• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/476

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

476 Cards in this Set

  • Front
  • Back

Nutrient agar

Basic media for non-fastidious bacteria

blood agar

enriched media


most pathogenic bacteria


allows for recognition of hemolysis

MacConkey agar

selective medium


gram (-) bacteria

Eosin Methylene Blue (EMB) agar

selective medium


gram (-) bacteria

Columbia Nalidixic Acid (CNA)

selective medium


gram (+) bacteria

Chocolate agar

for fastidious bacteria

Brilliant green agar

for salmonella

Trypticose Soy Broth

general purpose medium


aerobic bacteria

Buffered-peptone water

non-selective medium to low number of pathogens in environment and feed

Selenite broth

selective enrichment medium


Salmonella spp

Hayflick liquid medium

selective enrichment medium


Mycopasma spp

UVM medium

selective medium


Listeria spp

Selective media

-contains substances to either:


+enhance growth of particular organisms


+inhibit growth of unwanted organisms


-dyes (eosin, methylene blue), pH, NaCl, antimicrobials, etc


GasPak system

anaerobic bacteria


-use reducing media containing compounds like sodium thioglycollate


-plates placed in sealable containers utilizing chemicals to provide oxygen-free environment

Streak-plate method

Pour-plate method

Confirming presence of pathogenic bacteria


(3 ways)

-stained smears


-cultural & biochemical characteristics


-detection by immunological & molecular methods

Gram stain

Widely used
-crystal violet retained by gram (+)
-crystal violet not retained by gram (-)

Widely used


-crystal violet retained by gram (+)


-crystal violet not retained by gram (-)

Giemsa stain

Dermatophilus congolensis
Rickettsia
Babesia
Anaplasma
Borrellia

Dermatophilus congolensis


Rickettsia


Babesia


Anaplasma


Borrellia


Ziehl-Neelsen (acid-fast) stain

Mycobacterium spp
Actinomycetes
(red=positive)

Mycobacterium spp


Actinomycetes


(red=positive)


Carbol fuchsin stain

Campylobacter
Brachyspira
Fusobacterium
(stain red)

Campylobacter


Brachyspira


Fusobacterium


(stain red)

Basic criteria for presumptive ID

-colonial morphology and color


-presence/absence of hemolysis


-appearance on gram staining/ability to grow on MacConkey


-motility


-reaction to biochemicals (catalase & oxidase test)

Biochemical tests

-sugar fermentation


-triple sugar iron (TSI)


-sulfide indole motility (SIM)


-urease

Particular tests

-CAMP reaction


-Coagulase


-Hemagglutination


-Nagler test

ID'ing oxygen requirements

Immunological techniques

-fluorescent antibody tests (Leptospira, Clostridium)


-ELISA tests (Clostridium difficile)


-Agglutination tests (Salmonella typing, Taylorella)

Phage typing

-use of well-characterized lytic phages to ID specific bacteria


-causes lysis of bacteria


-special labs for Salmonella and Staphlyococcus

Molecular techniques

PCR tests


-Mycrobacterium paratuberculosis


-Mycoplasmsa bovis


-Moraxella differentiation


-Genotyping C. perfringens and C. difficile


-Leptospira


-Salmonella



DNA sequencing

Bacteria & Archaea

-prokaryotic


-no nuclei


-single chromosome (usually)


-asexual reproduction


-great majority don't cause disease


-archaea often isolated from extreme environments

Fungi

-eukaryotic


-have cell walls


-molds and yeasts

molds

-multicellular


-filamentous growth


-sexual and asexual spores

Yeast

-unicellular


-oval to round


-reproduce by budding

protozoa

-single-celled eukaryotes


-most capable of locomotion by pseudopodia, cilia, or flagella


-most asexual

algae

-unicellular/multicellular photosynthetic organisms


-make own food from CO2 and water using energy from sunlight

Viruses

-smaller than prokaryotes


-not visible by light microscope


-acellular


-obligate intracellular

prokaryotic cells

-nucleoid not surrounded by nuclear membrane


-usually single chromosome


-no membrane-bound organelles


-minute size


-binary fission


-no cytoskeleton


-ie bacteria

eukaryotic cells

-nuclear material surrounded by nuclear membrane


->1 chromosome


-membrane-bound organelles


-fairly large


-mitosis/meiosis


-cytoskeleton


-ie fungi, algae, plant, mammalian cells

prokaryotic capsule/glycocalyx

-gelatinous, sticky substance surrounding cell


-composed of polysaccharides, polypeptides, or both


+made inside cells and extruded onto cell's surface (K-antigen)


prokaryotic capsule/glycocalyx

-protect bacteria from immune system cells and desiccation


-virulence factor


-numerous pathogenic bacteria (Bacillus antracis, Klebsiella pneumoiae)

flagella

-mostly gram (-) bacteria


-bacterial movement


-virulence factor

flagella

3 parts:


-filament (flagellin protein)


-hook


-basal body (bacterium)



-differences in flagella proteins may allow classification of species into serovars

fimbriae

-for movement & adherence to each other & environment


-up to 100's on the cell


-shorter than flagella


-important function in biofilms



Pili (conjugation pili)

-transfer of DNA from one cell to another

Bacterial cell walls

-provide structure and shape


-protect cell from osmotic forces


-assist in attaching to other cells


-resisting antimicrobial drugs


-target for antibiotics


-give bacteria characteristic shapes


-mainly composed of peptidoglycan

Gram staining procedure

1. slide flooded with crystal violet, then rinsed in water. all cells purple


2. slide flooded in iodine, then rinsed in water. all cells purple


3. slide flooded in ethanol and acetone, then rinsed with water. Gram (+) remain purple, gram (-) colorless


4. slide flooded with safranin, then rinsed with water and blotted dry. Gram (-) pink.

Bacterial cytoplasmic membranes

-fluid mosaic model controls passage of substances into/out of phospholipid bilayer:


+hydrophilic heads


+hydrophobic hydrocarbon tails


-membrane proteins for recognition, enzymes, receptors, carriers, and channels


Plasma membrane function

-selectively permeable


-naturally impermeable to most substances


-proteins allow substances to cross membrane


-maintain concentration & electrical gradient


-site of electron transport for respiration

Passage of substances from membrane

-passive (smaller molecules)


+diffusion


+facilitated diffusion


+osmosis


-active processes


+active transport


+group translocation

cytoplasm

-water (mostly) + dissolved/suspended substances (ions, carbohydrates, proteins, enzymes, lipids, DNA, RNA, wastes)


-chemical reactions occur


-houses storage granules (lipids, starch, etc)

ribosomes

-sites of protein synthesis


-prokaryotic ribosomes different than eukaryotic


+50S + 30S


-some antimicrobial drugs target protein synthesis

nuclear material

-single haploid circular chromosome


-extensively folded with small amounts of protein & RNA


-some 2 circular chromosomes, 1 linear chromosome, plasmid

protein secretion systems

-mechanisms to transport large molecules through complex membranes and cell walls


-gram (-) bacteria (esp) have evolved secretion pathways

effector proteins

-proteins transported through secretion systems


-includes enzymes (proteases, lipases, cytotoxic/apoptosic proteins)

endospores

-produced for durability and pathogenicity


-high content of dipicolinic acid and calcium


-resistant to drying, pasteurization, radiation


-ie Bacillus anthracis, Clostridium tetani, Clostridium perfringens

biofilms

-bacterial populations adherent to each other &/or surfaces


-enclosed in a biopolymer matrix


-immobile form


-complex relationships among numerous microorganisms


biofilms

-develop extracellular matrix


-allows attachment to substrate


-drug penetration difficult


-microorganisms more harmful as part of a biofilm

formation of endospore

endospore germination

-initiated when conditions are favorable


-heat, warm weather, nutrients

microbial growth

increase in a population of microbes that results in either:


