. Mycobacterium

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43
Q

Cell wall component unique to gram negative bacteria

A

lipopolysaccharide

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44
Q

Gram positive staining in some bacteria is due to the presence of a:

A

Thick Peptiodoglycan

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45
Q

Acid fast staining in Mycobacteria is due to the presence of:

A

Mycolic Acid

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46
Q

Gram positive bacteria retains the color of the primary stain and Gram negative bacteria picks up the color of the counterstain. T/F

A

TRUE

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47
Q

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

A

Bacterial protein production by ribosomes

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48
Q

Translation

A

Production of protein

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49
Q

DNA sequence coding. Which of these organelles is used for bacterial phylogentic analystis?

A

Ribosomes

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50
Q

Is mitochondria present in bacteria?

A

NOPE

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51
Q

What are antimicrobials?

A

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

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52
Q

• When do you use antimicrobials?

A

When the patient have a treatable microbial infection

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53
Q

Antimicrobial vs antibotic

A

Antibotics- produced by living organism, Antimicobrial is a broader term

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54
Q

What should you know to proceed with treatment with antimicrobials?

A

location of the infections, likely pathogens involved, which antimicrobials are likely effective against a particular pathogen at a particular site

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55
Q

What are the other factors to consider in antimicrobial therapy?

A

Cost, (type, dose and duration), safety, ease of use, and possible emergence of resistance

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56
Q

Antibiotic

A

chemical substance produced by a microorganism that inhibits the growth of or kills other microorganisms.

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57
Q

Antimicrobial agent

A

a chemical substance derived from a biological source or produced by chemical synthesis that kills or inhibits the growth of microorganisms.

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58
Q

Natural (true antibiotics)

A

produced by bacteria or fungus (Streptomycin, penicillin, tetracycline)

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59
Q

Semi-synthetic

A

chemically-altered natural compound (ampicillin, amikacin)

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60
Q

Synthetic

A

chemically designed in the lab (sulfonamide, enrofloxacin, marbofloxacin)

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61
Q

Classification of Antimicrobial agents

A

A. Chemicalfamilystructure B. Mode of action C. Type of antimicrobial activity D. Spectrum of antibacterial activity

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62
Q

What do you need to know to treat with antimicrobial agents?

A

•Know the drugs •Know the microbiology •Know the patient

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63
Q

Mode of action of antimicrobial

A

inhibitors of cell wall synthesis inhibitors of protein synthesis inhibitors of membrane function inhibitors of nucleic acid synthesis (anti-metabolites)

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64
Q

Antibacterial Susceptibility Testing

A

Done to figure out which antimicrbioals are the best to treat certain infections

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65
Q

2 types of Antibacterial Suscpetibility Testing

A
  1. Dilution (broth/agar) 2. Diffusion (disk)- aka Kirby Bauer Test
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66
Q

What is a Susceptibility break point?

A

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

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67
Q

What is Minimum inhibitory concentration (MIC)?

A

Minimum amount of drug required to inhibit bacterial growth Drugs with lower MIC values are better choices

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68
Q

Disk Diffusion

A

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
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69
Q

Broth Dilution

A

• 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)

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70
Q

You always want to keep a dose (below or above) the MIC in the body?

A

above MIC in the body

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71
Q

Gradient diffusion test - E-Test

A

Measures MIC

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72
Q

Bactericidal

A

kills

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73
Q

Bacteriostatic

A

inhibits

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74
Q

Broad spectrum antibiotic

A

active against a wide variety of bacteria Eg. Tetracycline

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75
Q

Narrow spectrum antibiotic

A

affect only a narrow range of bacteria Eg. Penicillin

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76
Q

When do you use antimicrobial combinations?

A
  • 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)

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77
Q

Innate resistance

A

preexisting genomic property

i.e. Mycoplasa does not have a cell wall, Therefore, you can’t use beta lactones

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78
Q

Acquired resistance

A

new genetically encoded trait not representative of the species

(acquired by mutation or horizontal gene transfer)

Processes that bacteria can aquire virulence factors:

-conjugation

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79
Q

Mechanisms of Resistance

A
  • Enzymatic destruction or inactivation of drug
  • Prevention of penetration to target sites within microbe
  • Alteration of drugs target site
  • Rapid efflux of antibiotics
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80
Q

Strategies to Reduce Antimicrobial Resistance

A

• 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
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81
Q

What antimicrobial should you NOT use?

