Acidfast bacteria

Mycobacteria. Contain large amounts of waxes, making the cells impervious to harsh chemicals. No peptidoglycan.

Growth Factors

Preformed organic compounds that

all pathogenic bacteria need

Endospore

Condensed, walled-off nucleoid and cytoplasm surrounded by a spore coat (resistant to microwaves, chemicals, desiccation, heat, and antimicrobials)

Elementary Bodies (EB) and Small Cell Variants (SCV)

Condensed forms of obligate intracellular

bacteria taht are suited for survival

outside the host cell (metabolically inactive)

Cytotoxins

Exotoxins that are capable of

intoxicating multiple cell types

Effectors (Effector toxins)

Protein toxins that are injected from the bacterium directly into the cytosol of hte host cell via injectosomes

Endotoxins

LPS

Enterotoxins

Protein toxins that cause symptoms

associated with enteric disease

Exotoxins

Protein toxins that are exported from bacterial

cells in to the extracellular environment

Biofilms

Bacteria attached to surfaces and encased in a hydrated polymeric matrix containing polysaccharides, proteins, and nucleic acids

Minimum Inhibitory Concentration (MIC)

Lowest concentration of drug that visibly inhibits growth of bacteria after 18-22 hr incubation

Disk-diffusion susceptibility test (K-B)

Diameter of zone of inhibition correlates inversely with MIC

Resistant

Concentration of antimicrobial drug sufficient to inhibit isolate's growth in vivo not achievable and/or tolerated

Susceptible

Standard dosage of drug will usually achieve concentrations sufficient to inhibit isolate's growth in vivo

Breakpoint

Criteria for classification of results as "susceptible" or "resistant"

Penicillins

• Beta-lactam
• Inhibits cell wall synthesis
• Rapidly bactericidal
• Gram positive aerobes and most anaerobes susceptible
• Resistance aquared through production of beta-lactamases
• Calvulanic acid binds to B-lactamase and neutralizes it (clavamox = clavulanic acid + amoxicillin)
• Methicillin and oxacillin is resistant to B-lactamase
  

Cephalosporins

• Beta-lactam
• Inhibits cell wall synthesis
• Rapidly bactericidal
• Resistance acquired by production of beta-lactamases (not all B-lactamases work against both Penicillins + cephalosporins)
• First Generation: cephalexin, cefadroxil, cephapirin, cefazolin (gram-positives, some gram-negatives)
• 2nd Generation: cefoxitin (more gram-negative and anaerobe)
• 3rd Generation: less gram positive activity, more gram-neg activity
  

Tetracyclines

• Broad-spectrum
• Bacteriostatic by inhibiting protein synthesis (Binds to 30S and 50S subunits of bacterial ribosomes)
• Resistance through plasmid mediated efflux pumps
• Names include "-cycline"
• Provides cross resistance

Chloramphenicol, Florfenicol

• Broad-spectrum
• Bacteriostatic by inhibiting protein synthesis (ribosomes)
• Most resistace in plasmid mediated chloramphenicol acetyltransferases

Aminoglycosides

• Bactericidal
• Inhibits rate of protein synthesis and causes transcript misreads
• Uptake requires O2 dependent, active transport into bacterial cell.
• Primarily used for treatment of serious gram-neg infections. Limited gram-pos activity
• Resistance acquired primarily by plasmid-mediated enzymatic modification
• limited cross-resistance
• Gentamicin, amikacin, neomycin, streptomycin
  

Macrolides

• Bacteriostatic by inhibiting protein synthesis
• Active against gram0positive aerobes, mycoplasma, and anaerobes but NOT for gram negative aerobes
• Great for respiratory infections because drug concentrates in lungs
• Erythromycin, tilmicosin, azithromycin, clarithromycin, tylosin, tulathromycin

Lincosamides

• Bacteriostatic by inhibiting protein synthesis similar to macrolides
• Active against gram-positive aerobes, mycoplasma, and anaerobes, but poor gram-negative penetration
• -clindamycin, lincomycin, pirlimycin

Fluoroquinolones

• Rapidly bactericidal
• Targets 2 types of topoisomerases (doesn't allow for recoiling of bacterial chromosome and allows for rapid nuclease digestion)
• Potent,broad spectrum, but limited activity against anaerobes and streptococci
• Resistance through: mutations in DNA gyrase and topoisomerase genes, acquiring efflux pumps, conjugation (target not as susceptible to binding)
• Names have "floxacin" in it (baytril = enrofloxacin)