-discrete colony-aggregation of cells arising from a single parent cell


-biofilm-collection of microbes in the surface of a complex community

typical microbial growth curve

binary fission

generation time

time required for bacterial cell to grow and divide


-dependent on chemical and physical conditions

obligate aerobes

oxygen is essential

obligate anaerobes

oxygen is deadly


-toxic forms of O2 are highly reactive and excellent oxidizing agents


-resulting oxidation causes irreparable damage to cells

ID oxygen requirements

nitrogen requirements

-anabolism often ceases due to insufficient nitrogen


-acquired from organic & inorganic nutrients


-cells recycle nitrogen from amino acids and nucleotides


-nitrogen fixation by certain bacteria essential to life on earth

chemical requirements

-phosphorus-membrane/cell wall, DNA, RNA, ATP


-sulfur-disulfide bonds of proteins


-trace elements required in small amounts (se)


-growth factors-some amino acids, purines, pyrimidines, NADH, heme

effect of temperature on growth

-too low, membranes become rigid and fragile


-too high, membranes become too fluid



pathogenic bacteria usually can't grow outside specific temperature range

psychrophiles

-5C to 20C

mesophiles

most of the pathogenic bacteria



15C to 45C

thermophiles

42C to 80C

hyperthermophiles

polymerases for PCR reactions



67C to 105C

pH requirement

organisms sensitive to changes in acidity


-H+ and OH- interfere with H-bonding



Neutrophiles

grow best in narrow range around neutral (7) pH



most pathogens grow best around neutral pH

Acidophiles

grow best in acidic (<7) pH


-yeast (Candida) and Clostridium difficile

physical effects of water

-osmotic pressure


-hydrostatic pressure



-microbes require water to dissolve enzymes, nutrients


-most cells die in absence of water


-some have cell walls the retain water (Mycobacterium spp)


-Endospores & cysts-most metabolic activities stop

culturing microorganisms

-cultivating microorganisms


-inoculum introduced into medium

obtaining pure cultures

-cells arising from a single progenitor


-aseptic technique prevents contamination of sterile substances/objects


-streak plates


-pour plates

colony forming unit

-progenitor of cells

characteristics of bacterial colonies

culture media

some microorganisms don't require specific nutrients (E. coli), but some do (Haemophilus somni)


-liquid & solid media


agar

complex polysaccharide


-most microbes can't digest agar


-powdered agar dissolves at 100C


-solidifices at 40C

solid media

-blood agar


-MacConkey


-Hekton


-CNA


-urease slant


-citrate slant

defined media

know concentration of each ingredient in media

complex media

contains variety of nutrients released by partial digestion of yeast, soy, beef, or casein


-exact chemical composition unknown


-blood often added to provide NADH and heme

selective media

contains substance either to encourage growth of particular organisms or inhibit growth of unwanted organisms


-some dyes (eosin, methylene blue), pH, NaCl, antimicrobials used

differential media

used to differentiate microorganisms


-visible changes in medium or differences in appearance of colonies


-many media selective & differential

transport media

used for carrying clinical specimens


-feces, saliva, sputum, blood


-Amie's transport medium + charcoal

special culture techniques

-low-O2 culture-microaerophiles


-enrichment culture-enhancing growth of less abundant microbes in specimen


-cold enrichment-cold tolerant microbes (Listeria, Vibrio cholerae)


-animal-no growth in liquid media (M. laprae-armadillos; Treponema pallidum-rabbit)


-cell culture-viruses, rickettsias

direct method


(measuring microbial reproduction)

-serial dilution & viable plate counts


-membrane filtration


-most probable number


-microscopic counts


-electronic counters

serial dilution & viable plate count

membrane filtration

-used when population density is low



pic

cell counter

-no incubation required



pic

indirect methods


(measuring population size)

-metabolic activity


-turbidity


-dry weight


-genetic methods

metabolic activity

measure nutrient utilization, waste production, pH

turbitidy

MacFarland for antimicrobial susceptibility, spectrophotometer


dry weight

filtered, dried, weighed

genetic methods

isolate total DNA of microorganism


-perform real-time PCR


-UV spectrophotometry of DNA


-used to estimate number of microbes

refrigeration


preserving cultures

stores for short periods of time

deep-freezing


preserving cultures

stores for years

lyophilization


preserving cultures

stores for decades

role of HEPA filters

prevents human contamination from specimen



pic

tissue & organ specimens

-suitable portions placed in individual polyethylene bags/suitable leakproof container


-portions of intestine (tied off) should be packaged separately

swab specimens

-abscesses


-nasal passages


-pharynx


-tonsil


-eye


-ear


-skin


-vagina/cervix



prevent drying by using suitable transport medium

fecal specimen

-preferably obtained directly from rectum in manner that avoids contamination


-avoid submission of fresh droppings


-place in leak-proof container and ship immediately

milk specimen

collected aseptically using sterile screw-capped/stoppered vials (not bags)


-should be refrigerated immediately following collection


-deliver to lab under refrigerated conditions

urine specimen

collected aseptically


-refrigerated immediately


-avoid free-catch samples


-minimum 5mL urine

antrax, plaque, tularemia, foreign diseases


special considerations

clearly label all boxes & bags to avoid exposure to lab personnel

antrax


special considerations

cotton swabs soaked in extruded blood/blood taking from superficial ear vein


-swine-swabs taken from exudates & cut surfaces of hemorrhagic lymph nodes

blackleg, malignant edema


special considerations

submission of fresh affected tissues


-clostridium rapidly invades tissues after death


-2 impression smears on glass slides

clostridial enterotoxemia


special considerations

several ounces of fresh intestinal contents or tied-off section of affected intestine

Johne's disease


special considerations

fecal specimen from live animals

Campylobacteriosis


special considerations

-semen, preputial washing, fetal stomach contents, cervical mucus obtained aseptically


-refrigerated & delivered to lab within 5-6 hours of collections


-OR frozen as soon as collected with dry ice and shipped in insulated container with adequate amount of dry ice

Brucellosis


special considerations

placenta, stomach content of aborted fetus, mammary lymph nodes, milk samples preferred


-shipped under refrigerated conditions

Listeriosis


special considerations

submit brain stem sample and indicate Listeria is suspected

fungal isolations

take up to 3 week before reported out


-collect samples aseptically before antifungal therapy

fungal specimens

-superficial mycoses-hair & skin scrapings from edge of active lesions


+submit in small paper envelope


+saprophytic fungi will proliferate rapidly and overgrow ringworm fungi in sealed container


-deep-seated mycoses-tissues & organs as for bacteriology

drug

chemical that affects physiology in any manner

antimicrobial agent

-drug that treat infections


-kill or inhibit growth of susceptible microorganisms

Paul Erlich

-"magic bullets"


-arsenic compounds that killed Treponema pallidum (causative agent of syphillus)


Gerhard Domgak

-Prontosil red for Streptococi infections


-Converted to sulfanilamide in body by liver

Alexander Fleming

-Penicillin released from Penicillium sp.

Selman Wkasma

-Antimicrobial agents produced naturally by organisms


-Other antibiotics-streptomycin

Selective toxicity

more toxic to pathogen than host


-based on differences of biochemical, structural, or metabolic pathways between bacteria and eukaryotes

Bactericidal

drugs that kill bacteria

bacteriostatic

drugs that inhibit bacterial pathogenity

Ratio of drugs available

Antibacterial>antifungal>antiviral

Inhibition of cell wall synthesis

-prevent cross-linkage of NAM subunits in peptidoglycan layer


-prevent bacteria from increasing amount of peptidoglycan

Beta-lactams

-functional groups are beta-lactam rings


-bind to enzymes that cross-link NAM subunits



-Penicillins


Cephalosporins

Beta-lactams: affect existing peptidoglycan layer?

-NO!