A

Vancomycin

Vancomycin resistant Enterococcus (VRE)

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82
Q

Antimicrobials are used in agriculture for?

A

Growth Promotion

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83
Q

What is one of the main problems with use of antimicrobials in vet med?

A

Extra Label Use

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84
Q

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

A

D. Know the Client

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85
Q

T/F In general drugs with lower MIC values are better choices for treatment.

A

TRUE; because you can use a lower dose, but remember that MIC is not the only factor(microbe, site of infection etc)

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86
Q

Pure Culture of a bacteria is critical for obtaining accurate antimicrobial susceptibility pattern T/F

A

True- you MUST have a pure culture

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87
Q

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)

A

D. Kirby Bauer DOES NOT measured MIC accurately

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88
Q

Methods for IDing the agent

A
  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)

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89
Q
  1. Identification of the host immune response
A

Antibodies(Eg,Brucella infection),
Cell mediated immune response(eg.TB)—- very rare and only available for certain conditions

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90
Q

Ideal test has

A

Ideal test has high sensitivity and high specificity

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91
Q

Sensitivity

A

percentage of true positives in a sample population that are correctly identified as positive by a test.

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92
Q

Specificity

A

percentage of true negatives in a sample population that are correctly identified as negative by a test.

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93
Q

Positive predictive value

A

percentage of all positive test results that are true positives.

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94
Q

Negative predictive value

A

percentage of all negative test results that are true negatives.

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95
Q

Predictive values associated with individual test results vary

A

Predictive values associated with individual test results vary with disease prevalence

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96
Q

In a high prevalence herd, you will have a

A

more accurate results.

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97
Q

Specimen collection

A
  • 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
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98
Q

Can you submit a swab for a bx?

A

better to submit the material itself

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99
Q

What happens if you submit a fecal sample in a serum tube?

A

the bacteria will produce lots gas

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100
Q

Gram Staining

A

Gram Positive Purple(Crystal violet)
Eg: Streptococcus pyogenes

Stapylococcus aureus

Gram Negative- Pink (Safranin)

Escherichia coli Pasteurella multocida

Gram stain -Gram Positive = Thick Peptidoglycan

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101
Q

Acid Fast Staining (Kinyon’s stain)

A

Acid fast positive organism stains: Pink Acid fast negative organism stains: Blue

Acid fast stain –Acid fast + =mycolic acid

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102
Q

Largest Problem with direct staining

A

Sensitivity is very poor

Blood
• CSF
• Mycoplsama, spirochetes( can not be stained)

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103
Q

Urine

A

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

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104
Q

Transudates and exudates

A
  • Syringe
  • Remove air
  • Anaerobic transport medium

•Lavages or washes use a buffered solution •Saline vs. lactated ringer’s solution

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105
Q

Feces

A
  • 2-3 gms
  • Leak proof container
  • Repeated culture needed in shedding/chronic infections
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106
Q

Blood

A
  • Several specimens over a period of time, onset of fever,
  • 3- 4 in first 1.5 -3 hours
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107
Q

Tissue samples

A
  • Portion of a tissue
  • Multiple specimens
  • Collect first during necropsy
  • Sealed leak proof container
  • Refrigerate if delivery delayed
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108
Q

Interpretation

A

Normal flora Vs. Pathogens

Correlate with clinical signs and the organism

Quantitation- light, moderate, heavy

(Isolation of four or more organism; Most likely contamination)

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109
Q

False negative results

A

May be due to sampling, transport, storage issues, antimicrobial therapy, Fastidious organisms or when specific procedures needed

Consult with clinical microbiologist

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110
Q

The most dangerous pathogens are classified as

A

BSL-4

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111
Q

Principle of Secondary Containment

A

transport in secondary container that is leakproof, puncture proof and contains liquid absorbent

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112
Q

Rare bacteria are

A

Gram Negative cocci

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113
Q

Polymerase Chain Reaction

A

• 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
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114
Q

Antigen detection

A

(EIA, agglutination, FA, etc.)