Sulfonamides

• Bacteriostatic and slow acting
• Competitive analogs of p-aminobenzoic acid in the synthesis of folic acid
• Broad spectrum
• Cross resistance by plasmid-mediated alternative enzyme or over production of targeted enzyme
• Trimethoprim, ormethoprim = potentiated with sulfa and makes it bactericidal

Beta Lactam antimicrobials

Penicillins and Cephalosporins

Antibiotics inhibiting protein synthesis

Tetracyclines

Chloramphenicol

Florfenicol

Aminoglycosides

Macrolides

Antimicrobials that target topoisomerases

Fluoroquinolones

Antimicrobials that prevent folic acid synthesis

Sulfonamides

Antimicrobials for Gram Positive Aerobes

Beta-labtams

Chloramphenicol

Fluoroquinolones

Macrolides

Tetracyclines

Sulfonamides

Antimicrobials for Gram-positive Anaerobes

Beta-lactams

Chloramphenicol

Macrolides

Tetracyclines

Sulfonamides

Antimicrobials for Gram-negative Aerobes

Aminoglycosides

Beta-lactams

Chloramphenicol

Fluoroquinolones

Sulfonamides

Tetracyclines

Gram-negative Anaerobes

Beta-lactams

Chloramphenicol

Tetracyclines

Sulfonamides

Gram-positive aerobes

Staphylococcus

Stretpococcus

Enterococcus

Erysipelothrix

Listeria

Bacillus

Corynebacterium

Gram-positive anaerobes

Actinomyces

Clostridium

Peptostreptococcus

Gram-negative aerobes

E. coli

Salmonella

Klebsiella

Pasteurella

Pseudomonas

Proteus

Gram-negative Anaerobes

Bacteroides

Porphyromonas

Prevotella

Fusibacterium

Streptococcus

• Gram-positive coci occuring singly, in pairs, or in chains
• Commensals of mucosal membranes, mostly upper respiratory, genital, and digestive tracts. Infections mostly opportunistic
  
• Most require blood/serum components for growth
• Common dzz: URI, lymphadenitis, neonatal septicemia (failure passive transfer), secondary pneumonia, pyogenic infections in any body site
• Live for 6-8 wks in dried pus, soil, bedding, etc.. but susceptible to desiccation. (aerosol, direct contact/fomites = spread)
  
• Some cause contagious dz + transmit by convalescent carriers
  

Pathogenesis of Pyogenic Infection

• Pyogenic = pus (dead leukocytes, liquefied tissue, living and dead bacteria) encapsulation of liq tissue = abscess
  
• Bacteria enter tissues or attach and colonize (adhesins include M protein, capsule, teichoic acids)
• Initiate chemotactic leukocytic response
  
• Antiphagocytic factors: capsule and M protein
• Produce a variety of exotoxins:
  • Evoke vascular dilation, exudation of plasma and neutrophils
  • Hemolysins (leukotoxin), hyaluronidase, proteases)
  • B-hemolysis: clear zone @ colony on blood agar mostly pathogenic

Antimicrobial selection for B-hemolytic streptococci

• Predictable susceptibility: B-lactams (esp PENICILLINS), cchloramphenicol, trimethoprim/sulfas, macrolides, lincosamides
• Resistance: quinolones, aminoglycosides, tetracyclines
• Resistance mostly innate, due to lack of penetration through thick cell wall (not acquired genetic changes)

Major Streptococcus species

• Streptococcus pyogenes
• Streptococcus equi ssp equi
• Streptococcus equi ssp. zooepidemicus
• Streptococcus canis
• Streptococcus agalactiae
• Streptococcus suis
• Enterococcus spp
• Streptococcus pneumoniae

Streptococcus pyogenes

• B-hemolytic
• pharyngitis/tonsilitis of humans

Streptococcus equi ssp. equi

• B-hemolytic
• Strangles of Equidae
• Reservoirs & chronic carriers: chondroid in guttural pouch (10-30% up to 56 mos)
• Diagnosis: culture, PCR, serology for Abs to M protein
• Strangles Vaccine: attenuated bacterium with no capsule. IN application, fully virulent in tissue

Streptococcus equi ssp. zooepidemicus

• B-hemolytic
• Common pyogenic agent in many species of animals
• Most common pyogenic agent of horses (90% time)