-bacteria have weakened cell walls and eventually lyse due to increased osmotic pressure inside cell

Vancomycin & cycloserine mechanism

-interfere with particular bridges that link NAM subunits


-many gram (+)

Bacitracin mechanism

-blocks secretion of NAG and NAM from cytoplasm

Isoniazid and ethambutol mechanism

-disrupt mycolic acid formation in mycobacterial species

Semi-synthetic beta-lactam derivative benefits

-more stable in acidic environments (stomach)


-more readily absorbed


-less susceptible to deactivation


-more active against more types of bacteria

monobactams vs synthetics/semisynthetics (amoxicillin, ampicillin)

monobactams-effective ONLY against aerobic gram (-)



synthetics-more effective on gram (+)

Inhibition of protein synthesis

-prokaryotic ribosomes 70S (30S & 50S)


-eukaryotic ribosomes 80S (40S & 60S)


+mitochondria contain 70S-drugs can be more toxic with more adverse effects


-drugs selectively target translation

different mechanisms of inhibiting protein synthesis

Aminoglycosides

-used topically-not absorbed well orally


-little activity against anaerobes



-amikacin, kanamycin, neomycin, tobramycin, spectionomycin

tetracyclines

-block docking site of mRNA



-large spectrum


-shouldn't be used in pregnant animals



-textracycline, doxycycline, minocycline

chloramphenicols

-binds and blocks binding site of amino acids



-chloramphenicol, florfenicol

macrolides

-bind to 50S subunit, blocking proper mRNA movement through ribosome, stopping synthesis



-enytromycin, axithromycin, claritromysin, tylosin


-mainly affect gram (+) cocci and intracellular pathogens

disruption of cytoplasmic membrane

-form channel through cytoplasmic membrane and damage integrity

polymyxin

-disrupts cytoplasmic membranes of gram (-)


-toxic to kidneys

amphotericin b

-attaches to ergosterol in fungal membranes


-bacteria lack sterols, so not susceptible

inhibition of nucleic acid synthesis

-block DNA replication or mRNA transcription



-often affect eukaryotic & prokaryotic cells



-limited clinical use-except quinolones and fluoroquinalones

quinolones and fluroquinolones

-act against prokaryotic DNA gyrase and topoisomerase IV

rifampin

-inhibit RNA polymerase during transcription

reverse transcriptase inhibitors

-acts against enzyme of retroviruses


-don't harm mammalians because they lack reverse transcriptase

inhibition of metabolic pathways

-effective when metabolic processes of pathogen & host differ

sulfonamides

-structural analogs


 

-structural analogs


heavy metals

-inactivate enzymes

clinical considerations

-ideal antimicrobial agent


-spectrum of action


-efficacy


-routes of administration


-safety & side effects

ideal antimicrobial agent

-readily available


-inexpensive


-chemically stable


-easily administered


-nontoxic & nonallergenic


-selectively toxic against wide range of pathogens

spectrum of action

-number of different pathogens a drug acts against



-narrow-spectrum effective against few organisms



-best to perform antimicrobial susceptibility test before starting treatment

broad-spectrum

-effective against many organisms


-may allow for secondary or superinfections to develop


-killing of normal flora reduces microbial antagonism

efficacy

ascertained by


-diffusion susceptibility test


-minimum inhibitory concentration (MIC) test


-minimum bactericidal concentration test

minimum inhibitory concentration teset

-lowest concentration of antimicrobial that prevents visible growth of microorganisms in a broth dilution susceptibility test

Susceptible

an infection due to the isolate may be treated in body sites with the recommended dosage

resistant

isolates are not inhibited by the usual achievable concentration of a drug and not reliable in treatment

intermediate

infection due to isolate may be treated in body sites where high dosage of the drug can be used

no interpretation

no interpretative criteria established yet

routes of administration

-topical-external infections


-oral-no needles


-IM-via needle into muscle


-IV-via needle into bloodstream



must know how antimicrobial agent will be distributed to infected tissues

toxicity

-cause of many adverse reactions poorly understood



-may be toxic to kidneys, liver, or nerves



-pregnant animals need extra consideration

allergies

-rare, but may be life-threatening


-anaphylactic shock

disruption of normal microbiota

-may result in secondary infections


-overgrowth of normal flora causes superinfections


-greatest concern in hospitalized animals

resistance to drugs

-some pathogens naturally resistant



acquired in 2 ways:


-new mutations of chromosomal genes


-acquisition of R-plasmids via transformation, transduction, and conjugation

mechanisms of resistance

-produce enzyme that destroys or deactivate drug


-slow or prevent entry of drug into cell


-alter target of drug so it bind less effectively


-alter their metabolic chemistry


-pump drug out of cell before it can act


-biofilms retard drug diffusion and slow metabolic rate


-Mycobacterium tuberculosis produces MfpA protein, binds DNA gyrase depriving fluoroquinolones

multiple resistance

-pathogen can acquire resistance to more than 1 drug


-common when R-plasmids are exchanged


-develop in animal hospitals


+constant use of drugs eliminates sensitive cells


-superbugs

cross resistance

resistance to structurally similar drugs at the same time

limiting antibacterial resistance

-effective surveillance systems for collection of data at local & national level


-treatment based on susceptibility test results


-strict adherence to drug withdrawal periods in food-producing animals


-maintain high concentration of drug in patient for sufficient time


-use only when necessary


-use in combination

synergism

two agents enhancing the individual effects of drugs

Trueperella (Arcanobacterium) pyogenes pathogenicity

opportunistic causing suppurative lesions


-hemolytic toxin pyolysin causes pus formation


-neurominidases, extracellular matrix proteins, and fibria


-proteases

Trueperella (Arcanobacterium) pyogenes


species

cattle, pigs, sheep

Trueperella (Arcanobacterium) pyogenes


affected area

any organ system


-bovine pneumonia


-hepatitis


-osteomyelitis


-peritonitis


-cerebral abscesses


-lymphadenitis


-mastitis

Trueperella (Arcanobacterium) pyogenes


appearance on culture

-small hemolytic colonies in BAP


-typical pleomorphic cell morphology in gram stain

Trueperella (Arcanobacterium) pyogenes


treatment

-based on antimicrobial susceptibility test


-resistance to macrolides and tetracyclines



-feedlot cattle receive sub-therapeutic doses of tylosin (macrolide) as prophylaxis against liver abscessation



-no vaccine

Actinomyces bovis


disease

bovine actinomycosis-lumpy jaw


-assumed to invade following trauma


Actinomyces bovis


affected area

-mandible


-maxilla less common


causes chronic osteomyletis



-min involvement with regional lymph nodes


-swelling painful


-fistulous tracts

Actinomyces bovis


diagnosis

-advanced cases-distinctive clinical signs


-radiography


-bacterial culture

Actinomyces bovis


culture appearance

-filamentous branching


-non acid-fast (purple)

Actinomyces bovis


treatment

-small lesions: surgery


-adv cases: surgery unrewarding



prolonged therapy with penicillins



sodium iodine-IV multiple times

Actinomyces viscosis


disease

canine actinomycosis


-A. canis and A. hordeovulnaris also isolated in similar conditions

Actinomyces viscosis


affected area

extensive fibrovascular proliferation on the peritoneal and pleural surfaces


-with sanguinopurulent exudate


Actinomyces viscosis


gross apperance

Actinomyces viscosis


diagnosis

bacterial culture

Actinomyces viscosis


treatment

penicillins

Nocardia sp


characteristics

-gram (+)


-aerobic


-inhabitant of soils rich in organic matter


-opportunistic infections




Nocardia sp


smear characteristics

-smears: long, slender, branching filaments


+partial acid-fast


+gram staining (+)