(tests use antibody reagents to detect antigens in serum, feces, urine, tissue.)

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115
Q

Chemical detection

A

(HPLC, GLC, MALDI-TOF- MS) (analysis of total cell fatty acids/proteins; limited use on clinical specimens)

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116
Q

Biological detection

A

(Limulus amoebocyte assay) (test for LPS, adapted from clotting mechanism of horseshoe crab)

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117
Q

Detection of Specific Immune

Response to a bacteria or fungus

A

• 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

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118
Q

False positives for immune tests can mean

A

prior antigen exposure, vaccination, cross-reactions

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119
Q

False negatives for immune tests can mean…

A

anergy, immunosuppression

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120
Q

Beta Lactam(b-Lactam) antimicrobials

A

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

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121
Q

Mechanism of action of Beta Lactam antimicrobials

A

Mechanism of action

Inhibit Cell wall synthesis(transpeptidation step) in the peptidoglycan synthesis, Stimulate autolysins which degrade peptidoglycan

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122
Q

Resistance mechanisms of b-Lactamase

A

Resistance mechanisms;
• b-Lactamase(enzyme which cleaves b lactam ring) production • Extended Spectrum b lactamase
• Alteration in penicillin binding proteins

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123
Q

cell wall synthesis inhibitors

A
  • Glycopeptides(Vancomycin, daptomycin)
  • Last resort antimicrobial in S. aureus, and Enterococcus

• Fosfomycin, bacitracin

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124
Q

Gram positive cocci

A

Staphylococcus

Streptococcus

Enterococcus

Micrococcus

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125
Q

Staphylococcus

A

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

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126
Q

Staph in a dog is is almost always…

A

S. pseudintermedius

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127
Q

What is Coagulase?

A

Enzyme which Convert fibrinogen to Fibrin

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128
Q

Staph causes

A

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

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129
Q

pyogranulomatous

A

Chronic persistent relapsing infections in staph infections

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130
Q

Toxin Mediated Diseases from Staph

A
  • 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!

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131
Q

Superantigen

A

Causes indiscriminate binding to MHC Class II receptor and releasing lots of cytokines and T cells

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132
Q

Virulence factors of Staph

A
  • 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
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133
Q

Staph in Dogs

A

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
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134
Q

Why do dogs get staph so easily?

A

“Epidermal barriers are less well developed” ???

Thin stratum corneum Lack of Follicular Plug

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135
Q

Diagnosis of Staph

A

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)

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136
Q

What kind of culture do you use with Staph

A

anerobic

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137
Q

Greasy Pig Disease

A

Exudative epidermitis caused by S. hyicus

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138
Q
A

Cattle: S. aureus
• Sub-acute chronic or acute mastitis

• Per-acute mastitis (Gangrenous mastitis)

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139
Q
A

Ulcerative Pododermatitis (S. aureus)

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140
Q
A

BIRDS Bumble foot; S. aureus

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141
Q

Botryomycosis

A

Botryomycosis- Rodents, Human, Horses Chronic pyogranulomatous inflammation Most common isolate : S. aureus

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142
Q

Treatment of staph

A

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

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143
Q

All staphylococcus isolates which are macrolide(erythromycin) resistant should be

A

All staphylococcus isolates which are macrolide(erythromycin) resistant should be considered Clindamycin resistant unless otherwise confirmed by a D-test

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144
Q

Antimicrobial resistance in Staph bacteria

A

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
Q

How would you determine whether staphylococcus sp. isolated from the owner and pet are the same?

A

Pulse Field Gel Ectrophoreisis

146
Q

What is the best treatment for a mature staphylococcal abscess?

A

open, flush and use local treatment- YOU DON”T NEED AN ANTIMICROBIAL!