Streptococcus canis

• B-hemolytic
• Neonatal septicemia (in failure of fetal transfer)
• Genital, skin, and wound infections
• Canine streptococcal toxic shock syndrome and necrotizing fasciitis

Streptococcus agalactiae

• Chromic bovine mastitis
• Only obligate parasite of udder
• Only CAMP positive org: synergistic "arrow-head hemolysis at intersection of Strep. and Staph. streak lines on BA

Streptococcus suis

• Pneumonia, septicemia, arthritis, meningitis
• Sporadic-major issue
• Zoonotic and causes meningitis with high morbidity

Enterococcus spp

• Very close to strep, but survive well in GI
• a-hemolytic (so not usually pyogenic)
• endocarditis and 10-15% canine urinary tract infections (UTI

Staphylococcus

• Gram positive cocci that tend to be in clusters
• Commensals of upper respiratory tract and skin of all endotherms
• Unlike strep, prolonged survival in inanimate environ.
  
• Spread of strains b/w diff animal species very limited
• Pyogenic, associated with abscess formation and suppuration
• Invasive enzymes: hyaluronidase, protease, lipase, fibrinolytic enzymes
• Capsules and Protein A = antiphagocytic (fxns as Fc receptor)
• Exotoxins (leukotoxins and cytolysins = alpha toxin, which is a pore forming hemolysin) can cause cell death and release of inflammatory mediators
• Superantigens cause massive T cell stimulation

Importance of Urease in UTI caused by Staphylococcus

Urease hydrolyzes urea into ammonia, which

increases the pH and reduces the solubility of

salts, which precipiates out of solution and

forms phosphate (struvite, apatite) uroliths).

Identifying characteristics of Staphylococcus

• Coagulase test positive strains correlate well with pathogenicity/virulence
  
  • S. aureus and S. intermedius groups are coagulase +
  • Coagulase - strains considered normal skin flora with limited virulence
• Hemolytic reactions can be complete, incomplete, or nonhemolytic.
  • Double zone of hemolysis (2 diff hemolysin toxins produced) produced by animal strains correlates with coagulase+)
    
• Isolation of Staph spp must be interpreted with caution (should be isolated in assoc with lesion, from deep within tissue, abscess or pustule)
  

Species in Staphylococcus intermedius group (SIG)

Staphylococcus pseudintermedius

Staphylococcus delphini

Staphylococcus intermedius

Common Staphylococcus strains outside of SIG

Staphylococcus aureus

Staphylococcus hyicus

>40 spp of coagulase - Staphylococcus

Staphylococcus pseudintermedius

• MOST common pyogenic agent of dogs: pyoderma, infections of respiratory tract, bones, joints, wounds, etc...

Staphylococcus delphini

• From dolphins, horses, camels, mink, domestic pigeons
• Most common SIG from horses

Staphylococcus intermedius

Only isolated from wild pigeons

Staphylococcus aureus

• Humans and many animal species: abscesses, mastitis, osteoyelitis, etc...
• Bumble-foot, botryomycosis in birds

Staphylococcus hyicus

• Exudative epidermitis (greasy pig disease of piglets)
• Very devastating

Coagulase-negative Staphylococcus

• Aka Staphylococcus epidermidis
• Can only differentiate via genomic studies
• Infections associated with medical devices
• Common cause of subclinical bovine mastitis

Antimicrobial selection for Staphylococcus

• Penicillinase-resistant penicillins, cephalosporins, clavulanate/amoxicillin, macrolides, trimethoprim/sulfas, chloramphenicol, aminoglycosides, quinolones
• 60-80% has B-lactamase
• Resistance issues with B-lactams and tetracyclines
  • Transduction of B-lactamase gene
  • Inducible B-lactamase genes
  • Broad spectrum B-lactamases (cephalosporins)
  • Methicillin resistance

Methicillin resistance in MRSA and MRSP

• mecA resistance gene (penicillin binding protein with affinity to B-lactams and methicillin)
• MRSA contains staphylococcal cassette chromosome
  • Mobile genetic element wth integrated copies of plasmids
  • No phage-related genes, but mobility due to two recombinases

Rhodococcus equi

• Gram-positive coccobacillus
• Occurs in soil, manure, + the intestine of mammals and birds
• Foal intestine serves as incubator
• Acquired by inhalation of dust, ingestion, umbilicus?
• No diff in # of orgs on prob farms vs. okay farms because problem farm strain has plasmid containing virulence factor