Nocardia sp


pathogenesis

-assc with immunosuppression or heavy challenge


-usual mode of infection: inhalation


+may occur by skin wounds and teat canal


-supreoxide disnutase, catalase, and thick peptidoglycan confer resistance


Nocardia sp


culture characteristics

-culture: produce aerial filaments


+may have spores


+white, powdery, odorless, firmly adherent to agar



-grow in Sabouraud agar



Nocardia sp


sequencing

-16S rRNA DNA sequencing

Nocardia asteroides


common name

Canine nocardiosiis

Nocardia asteroides


affected systems

-pulmonary


-cutaneous


-CNS

Nocardia asteroides


pulmonary

-develop from inhalation


-not typically seen


-mostly in dry, warm climates

Nocardia asteroides


cutaneous

-result from intro of bacteria into wounds


-may produce mycetoma

Nocardia asteroides


CNS

-result from spread of bacteria in blood


-meningitis in humans-inhfalation to blood

Nocardia asteroides


tx + control

-tx less effective than for canine actinomycosis


+intrinsically resistant


-susceptibility using broth microdilution


-amikacin, imipenem-cilastatin, TMX usually effective


-prevention-avoiding exposure to bacteria in soil

Bovine nocaridal mastitis


characteristics

-chronic bovine mastitis


-usually sporadic cases


-diffuse or multifocal fibrosis


-white clots intermittently in milk


-systemic reactions may be induced during early lactation

Bovine nocaridal mastitis


tx

-difficult to treat


-dry-cow therapy with neomycin could be effective

Bovine nocardiosis


common name + distribution

bovine farcy


-limited to tropical areas


-Mycobacterium spp also isolated

Bovine nocardiosis


systems affected

chronic infection of superficial lymphatic vessels and lymph nodes


+thickened and cord-like


-nodules on the medial aspects of legs and on neck

Actinobaculum suis


common name/disease

porcine cystitis and pyelonephritis

Actinobaculum suis


pathogenecity

-causes cystitis and pyelonephritis in breeding pigs (mostly female)


-ascending infection


Actinobaculum suis


predisposing conditions

-mating


-trauma to urogenital tract


-presence of other organisms


-water restriction


Actinobaculum suis


presentation

-sudden death with or without clinical signs


-hematuria, azotemia


-mild fever


-painful urination


-arching of back

Actinobaculum suis


diagnosis

-gram stain (+)


-culture


-PCR


-immunofluoresence

Actinobaculum suis


tx

penicillin


ampicillin

Dermatophilus congolensis


smear characteristics

-gram (+)


-filamentous


-branching


-produces motile coccal zoospores

Dermatophilus congolensis


predisposing factors + pathogenesis

-maybe present in skin of healthy animals


-trauma and persistent wet conditions


-when activated, zoospores produce germ tubes and invade epidermis



-cyclical pattern or invasion/regeneration of epidermis, serous exudation and microabscess formation lead to raised scab-like crusts

Dermatophilus congolensis


virulance factors

-phospholipases


-proteolytic enzymes


-ceramidase

Dermatophilus congolensis


dx

-clinical picture


-scab material & skin in formalin


-smears from undersurface of scabs for Giemsa


-cultured on BAP


+small, yellowish, hemolytic colonies


-no growth in Sabouraud agar


-16S DNA sequencing

Dermatophilus congolensis


clinical picture

-dorsal areas of animals


+prolonged rainfall


+warm environment


-early lesions appear as papules


-serous exudate and inflammation produces adherent scabs

Dermatophilus congolensis


tx

-localized lesions can resolve spontaneously


-systemic long-acting oxytetracycline or penicillin/streptomycine


-topical tx ineffective

Nocardioform placentitis


causative agents

Crossiella equi


Amycolatopsis spp

Nocardioform placentitis


pathogenesis

gram (+) filamentous branching bacteria


-causes brown mucoid placentitis


-sporadic

Nocardioform placentitis


clinical signs

-premature udder development/lactation


-vulvar discharge



<1/2 mares exhibit signs

Nocardioform placentitis


dx

-ultrasound exam

Nocardioform placentitis


outcomes

-abortion


-premature foal


-term, but compromised foal


-normal foal



mare clears infection rapidly, rebreeds normally, not at increased risk of subsequent abortion

Trueperella (Arcanobacterium) pyogenes

Actinomyces bovis

Nocardia asteroides


canine nocardiosis

Dermatophilus congolensis

Nocardioform placentitis


Crossiella equi


Amycolatopsis spp

Diseases associated with Staphylococcal sp

infections of dogs and cats, S. intermedius(S. pseudointermedius)
staphylococcal mastitis, S. aureus
exudative epidermitis–S. hyicus
Omphalitis– S. aureus
Botryomycosis– S. aureus
Tick Pyemia– S. aureus
Methicillin resistant Staphylococcal infections

Causative agent of Staphylococcal infections in dogs and cats

S. intermedius(S. pseudointermedius)

Staphylococal infections of cats and dogs are
opportunistic pathogens
staphylococcal diseases of cats and dogs cause

suppurative conditions: dermatitis, pyoderma, otitis externa, endometritis, cystitis, osteomyelitis and wound infections

symptoms of staphylococcal diseases of cats and dogs
fever, pain, loss of appetite, itching, pus filled lesions such as pyoderma
who is more susceptible to staphylococcal diseases of cats and dogs and why

younger and older dogs due to weak immune system

staphylococcal diseases of cats and dogs; cystitis cases signs and symptoms

often urination, urinalysis may indicate increased protein and hemoglobin

staphylococcal diseases of cats and dogs; diagnosis
clinical signs
gram staining of clinical specimen
culture and/or biopsy
When obtaining specimen for bacteriological culters one must

–avoid superficial contamination
–special swab protected by a sterile otoscope for otic specimens
–skin shaved and disinfected for blood specimens
–urine collected by cystocentesis, catherter or midstream(clean catch)
–swabs should be kept in transport media, kept cold and submitted to lab ASAP

staphylococcal diseases of cats and dogs: Tx

–stop itching and scratching for skin diseases
topical therapy may be effective in uncomplicated superficial infections (combinations of silver sulfadiazine, mupiracin, fusidic act etc)
–susceptible to antimicrobials including beta lactams though some multi resistance strains(MRS) detected
–for urinary infections drugs excreted by urine should be chosen for up to 2 weeks

Staphylococcal mastitis
common form of mastitis worldwide caused by S. aureus
–can be subclinical, chronic, and acute
–necrosis due to alpha toxins
transmission of Staphylococcal mastitis
contaminated hands and milking equipment
what could cause systemic reaction and be lethal in staphylococcal mastitis
peracute and gangrenous forms
symptom of gangrenous form of staphylococcal mastits

effected quarter is cold, dark and eventually sloughs

Staphylococcal mastitis Tx
–Cephalosporins, cloxacillin, erythromycin, penicillin
–if susceptible penicillin can be combined with novobiocin, pirliycin, tylosine or tilmicosin
Staphylococcal mastitis Tx concerns

–Antimicrobials administered by parenteral or intrammamary routes
–difficult to treat with success rate up to 60%
–intrammamary route advised: parenteral could be used during acute mastitis
–culture and susceptibility should be done

Desirable characteristic of antimicrobials to treat mastitis

–low MIC for pathogen
–high distribution and availability in mammary tissue
–low serum protein binding activity
–long half life

control plan for mastitis

–properly maintain of milking equipment
–hygienic milking practices
–post–milking teat disinfection
–antibiotic therapy for clinical cases and for dry cows
–culling of persistently infected cows

Exudative epidermitis
caused by S. hyicus in suckling and weaned pigs
characteristics of exudative epidermitis
widespread sebaceous secretion and exudation on skin surface and highly contagious
symptoms of exudative epidermitis
anorexic, depressed, febrile and non prutic dermatitis with greasy exudate
Mobidity/mortality of exudative epidermitis
20–100%/can reach 90% in litters
S. hyicus can be isolated from
healthy pigs' vaginal mucosa and skin
Exudatie epidermitis transmission
via minor abrasions on the skin
exudative epidermitis predisposing factors/major virulence factor
weaning/ exfoliative toxin
exudative epidermitis diagnosis
clinical: high mortality rate in oung pigs with exudative, non prutic skin lesions
laboratory: isolation and identification of S. hycus by culture
Tx of exudative epidermitis
early systemic antibiotic combined with topical antiseptics and/or antibiotics
control of exudative epidermitis