147
Q

T/F A disease can be diagnosed by identifying the infectious agent and the host immune response to that agent.

A

TRUE-

148
Q

Humoral immune response is measured by screening for:

A

Antibodies

149
Q

Cell- mediated immunity measures

A

T Cells

150
Q

Ability of a test to accuratley ID an infected agent as postive is known as

A

Sensitivity

151
Q

Ability of a test to accurately ID a non-infected animal as negative is known as

A

Specificity

152
Q

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?

A

Herd A

The higher the prevalence of a disease, the higher the predicitive value

153
Q

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

A

D. Urine collected and shipped to the lab in a syringe with a needle attached to it

154
Q

Streptococcus

A

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
Q

Streptococcal Diseases

A

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
Q

Lancefield classification

A

used for Strep

based on cell wall carbohydrates (A,B,C, D,E, F, G,H)

157
Q

Streptococcus Cell-Associated Virulence Factors

A

Capsules

Peptidoglycan Teichoic/lipoteichoic acid
M protein- VERY IMPORTANT IN STRANGLES
Ig binding proteins
Streptokinase,
Streptococcal pyrogenic exotoxins (superantigens)

158
Q

S. pyogenes

A

Scarlet fever in humans

159
Q

S. canis

A

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
Q

Streptococcus suis

A

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
Q

What is the strains of Strep that is highly zoonotic?

A

Streptococcus suis

and streptococcus iniae

162
Q

Streptococcus iniae

A

Acute fulminating septicemia in fish
chronic form limited to the central nervous system.
meningoencephalitis, perineuritis, polyserositis, epicarditis, myocarditis, and cellulitis.

163
Q

This is caused by….

A

Streptococcus porcinus

Jowl Abscess in pigs

164
Q

Viridans group of Streptococcus

A
  • 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
Q

Streptococcus pneumoniae

A
  • Streptococcus pneumoniae: pneumococcal pneumonia, septicemia and meningitis in humans
  • Pneumonia in guinea pigs and rodents • Domestic pets can act as carriers
166
Q

S. equi

A
  • 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
Q

What causes Strangles in horses?

A

S. equi

Abscessation of regional lymph nodes in the intermandibular area usually caused by infection with S. equi

168
Q

S. equi: virulence factors

A

• Cellular - hyaluronic acid capsule - M protein

  • IgG Fc binding proteins
  • peptidoglycan/teichoic acid

•Extracellular -streptokinase, hyaluronidase

Streptolysin S,
DNAase
Streptococcal Pyrogenic Exotoxins

169
Q

S. equi: Transmission

A

Direct: contact with horse shedding bacterium

Indirect: contact with contaminated environments
(buckets, feed, walls, floor, grass, flies, water troughs)

170
Q

S. equi: Clinical Signs

A

(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)
171
Q

S. equi: Potential Complications

A
  • Disseminated infection (bastard strangles)—- CAN SPREAD TO ALL OF THE LYMPHNODES
  • Purpura hemorrhagica (immune complex mediated vasculitis)
172
Q

Guttural Pouch Empyema

A

(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

173
Q

Chondroids

A

Guttural Pouch Chondroids

  • Chondroids = accumulation of soft or hard concretions in one or both guttural pouches
  • Associated with chronic empyema
174
Q

S. equi: Carriers

A

• 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)

175
Q

S. equi: Recovery and Immunity

A
  • Infected animals usually recover after abscesses mature and rupture
  • Most (>75%) animals have strong immunity following recovery
176
Q

S. equi: Diagnostic Tests

A

• 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)

177
Q

S. equi: Vaccines

A

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)

178
Q

Enterococcus

A
  • Inhabit GI tract
  • Survive in environment
  • Nosocomial infections(systemic infections) • Persistent UTI

• Vancomycin resistance pathogenicity island • In vivo resistance

179
Q

Gram Positive rods

A
  • Listeria
  • Erysipelothrix
  • Bacillus
  • Corynebacterium
  • Rhodococcus
  • Nocardia
  • Actinomyces, Trueperella, Actinobaculum, Dermatophilus • Anaerobes(Clostridium)
  • Mycobacterium
180
Q

Listeria

A

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

181
Q

most frequent listeria

A

Listeria monocytogenes

182
Q

Clinical significance of Listeria

A

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

183
Q

Pathogenesis of Listeria

A

• 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
184
Q

Disease presentations of Listeria

A

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

185
Q

Virulence factors of Listeria

A
  • Internalin: adhesion, entry, phagocytosis
  • Listeriolysin O) (Hemolysin): required for intracellular multiplication

Facilitate bacterial release from phagosomes • Act A: intracellular movement

186
Q

If you are doing a necropsy and you suspect Listeria, what tissue do you want to send off for testing?

A

brain stem

187
Q

Which listeria uses uses host actin filaments to travel between cells

A

L. monocytogenes, THUS THEY CAN GET AWAY FROM THE IMMUNE SYSTEM

188
Q

Diseases from Listeria

A
  • 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
189
Q

Circling Disease is from

A

Listeria there is also Unilateral signs of trigeminal and facial paralysis

190
Q

Lesions of Listeria

A

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)

191
Q

Diagnosis of Listeria

A

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

192
Q

Post Mortem for Listeria

A
  • 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

193
Q
A

Listeria

194
Q

Therapy for Listeria

A
  • 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.
195
Q

Control of Listeria

A

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

196
Q

Erysipelothrix spp

A

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

197
Q

Disease Outcome

A
  • Number of organisms exposed to •Route of exposure
  • Virulence of strain
  • Immune status of host

going to be an exam question

198
Q

Erysipelothrix rheusiopathiae

A

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)

199
Q

Erysipelothrix tonsillarum

A

Erysipelothrix tonsillarum – less common
Not virulent for pigs. Has been associated with disease in dogs.

200
Q

Transmission and virulence factors for Erysipelothrix

A

• 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
201
Q
A

Erysipelothrix

rhomboid lesions

202
Q

Diseases of Erysipelothrix

A

• 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)
203
Q
A

common in Erysipelothrix

204
Q

Diagnosis, Treatment, Control of Erysipelothrix

A
  • 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)

205
Q

The most common Staphylococcus isolates from dogs belongs to the species..

A

Staphylococcus pseudintermedius

206
Q

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?

A

Staph pseduintermedius

207
Q
A

Streptococcus- chain of cocci

208
Q
A

Staphylococcus

209
Q

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

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

210
Q

Bacillus spp

A

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

211
Q

Pathogenic Bacillus spp.

A
  • 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

212
Q

Bacillus anthracis

A

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

213
Q
A

Medusa head colonies as seen in Bacillus antracis

214
Q

Virulence Factors for bacillus anthracis

A

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

215
Q

Bacillus anthracis capsules

A

• 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
216
Q

McFadyean Reaction

A

Bacillus anthracis

Capsule stain as a pink shadow with Polychromatic methylene Blue

217
Q

Anthrax toxin

A

(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

218
Q

Habitat of Bacillus anthracis

A

• 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)

219
Q

Predisposing factors that increase exposure

of animals to anthrax spores in soil

A
  • 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

220
Q

Disease Pathogenesis of Bacillus anthracis

A

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

221
Q

Forms of Anthrax

A
  • 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)

222
Q

Antemortem signs of anthrax

A

rapidly fatal disease
high fever, bleeding from orifices, shock, respiratory distress

223
Q

Postmortem signs of anthrax

A

Dark, unclotted blood,

Incomplete rigor mortis
Splenomegaly: large, “current-jelly” spleen, widespread edema bacteremia(80% of bacteria in blood at time of death)

224
Q
A

Anthrax

225
Q

Diagnosis, Treatment, Control of Anthrax

A

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

226
Q

If you did a necropsy on an animal with anthrax, what would you see?

A

Hypertrophy of the spleen

227
Q

Diagnosis of Anthrax

A

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

228
Q

Treatment of anthrax

A

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)

229
Q

Response to anthrax in range/pastured cattle

A

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

230
Q

How do you dispose of anthrax animals that have died?