–strict isolation of infected pigs
–cleaning and disinfecting of contaminated buildings
–sows should be washed prior to farrowing with antiseptic soap

S. aureus infections in poultry

omphalitis– infection of yolk sac can be seen in young chicks
–skin injuries may cause localized abscesses like on the foot(bubblefoot)
–may also cause invasive infections in bones, joints, tendon sheaths, and sternal bursa

omphalitis causes
decreased weight gain and egg production and mortality
S. aureus infections in poultry diagnosis
E. coli and Pasteurela multocida may cause similar lesions in poultry so identification by culture
S. aureus infections in poultry Tx
AST must be performed due to common drug resistance
S. aureus infections in poultry prevention
–proper management to reduce injury and immunosuppression
–elimination of wood splinters, protruding wires of cages and fighting
–good litter management and hatchery management
Botryomycosis

–a chronic, suppurative condition often caused by S. aureus
–can occur within a few week of castration of horses due to infection of spermatic cord(schirrhous cord)
–can also happen in mammary tissues of sows, composed of fibrous tissue and pus

Tick pyemia
characterized by either septicemia and rapid death or by localized abscesses in many organs
predisposing factor for tick pyemia
Anaplasma phagocytophilum transmitted by ticks
confirmatory test for tick pyemia
microscopic identification of S. aureus in pus and isolation
tick pyemia Tx
–limited value
–prophylactic Tx of lambs can be initiated at age week 1
most MRS strains are
coagulase positive
MRS Tx

– limited options
–antimicrobial susceptibility must be performed
–vancomycin often the only drug of choice as well as oxazolidiones like Linezolid but never be used as a single agent to Tx MRSA infections

Diseases/important species of Streptococcus spp

–Strangles–S equi subsp equi
–Purpura hemorrhagca
–S. zooepidemicus and S.equisimilis
–S. canis
–Bovine streptococcal mastitis
–S. suis
–enterococcus spp

Strangles

–a febrile disease, with abscessation of lymph nodes, commonly in young horses that's highly contagious disease of horses
reportable disease

transmission of strangles
via purulent exudates or discharging absesses
–sales, shows, race–tracks increase the risk
Strangles:Clinical signs

–incubation period 3–6 days
–high fever, depression, and anorexia followed by oculonasal discharge which becomes purulent
–lymph nodes are swollen and painful characteristically submandibular lymph nodes are effected and eventually rupture discharging purulent highly infectious material
–guttural pouch empyema common
–most horses become immune with reinfection occurring in some horses

Strangles Morbidity/mortality
–up to 100%/less than 5%
–death due to complications
Strangles– diagnosis
–clinical signs and history of recent exposure to suspect animal
–must be differentiated from S. zooepidemicus and S. equisimilis for causing similar problems
–culture and PCR(tests are very sensitive to detect)
–colonies are beta hemolytic slightly mucoid
sugar fermentation tests help to differentiate
Strangles Tx

–Penicillin to in contact animals
–antimicrobial therapy is controversial for infected horses and limited if abscesses have formed
–carriers may be treated with local antibiotic treatment of guttural pouch
–ruptured abscesses should be flushed with 3–5%povidine–iodine solutions
–anti–inflammatory drugs for pain and fever

Strangles– Control

–isolation of suspected and infected horses
– isolated for 2 weeks when first introduced or when returning to property
–guttural pouch should be examined and tested by PCR to detect carriers
–live attenuated vaccines though may cause infections and side effects
–predisposing factors such as overcrowding should be avoided
–buildings and equipments should be cleaed following outbreaks

Purpura hemorrhagica

Strangles
Purpura hemorrhagica

immune mediated disease that may occur due to strangles
type 3 immune mediated vasculitis by damaging blood vessels leading to edema of head, ventral abdomen and libs and petechial hemorrhages of mucous membranes

Tx of purpura hemorrhagica

–dampening the immune response and removing the inciting cause
–started on dexamethasone to suppress the immune reaction
–then put on antibiotics to eliminate any underlying respiratory infections

Ascending placentitis associated with S. zooepidemicus and S. equisimilis being number 1 reason in horses

S. zooepidemicus and S. equisimilis

–mucosal commensals, opportunistic pathogens
–causes abortion, respiratory infections and suppurative conditions in horses, cattle, sheep and pigs

strangles like syndromes in horses reported in
S. zooepidemicus and S. equisimilis cases
Differentiation of S. zooepidemicus and S. equisimilis

–beta hemolytic colonies
– sugar fermentation tests and PCR
–must be differentiated from S. equi

Tx of S. zooepidemicus and S. equisimilis

–in early phase susceptible to beta lactams
–in early detection of placentitis tx could be effective
–no vaccines available

S. canis
S. canis
S. canis

–opportunistic pathogen causing neonatal septicemia, suppurative conditions(otitis externa, pneumonia, pleuritis, dermatitis, myositis, nephritis) and toxic shock syndrome in carnivores
–severe infections in puppies and kittens

S. canis infections diagnosis

–gram staining of exudate may reveal streptococci in chain
–culture of affected tissure reveals the presence of S. canis

Tx of S. canis
–usually susceptible to beta–lactams but Tx may not always be successful
–draining and flushing the abscesses hasten recovery
–dose could be higher than normally recommended because organisms could be harbored in the tonsillar crypts and pus
–cats with diskospondylitis may require up to 6 months of antimicrobial, usually starting with a parenteral injection then subsequent oral meds
Bovine streptococcal mastitis
three kinds
S. agalactiae
S. dysgalatiae
S. uberis
S. agalactiae
bovine streptococcal mastitis which colonizes milk ducts and produces intermittent acute infections
S. dysgalatiae
bovine streptococcal mastitis which is found in the buccal cavity, genitalia and skin and causes acute mastitis
S. uberis

bovine streptococcal mastitis which is a normal inhabitant of skin tonsils and vaginal mucosa, a major causative agent of mastitis usually without systemic signs.

Bovine streptococcal mastitis diagnosis
–clinical sins–inflammation of mammary tissue and clots in milk
–milk samples should be sent to lab for culture
differentiation of mastitis causing streptococci
by CAMP test and sugar fermentation tests
PCR also available
Tx of bovine streptococcal mastitis
susceptible antimicrobials following culture–tx success is high especially for S. agalactiae
for environmental streptococci dry season therapy
bovine streptococcal mastitis control

–milking hygiene
– biosecurity to limit reintroduction
–avoid cross–suckling in calves
–avoid any nutritional deficency
–minimize teat sealants prepartum
–cows that are refractory to tx should be culled

S. suis is recognized as
significant losses to pig industry
S. suis Lancefiled group D

–at least 35 serotypes with varying virulence
–serotype 2 is the most prevalent serotype

S. suis is associated with
–meningitis, arthritis, septicemia and bronchopneumonia of all ages
–sporadically can cause endocarditis, neonatal deaths and abortions
–respiratory cases are in conjunction with Mycoplasma spp and Pasteurella spp
S. suis pathogenesis
–capsule and an opacity factor are both essential pathogenic factors
–strains positive for suilysin, extracellular factor(EF), and muramidase released protein(MRP) are mose virulent
–adhesions such as fibronectin–binding protein are other factors
–hyaluronidase may facilitate local spread
S. suis Tx
–most strains susceptible to beta–lactams
–prophylactic long–acting penicillins can be given by injection to sows 1 week before farrowing and piglets during first 2 weeks of life
S. suis control
–bacteria tend to be endemic in a herd and eradication is not feasible
–improved husbandry needed
–vaccine are available but may not be effected mostly due to serotype differences
Enterococcus species

can cause opportunistic infections such as UTI and otitis in dogs, mastitis in cattle with E. faecalis most frequently isolated