A

incineration or deep burial (>6.5 ft) under layer of quicklime (anhydrous calcium oxide)

231
Q

Anthrax and Humans

A

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

232
Q

A bacteria which uses host actin filaments to travel between cells….

A

Listeria monocytogenes

233
Q

What are the intercellualar pathogens?

A

Listeria

234
Q

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

A

D. Hepatic necrosis is in YOUNG ANIMALS and monogastric animals

235
Q

Toxin and capsule are required for the virulence of bacillus anthracis T/F

A

TRUE

236
Q

Capsule of anthrax bacilli is composed of a polysaccharide T/F

A

FALSE- the capsule is polylucemic acid

237
Q

McFayden staining reaction is used for detecting….

A

capsule of anthrax bacilli

238
Q

In avirulent forms of Bacillus anthracis presence of toxin is essential for protective immune response.

A

TRUE

239
Q

T/F Anthrax is a contagious disease

A

FALSE- Anthrax is an infectious disease– this is why there are sporative outbreaks

240
Q

Corynebacterium spp.

A

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

241
Q

Contagious Bovine PyelonephritiS

A

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

242
Q

Antemortem signs of Contagious Bovine Pyelonephritis

A

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

243
Q

Postmortem findings of contagious bovine pyelonephritis

A

Multifocal abscesses in renal cortex, medulla,

pelvis

Enlarged renal lymph nodes

Uremia

Diagnosis: culture (urine or renal tissues)

244
Q

Diseases from Corynebacterium

A

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.

245
Q

Virulence factors and pathogenesis of Corynebacterium

A

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

246
Q
A

Corynebacterium tuberulosis-

THIS IS CONTAGIOUS

247
Q
A

Caseous Lymphadenitis (C.pseudotuberculosis)

248
Q

Caseous necrosis

A

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.

249
Q

Diagnosis of Corynebacterium

A

Culture of purulent materials

250
Q

Diagnosis by Serology of corynebacterium tuberoslosis

A

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

251
Q

If you see antibodies from an ELISA test for Corynebacterium psuedotuberolosis what can that mean?

A
  1. could have the infection now
  2. exposure
  3. previous infection

YOU CAN NOT TAKE A POSITIVE RESPONSE AS A POSITIVE TEST RESULT.

252
Q

Treatment and control of corynebacterium psuedotuber

A

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,

253
Q

Control of corynebacterium

A
  • Biosecurity practices
  • Culling of infected animals
  • Hygiene and management practices
  • Vaccines are available but strictly adhere to the label • Purchase animals from negative herds
254
Q

Corynebacterium kutscheri

A

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

255
Q

Corynebacterium bovis

A

Dermatitis, Hyperkeratosis in mice

256
Q

Virulence Factors of R. equi

A

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

257
Q

Rhodococcus equi

(Foal pneumonia)

A

(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

258
Q

Enviornment of Rohodococcus Equi

A

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)

259
Q

Rhodococcus equi

A

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.

260
Q

Things found in a necropsy for R. equi

A

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

261
Q

Rhodococcus equi in other species

A

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

262
Q
A

R. equi

ddx: could also be herpes

263
Q

Diagnosis: screening tests for R. equi

A

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

264
Q

Diagnosis: diagnostic tests for R. equi

A

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

265
Q

Treatment for R. equi

A

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

266
Q

Prevention of R. equi

A

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

267
Q

Nocardia

A
  • 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.

268
Q

N. asteroide

A

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.