Enterococcus species identification
–forms short chains and pairs and lacks a capsule
–previously classified with group D streptococci and reclassified as a separate genus
enterococcus species are found in
the human colon though rarely pathogenic at this site and can cause disease if introduced into other parts of body
Tx of enterococcus species

intrinsically resistant to many antimicrobials so difficult to treat making it a possible major health concern in humans

Enterococcus spp differ from streptocci by

–not sensitive to bile salts so will grow on MacConkey Agar
– some are motile

prevention of enterococcus spp

–difficult in health care setting
–patients often have weakened immune systems

bubblefoot from omphalitis

omphalitis

Staphylococcal infections in dogs and cats

Staphylococcal infections in dogs and cats

Staphylococcal mastitis

Corynebacterium spp morphology

–small, pleomorphic, gram +
–in stained smears appear Chinese letter characters
–relatively slow growth in lab media

Differentiating factors of corynebacterium spp

–most are catalase +, oxidase –,
–non spore forming
–pathogenic bacteria are non motile
–cause pyogenic infections

corynebacteriu spp pathogenesis and pathogenicity

–opportunistic pathogens
–pyrogenic organisms(with the exception of C. Bovis which can be isolated from teat canal of healthy cattle)

C. presudotuberculosis can surviv and replicate in

phagocytes
virulence in C. presudotuberculosis is linked to
–cell wall lipid and an exotoxin(phospholipase D(PLD)) and Corynebacteial secreted protease 40(CP40)
what may enhance survival and multiplication of corynebacterium spp
PLD

CP40 induces

strong immune response which may provide protection

What do C. pseudotuberculosis and C. ulcerans produce

diphtheria–toxin which the presence of in milk may have public implications
C.renale group are
–urinary tract pathogens and produce urease
–also posses fimbriae for attachment to urogenital mucosa
Diagnositc procedures of Corynebacterium spp

–animals species affected and clinical signs may suggest a specific infection
–suitable specimens for the lab: pus, exudate, affected tissue, midstream urine
–direct examination of gram stained smears may reveal corynebacteria
–culture media: blood agar, McConkey and CNA incubated up to 5 days at 37C

Corynebacterium spp identifying diagnostic procedures

–colonial characteristics
– presence of hemolysis
–absence of growth in McConkey, presences of growth in BAP and CNA
–typical corynebacterium polymorphism on gram stain
–biochemical tests

Caseous lymphadenitis is

a chronic suppurative condition of sheep, goat, and rarely cattle caused by C. pseudotuberculosis with organisms surviving in the environment for several months
Caseous lymphadenitis transmission route

–skin wounds, arthropod bites, or dips
–ruptured abscesses
–hematogenous spread causes abscesses in internal lymph nodes

caseous lymphadenitis clinical signs
–abscessation and enlargement of superficial and internal lymph nodes
–goats usually develop superficial, subcutaneous abscesses usually in the head and neck
–ill–thrift and pneumonia may be present
–visceral form may not be detected antemortem

caseous lymphadenitis

incubation period of caseous lymphadenitis

around 3 months

Caseous lymphadenitis diagnosis

–clinical (or postmortem) findings
–smears from lesions by gram stain
–isolation and identification of bacteria via submitted swabs to lab
–serological diagnosis:ELISA (individual and flock screen)
–interferon–gamma test as flock screen

Caseous lymphadenitis: Tx

susceptible to many antimicrobials but therapy is usually ineffective due to intracellular survival ability of bacteria and inability of drugs to penetrate into abscesses

caseous lymphadenitis: control

–import animals from countries/states/flocks free of caseous lymphadenitis
–animals should be subjected to pre–importation screening tests such as ELISA
–imported animals should be quarantines up to 3 months
–infected animals should be slaughtered
–contaminated buildings and equipment should be disinfected
–vaccines available

ulcerative lymphangitis is/caused by

– slow and chronic either lymphangitis of lower limbs or abscessation of pectoral region(also called pigeon fever)
–C. pseudotuberculosis in horses and rarely in cattle
–prevalent in fall and early winter

ulcerative lymphangitis is transmited by

skin wounds, arthropod bites or contact of infected animals

ulcerative lymphangitis

ulcerative lymphangitis
ulcerative lymphangitis clinical signs

–lymphatic vessels swollen and firm with nodules forming along their length
–edema develops in affected limbs and ulcerated nodules exude a thick odorless, greenish blood–tinged pus

ulcerative lymphangitis diagnosis

based on isolation and identification in the lab

Tx and control of ulcerative lymphangitis

–systemic antimicrobials may be combined with topical Tx
– affected animals should be isolated and contaminated areas disinfected

Bovine pyelonephritis causative agent

C. renale– which may be isolated from healthy cattle vulva, vagina and prepuce

Bovine pyelonephritis acquired by

stress of parturition and short urethra in cow may predispose to infection

Bovine pyelonephritis
–ascending infection from bladder to ureters can result in pyelonephritis with chronic infections possibly leading to extensive renal damage

Bovine pyelonephritis: clinical signs

–fever, anorexia and decreased milk production
–restlessness and kicking in the abdomen may indicate renal pain
–dysuria and blood tinged urine are present
–clinical signs may suggest UTI
–red blood cells and protein are present in the urine
– thickened ureter and enlarged kidneys may be detected by renal palpation and or ultrasonography: unilateral
–culture of C. renale frome urine is confirmatory

Bovine pyelonephritis: Tx

–antimicrobial tx based on susceptibility test, should start early for at least 3 weeks
–penicillin is usually good choice for high excretion in urine

Ulcerative balanoposthitis

–caused by C. renale
–characterized by ulceration around prepucial orifice with a brownish crust developing over the lesion
–similar lesion may happen on the vulva of ewes
–castrated sheep more prone
–untreated cases may progress to total occlusion of preputial orifice

C. renale may cause mucosal irritation and ulceration by

hydrolyizing urea into ammonia

predisposing factor of Ulverative balanoposthitis

high urea level in the urine due to high protein intake

ulcerative balanoposthitis

rhodococcus equi morphology

–gram positive rods or cocci
–salmon–pink, mucoid, non–hemolytic colonies
–aerobic, non motile
–CAMP test positive
–major respiratory pathogen of foals

Rhodococcus equi

Rhodococcus equi– suppurative bronchopneumonia epidemiology

–one of the most common causes of pneumonia in folas
–generally acquired by inhalation of dust
–may be present in high number in horse feces
–environmental influences–dry weather, poorgrass coverage
–high foal density
–only young foals susceptible

Rhodococcus equi– suppurative bronchopneumonia pathogenesis

–ability to survive and multiply in macrophage
–virulence is principally associated with a large??(not on slide)
–encodes several proteins most important VapA
–only equine isolates have VapA gene
–capsular polysaccharides, mycolic acids and exoenzymes

Rhodococcus equi– suppurative bronchopneumonia clinical signs

–usually less than 4 weeks old foals
–sudden onset of fever
–anorexia
–signs of bronchopneumonia
–could be insidious in 2–4 month old foals
–coughing, dyspnea, weight loss, exercise intolerance
–loud, moist rales on auscultation

Rhodococcus equi– suppurative bronchopneumonia

Rhodococcus equi– suppurative bronchopneumonia: diagnosis

–differentiating lower respiratory trac infections problematic
–WBC, fibronegen, radiography, ultrasonography,
–bacterial culture from tracheobronchial aspirate
–salmon color mucoid colonies on BAP, CAMP test
–PCR tests

Rhodococcus equi– suppurative bronchopneumonia: Tx

–combination of oral rifampin and a macrolide for up to 10 weeks
–severely affected foals have poor prognosis
–response to therapy monitored by radiography/ultrsonagrophy and plasma fibrinogen
–supportive therapy: rehydration and bronchodilatotory agents or expectorants

Rhodococcus equi– suppurative bronchopneumonia: control

–vaccines not available
–screening of foals twice a week clinical examination
–prevention of dust ihalation
–limit the foal density
–limited time spent indoor
–foaling at pasture may reduce the occurence
–passive immunization–hyperimmune plasma
–chemoprophylaxis–conflicting evidence and danger or resistance
–development of active immunization highly needed(aka vaccine)

Symbiosis

"live together"

mutualism

benefits mammal


benefits bacteria

commensalism

benefits bacteria


neither harms/benefits mammal

parasitism

benefits bacteria


harms mammal

resident microbiata

"normal flora"


"indigenous microbiota"


not normally causing disease


-resident


-transiet

resident microbiota

-part of the normal microbiota throughout life


-mostly commensal

transient microbiota

-remain in body for short period


-found in same regions as resident


-cannot persist in body


-competition from other microorganisms


-elimination by body's defense cells

acquisition of normal microbiota

-development in womb free of microorganisms


-microbiota begin to develop during birthing process


-much resident microbiota established during first months of life


-communities tend to be host-specific or organ-specific


-normal microflora primes the immune system

Opportunistic pathogens

-normal microbiota that cause disease under certain circumstances


-introduction into unusual site


-immune suppression


-changes in relative abundance may allow opportunity for member to thrive and cause disease

reservoirs of infectious disease

-most pathogens cannot survive for long period outside of their host


-sites where pathogens are maintained as a source of infection


-3 types


+infected animals


+carriers


+nonliving reservoir

infected animal

transmit disease by excretions


-aerosol


-direct


-feed


-venereal

carriers

-infected individual who are asymptomatic but infective to others


-some eventually develop illness, others never get sick


-healthy carriers may have defensive systems that protect them

nonliving reservoirs

-soil


-food


-water


contaminated often by feces or urine

zoonoses

-diseases naturally spread from animal host to humans

acquisition of zoonoses

-direct contact with animal/waste


-eating animals


-bloodsucking arthropods



humans usually dead-end host


contamination

the mere presence of microbes in/on the body

infection

when organism evades body's external defenses, multiplies, and becomes established in the body

portals of entry

-sites where pathogens enter body


-skin


-ear


-mucous membranes


-placenta


-parenteral route

portals of exit

-where we obtain specimens


-ear


-blood


-skin


-urine


-feces


-semen/vaginal excretions


-eye tears


-nose secretions


-saliva


-milk


pathogen

infectious biological agent causing disease to its host


-must find appropriate niche


-must compete with normal microflora


-must evade/overcome host defese

pathogenisis

-express proteins, adhesins, and other virulence factors to cause disease

virulence genes

many encoded within mobile genetic elements


-plasmid


-bacteria phage


-composon



some encoded in bacterial chromosome

antibiotic resistance genes

carried in plasmids


-makes other bacteria resistant to AB

adhesion in infection

-process by which microorganisms attach themselves to other cells


-required to successfully establish colonies in host


adhesion of pathogens to host cells

adhesion factors

-specialized structures


-attachment proteins

role of adhesion

-attachment proteins help in adhesion


-changing/blocking ligand or its receptor can prevent infection


-inability to make attachment proteins/adhesins renders microorganisms avirulent


-some bacterial pathogens attach to each other to form a biofilm

attachment proteins

-found on viruses and many bacteria


-viral/bacterial ligands bind host cell receptors

virulence factors

-adhesion factors


-biofilms


-extracellular enzymes


-toxins


-antiphagocytic factors

pathogenicity

ability of microorganism to cause disease

virulence

degree of pathogenicity


virulence factors


extracellular enzymes

-secreted by pathogen


-dissolve structural chemicals in body


-help pathogen maintain infection, invade, and avoid body defenses

extracellular enzymes

toxins

virulence factors


toxins

chemicals that harm tissues or trigger host immune responses that cause damage


-endotoxins


-exotoxins

toxemia

toxins in bloodstream that are carried beyond site of infection

virulence factors


antiphagocytic factors

prevent phagocytosis by the host's phagocytic cells


-bacterial capsule


+composed of chemicals not recognized as foreign


+slippery-difficult to engulf


-antiphagocytic chemicals


+prevent fusion of lysosome and phagocytic vesicles


+leukocidins directly destroy phagocytic WBCs

infection

the invasion of the host by a pathogen

disease

results if the invading pathogen alters normal bodily functions


-aka morbidity

stages of infectious disease

symptom

subjective characteristics of disease felt only by patient

sign

objective manifestations of disease observed/measured by others

syndrome

symptoms & signs that characterize disease/abnormal condition

asymptomatic/subclinical

lack symptoms, but may still have signs of infection

acute diseases

relatively sudden onset of symptoms that are usually severe

chronic disease

disease that persists for a long time. A chronic disease is one lasting 3 months or more

subacute

poorly defined state between acute and chronic

latent disease

remaining in an inactive or hidden phase

communicable disease

illness caused by an infectious agent or its toxins that occurs through the direct or indirect transmission of the infectious agent or its products from an infected individual or via an animal, vector or the inanimate environment to a susceptible animal or human host

contageous disease

An infectious disease that is spread through contact with infected individuals

principal challenge of host response

detection of pathogen & mounting a rapid defensive response

innate immunity

-external physical barriers


-internal protective cells

external physical barriers

-skin


-mucous membranes

internal protective cells

-macrophages


-neutrophils


-anti-microbial peptides


-interferons, complement inactivating pathogens

inflammation

adaptive immunity

acquired immunity against unique species of pathogens by highly specialized immune cells

5 attributes of adaptive immunity

-specificity


-inducibility


-clonality


-unresponsivesness to self


-memory

4 functions of antiboides

-neutralization


-opsonization


-oxidation


-agglutination

cellular immune response

etiology

-study of the cause of disease

germ theory of disease

disease caused by infections of pathogenic microorganisms

Koch's postulates

-suspected agent must be present in every case of the disease


-agent must be isolated and grown in pure culture


-cultured agent must cause disease when it is inoculated in a healthy, susceptible experimental host


-same agent must be reisolated from the diseased experimental host

exceptions to Koch's postulates

-some pathogens can't be cultured in lab


-disease caused by combo of pathogens & other cofactors


-ethical considerations prevent applying Koch's postulates to pathogens that require a human host

difficulties in satisfying Koch's postulates

-disease can be caused by more than 1 pathogen


-pathogens that are ignored as potential causes of disease

Staphylococcus spp morphology

–gram–positive cocci in clusters resembling branches of grapes
–nonmotile
–facultative anaerobes
–catalase positive
–commensals on mucous membranes and skin
–moderately sized white or golden colonies

Staphlycoccus gram stain

Differentiating features

–salt tolerant
–some species produce coagulase
–some produce hemolysis on blood agar
–tolerant of dessicantion–survive on environmental surfaces
–causes pyogenic infection

biochemical reactions for differentiation of important veterinary Staphylococci

–Maltose, mannitol, and trehalose fermentation tests
–some could be beta–hemolytic(S. aureus)
–coagulase test

Laboratory diagnosis of Staphylococcus

–gram stained on smears
–specimens from lesion cultured on blood agar, McConkey(or EMB) agar

Laboratory diagnosis of Staphylococcus identification criteria

–colonial characteristics:mid size white or golden
–presence of hemolysis
–absence of growth on MacConkey agar
–Catalase and coagulate tests
–biochemical profile
–PCR
PCR for Mec gene used to detect MRS

virulence factors of Staphlococcus spp

Streptococcus morphology

–gram–positive cocci arranged in chains or occasionally pairs
–falcultative anaerobes
–small usually hemolytic colonies
–catalase negative–requiring enrichment media to grow