269
Q

Cutaneous nocardiosis

A

Cutaneous nocardiosis in cattle, called “bovine farcy”, is caused by N. asteroides (formerly called N. farcinica); lesions are typically associated with lymphangitis and lymphadenitis

270
Q

Nocardia asteroides

A

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

271
Q

In horses, N. asteroides and N. braziliensis can cause

A

n horses, N. asteroides and N. braziliensis can cause fibrinopurulent pneumonia and pyothorax with sulfur granules

272
Q

In humans, most patients with N.asteroides infections have

A

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

273
Q

Disease for Norcarida

A

Not usually pathogenic for immunocompetent individuals

• Causes pyogranulomatous infections

(thorax, skin, mammary gland, systemic)

Feline pyothorax

274
Q

Malitof

A

mass spec is what we use

275
Q
A

Nocardia mastitis

276
Q

Diagnosis, Treatment, Control for Norcarida

A
  • 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)

277
Q

Casoeus lymphadenitis in sheep is caused by:

A

Corynebacterium psuedotuberculosis

278
Q

Casoeus lymphadenitis is a contagious disease T/F

A

TRUE

279
Q

Positive antibody titers to phospholipase D extoxin of c. Pseduotuberculosis is diagnostic for Caseous lymphadentitis.

T/f

A

FALSE- one titer is not diagnostic; it can be positive due to exposure or previously having the disease

280
Q

Rhodococcus equi is an olbigate intracellular pathogen T/F

A

FALSE- It is NOT obligate- it can be extracelluar as well as intracellular

281
Q

Toxin and capsule are required for the virulence of bacillus anthracis. T/F

A

TRUE

282
Q

Antibiotics from Actinomycets

A

Amphotericin Chloramphenicol
Tetracycline

Erythromycin

Neomycin

Streptomycin

Gentamicin

283
Q

actinomycets

A

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”

284
Q

Actinomyces, Actinobaculum and Trueperella

A

Frequently associated with pyogenic infections in livestock,

Eg. Trueperella pyogenes
(formerly Corynebacterium, Actinomyces, and Arcanobacterium pyogenes)

285
Q

Disease from actinomycetes

A

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)

286
Q

Actinomyces bovis

A

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).

287
Q

Actinomyces hordeovulneris

A

Foxtail (grass awns)

288
Q

Diagnosis, Treatment, Control for Actinomyctes

A

• 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

289
Q

Dermatophilus congolensis

A

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.

290
Q

Disease for D. congolensis

A

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
291
Q
A

D. congolensis

292
Q
A

Rain Scald- D. Congolensis

293
Q
A

D. congolensis or strawberry foot rot in cattle

294
Q

Diagnosis, Treatment, Control for D. congolensis

A
  • 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

295
Q
A

D. congolensis- on cows in St. Kitts

296
Q

Trueperella pyogenes

A

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

297
Q

Trueperella pyogenes in Cattle

A

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

298
Q
A

Trueperella pyogenes

299
Q

Actinobaculum suis

A

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
300
Q

Summer mastitis

A

is a communicable disease among pastured daily cattle during the dry period

Trueperella pyogenes in Cattle

301
Q

What are the two spore forming bacterias?

A

Anthrax and Clostridium

302
Q

Tyzzers disease

A

Clostridium piliforme
A Gram negative Clostridium which causes Tyzzers disease in laboratory animals

303
Q

Clostridium spp.

A

Large, endospore-forming, Gram-positive rods

Except for

Clostridium piliforme
A Gram negative Clostridium which causes Tyzzers disease in laboratory animals

304
Q

Clostridium

A

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)

305
Q

Virulence Factors of Clostridium

A

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

306
Q

Clostridium tetani

A
  • 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

307
Q
A

Clostridium tetani;

called “wooden horse” in horses

308
Q

Diagnosis of C. tetani

A
  • 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
309
Q

Treatment of C. tetani

A

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

310
Q

Control of C. tetani

A

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

311
Q

Clostridium botulinum

A
  • 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”
312
Q

Clinical Signs of C. Botulinum

A

• 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

313
Q
A

C. botulinum

314
Q

botulism is called _____ in poultry

A

limberneck

315
Q

Diagnosis of C. botulinum

A

Demonstration of toxin in serum of animal Demonstration of toxin in food/stomach contents (mouse bioassay/neutralization test- gold standard) MALDI TOF

316
Q

Treatment of C. botulinum

A

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)

317
Q

Control of C. botulinum

A

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)

318
Q

botulism is very common in_____

A

aquatic birds because they eat maggots

319
Q

Histotoxic Clostridia

A

C. chauvoei

C.septicum
C. novyi

Less potent

Toxins Invasive

infections Myositis

320
Q

Histotoxic Clostridial Diseases

A

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

321
Q

Clostridium species frequently associated with

A

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

322
Q

Gas gangrene, Black disease(necrotic hepatitis)

A

C. novyi (A, B , C)

323
Q

Black leg

A

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
324
Q

Malignant edema, Braxy, Necrotic dermatitis (chicken)

A

C. septicum

325
Q

Necrotic hepatitis

A

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

326
Q

Disease of Clostridium

A
  • 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

327
Q

Malignant edema

A

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.