Streptococcus spp cause

invasive and non invasive pyogenic infections
–mastits
–metritis
–polyarthritis
–meningitis
–strangles
–abortion
–respiratory tract infections in horses

streptococci virulence factors

–hyaluranidase
–most virulent strains have capsules
–streptolysin S
–streptokinase
–Antiphagocytic M protein(SeM or emm)
–pyogenic exotoxins

Streptococci–diagnosis
–type of hemolysis on blood agar
–chains of gram–positive
–No growth on MacConkey(or EMB)
–Negative catalase test

Streptococcis diagnosis
often categorized based on Lancefield classification

–divided into serotypes based on bacteria's antigens
–Lancefield groups B, C, D, E and G include the significant animal pathogens

streptococci blood agar plate
top left– complete
top right– incomplete
bottom– no hemolysis

Bacillus morphology

–large, gram positive
–aerobic or facultative anaerobic
–endospores produced
–majority of species are non pathogenic, environmental

bacillus anthracis causes

anthrax

B. licheniformis is implicated in
sporadic abortions in cattle and sheep
differentiation of Bacillus spp

–grow aerobicall and produce catalase differentiating other spore forming bacteria such as Clostridium sp
–B. anthracis colonies up to 5mm, flat dry, ground glass appearance
–B. cereus similar to B. anthracis but slightly larger and with greenish tinge
–B. licheniformis are dull, rough, wrinkled and strongly adhere to agar: colonies similar to lichen
–commercial biochemical and PCR tests available

diseases associated with Bacillus spp

–infections with B. licheniformis
–anthrax

infections with B. licheniformis
–widespread in the environment
–recognized as a cause of abortion in cattle in britain
–an association with feeding of silage or moldy
–considered significant only when obtained in pure culture from stomach content in abortion cases
anthrax is

–reportable severe disease that virtually affects all mammalians including humans caused by B anthracis
–worldwide and endemic in some countries or areas

animal susceptibility of anthrax

–ruminants high, developing fatal septicemia
–pigs and horses moderate
–carnivores more resistant
–birds almost totally resistant possibly due to high body temperatures

anthrax epidemiology

–endospore formation surviving for years
–outbreaks may be seen in pastures where buried carcasses are
–spores may be brough to surface by flooding, excavation, worms
–sporadic cases with contaminated meat
–animal acquire bacteria by ingestion or inhalation

anthrax pathogenesis

–virulence genes are encoded in 2 plasmids
+capsule composed of poly–gamma–D–glutamic acid

anthrax pathogenesis complex toxin consists of
–protective antigen– induces antibody and acts as binding moiety
–edema factor–causes increasing levels of cAMP
–lethal factor
anthrax clinical signs and pathology
incubation period: hours to days
most animals found dead in others theres pyrexia, depression, congested mucosa and petechial may be seen
anthrax clinical signs and pathology: in cattle

disease is septicemic and fatal

anthrax clinical signs and pathology: postmortem findings in cattle
–rapid bloating
–incomplete rigor mortis
–widespread petechial hemorrhages and edema
–dark–clotted blood and blood stained fluid in body cavities
–extremely large soft spleen
anthrax clinical signs and pathology: postmortem findings in pigs and dogs
–edematous swelling of throat and head along with regional lymphadenitis
–may prevent breathing
–multifocal hemorrhagic enteric lesions
anthrax clinical signs and pathology: postmortem findings in horses
–clinical course prolonged
–extensive subcutaneous edema of thorax, abdomen or legs
–swelling of pharynx
–less commonly enteric lesions
anthrax diagnosis

–carcasses are bloated, putrefied with no rigor mortis
–dark unclotted blood may come from mouth, nostrils and anus
–necrosis discouraged due to sporulation risk
–peritoneal blood from vein of ruminants can be collected for special capsular staining and culture
–BAP and MacConkey inoculated
–biochemical and PCR test

BAP and MacConkey inoculation of anthrax will yield
–colonial morphology
–gram stain(large rods with endospores)
–absence of growth in MacConkey
Anthrax Tx

–early in infection:high doses of long acting penicillins or ox tetracycline
amoxicillin, ciprofloxacin, doxycycline, erythromycin and sulfonamides can also be used
–beta lactamase resistance is rare

anthrax control in endemic regions

–suspected cases must be reported immediately
–annual vaccination with sterne strain, –chemoprophylaxis(long acting penicillins) during outbreaks, and
– vaccination of humans

Anthrax control in non endemic regions

–movements of animal and animal waste must be prohibited
–PPE use and disinfection before leaving affected farm
–contaminated buildings should be fumigated
–immediate disposal of carcasses, bedding, manure
–prevent scavenger animals
–in–contact animals should be isolated

anthrax in humans
–a bioterroism agent
–disease maybe fatal if untreated
–extensive studies going on for better diagnostic and vaccine
3 main forms of anthrax in humans

–cutaneous anthrax (malignant pustule)
–pulmonary anthrax
–intestinal anthrax

Clostridium key points
–large gram + rods
–endospore producing
–anaerobic
–colonies of C. perfringens with double hemolysis
–may be present in healthy animals feces
–produce diverse forms of diseases in aimals
Pathogenic clostridia groups
neurotoxic
atypical
histotoxic
enteropathogenic and enterotoxemic
Neurotoxic clostridia include
C.tetani
C. botulinum
histotoxic clostridia include
don't care
enteropathogenic and enterotoxemic clostridia include
don't care
atypical clostridia include
C. piliforme
Specimen collection of clostridium spp
–ensure survival of these anaerobic bacteria
+obtain specimen from live of recently dead animals
+specimens put in anaerobic transport media
+BAP enriched with yeast extract and vitamin K for growth
+anaerobic conditions for bacterial growth needed
clostridium detection and differentiation
–colony morphology
–miniaturized biochemical tests
–PCR and FA(fluorescence assay) tests
–bioassays and ELISA for toxin presence
diseases associated with clostridium
–Neurotoxic clostridia Tetanus
Tetanus
–acute potentially fatal intoxication with horses and humans being most susceptible: carnivore relatively resistant, poultry not susceptible
–spores produce drumstick appearance
etiologic agent causing tetanus
C. tetani
tetanus endospores resistant to
chemicals and pasteurization but not to autoclaving
infections of tetanus occurs when
endospores introduced into traumatized tissue
common sources for tetanus is
deep penetrating wounds
when are tetanus spore germinated
in anaerobic environments
tetanus produces
potent toxin, tetanospasmin, responsible for clinical signs of tetanus
tetanus pathogenesis
–effect of toxin on a pair of antagonistic muscles
–spastic paralysis occurs
–bound toxin is not neutralized by antitoxin
–recovered animas may not necessarily immune
tetanus clinical signs
–incubation period 5–10days up to 3 weeks
–wounds on head or near head associated with shorter incubation and increased chance of generalized tetanus
–stiffness,
–localized spasms which may lead to lockjaw
–altered heart and respiratory rates
–dysphagia and altered facial expression
–generalized muscle stiffness can lead to saw horse
tetanus diagnostis is
usually presumptive and based on clinical signs and recent history of trauma
tetanus diagnostic procedures
–to differentiation from strychnine poisoning–perform gram stain
–anaerobic culture not always successful
–PCR tests developed
–bioassays on mice
Tetanus Tx
–antitoxin administered promptly
–toxoid(vaccine) can be given even to those receiving antitoxin
–large doses of penicillins iv or im
–affected animals should be housed in quiet and dark environment
–fluid replacement therapy, sedatives and relaxants

tetanus control

–farm animals should be vaccinated with tetanus toxoid
–a booster dose may be needed
–prompt surgical debridement of wounds in horses
–for unvaccinated animals that have deep wounds give antitoxin