328
Q

Diagnosis, of clostridial necrotic myositis

A

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

329
Q

Treatment, Control of necrotic myositis

A

Treatment: antimicrobial treatment (penicillin) (only effective if given early)

hyperbaric oxygen
surgical debridement/amputation

• Control: routine vaccination of farm animals with multicomponent bacterin/toxoids

330
Q

Enteric Clostridium

A
  • C. perfringens
  • C. difficile
  • C. spiroforme necrotic/hemorrhagic enteritis, necrotic hepatitis enterotoxemia
331
Q

C. perfringens

A

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

332
Q
A

C. perfringens

333
Q

C. perfringens Type D enterotoxemia

A

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)

334
Q
A

C. perfringens Type D enterotoxemia

335
Q

pulpy kidney disease

A

Rapid postmortem autolysis of the kidneys

C. perfringens Type D enterotoxemia

336
Q

Diagnosis and treatment for C. perfringens Type D enterotoxemia

A

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

337
Q

Clostridium difficile enterocolitis

A

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
338
Q

Actinomyces bovis can be acid fast positive by Kinyoun’s staining protcol. T/F

A

FALSE- it doesn’t have mycolic acid

339
Q

What type of culture would you request from a lesion like this in a dog?

A

Aerboic and anerobic culture- absyess submit both!

340
Q

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

A

C

341
Q

Trueperella pyogenes is a common bacterial isolate form pyogenic lesions of internal organs in cattle. T/F

A

True

342
Q

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

A

B

Corynebacterium renele causes pyelonepritis in cattle

343
Q

Dysbiosis

A

when the normal flora of the GI tract is disturbed- these cause Pseudomembraneous colitis which causes

344
Q

Clostridium difficile toxins

A

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

345
Q

Approaches to diagnosis of Clostridium difficile diarrhea

A

• 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)

346
Q

Approaches to treatment of C. difficile diarrhea

A
  • 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)
347
Q

Clostridium spiroforme and Rabbits

A

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.

348
Q

Tyzzer’s Disease

A

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

349
Q

Non-Sporeforming Anaerobes

A

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

350
Q

Virulence Factors OF Non-Spore forming Anaerobes

A
  • 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

351
Q

Anaerobic Infections

A

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

352
Q

Signs consistent with anaerobic infection

A
  • 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

353
Q

Fusobacterium necrophorum

A

leukotoxin- kills leukocytes

354
Q

Anaerobic, Non-sporeforming Gram-

negative Rods

A

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)

355
Q

Fusobacterium necrophorum

A

Liver abscess

Foot Rot

extensive necrosis and keratinolysis in severe cases

356
Q

Control of Fusobacterium necrophorum

A

• Control:

  • keep feet dry, avoid mechanical injury
  • parasite control, routine immunizations,

good nutrition, dental prophylaxis, etc.
- vaccines: sheep & cattle (Fusobacterium necrophorum)

sheep (Dichelobacter nodosus

357
Q

aminoglycosides you don’t use in

A

anerobic infection

358
Q

Diagnosis, Treatment, Control of fusobacterium ncrophorum

A
  • Diagnosis:
  • Culture, (PCR?) • Treatment:
  • remove necrotic tissue, oxygenate, antiseptic foot baths - antimicrobials - penicillin, metronidazole, clindamycin,

chloramphenicol, doxycycline

(aminoglycosides, sulfonamides not effective)

359
Q

Anaerobe identification

A

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)

Bact (34 decks)

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