Pathogenesis of Rhodococcus equi

• Foals at-risk as MAb declines (peak incidence 6-12 weeks) Passive transfer important
• Neutrophils are fully competent bactericidal defense
• Infection largely within macrophages/monocytes b/c virulence factor allows entry into macrophage (Entry via non-Fc recep (CRs) allows evasion of Ab-mediated killing in macrophages and intracellular survival). Presence of vapA plasmid necessary to arrest phagosome maturation
• chronic pyogranulomatous inflammation
  

Immunoprophylaxis/Treatment of Rhodococcus equi

• Commercial vaccines not approved in US due to lack of efficacy
• Passive immunization via hyperimmune plasma presumably vs. Vaps
• Macrolides are best with Rifampin (combo to limit resistance) - Erythromycin gentamicin,clarithromycin
• Lots of resistance issues because high freq of emergence of resistant mutants
• Hard to get antimicrobials to penetrate intracellular and abscess

Biotypes of Corynebacterium psuedotuberculoses

• Ovine and equine biotypes
• In sheep/goats: caseus lymphadenitis which is chronic with multiple chronic  abscesses resuting in debilitation, weight loss, poor production. 3rd leading cause of economic loss in western US sheep indust.
• In horses: ulcerative lymphangitis (pigeon breast, pigeon fever, dryland distemper) in horses. Results in deep abscesses in inguinal and pectoral regions

Corynebacterium pseudotuberculosis

• Small, pleomorphic gram-positive rods. Diphtheroids (Palisades, Chinese letters, club and filamentous)
• Occurs on the skin and mucous membranes and in legions
• Survives on exposed pen floor 10 days, in hay and bedding >1 yr
• Enters through abrasions, shearing wounds, insect bites

Caseous lymphadenitis

• Caused by ovine biotypes of Corynebacterium pseudotuberculosis
• Incubation period from 25-140 days
• Faculatative intracellular pathogen, having capacity to replicate within and ultimately escape from macrophage phagolysosomes
• Abscesses form in lymph nodes with onion-like concentric layers
• Susceptibility: penicillins, tetracyclines, sulfonamides, macrolides
  
• Virulence factors:
  • toxic cell-wall lipid (protects from lysosomal enzymes)
  • Sphingomyelinase-specific phospholipase D (exotoxin) causes hemolysis, increased vascular permeability, and cytolysis
    

Ulcerative lymphangitis

• Pigeon breast, pigeon fever, dryland distemper
• Caused by equine biotype of Corynebacterium psuedotuberculosis
• Deep abscesses in inguinal and pectoral regions
• Seasonal occurence
• Susceptibility: Penicillins, tetracyclines, sulfonamides, macrolides
• Treatment ineffective in walled off abscesses

Diagnosis of Corynebacterium pseudotuberculosis

• Serology: no correlation between Ab titer and extent of lesion development
• Multiplex PCR can identify and differentiate from other corynebacteria
• Readily grows on standard lab media

Immunization for Corynebacterium pseudotuberculosis

• Toxoid vaccines provide good protection vs. dz in sheep and goats
• Bacterins provide variable protection and reduce number of abscesses

Corynebacterium renale

• Short, pleomorphic, gram positive rods
• Inhabits lower genital tract of cattle
• Transmitted via direct contact and by urine splashing
• Pili-mediated attachment to uroepithelium is critical in pathogenesis
• Predilection for urinary tract due to bacteria's ability to metabolize large quantities of urea (urease). Mucosal damage results from chem irritation when urease -> ammonia
  
• Causes chronic ascending pyonecrotic urinary tract infection (bovine pyelonephritis)
• Ovine posthitis (pizzle rot) necrotizing inflammaiton of prepuce
• Penicillin is antibiotic of choice
  

Arcanobacterium pyogenes

• Small gram-positive rods (facultative anaerobe)
• Commensal of mucous membranes and skin of suscleptible animals (cattle, goats, sheep and pigs)
• Causes suppurative processes (usually complicated by other potential pathogens or debilitated tissues, chronically progressing to thick walled abscesses
• The most common pyogenic agent of cattle
• Susceptible to penicillins, tetracyclines, sulfas

Listeria

• Small, motile gram-positive rods
• L. monocytogenes is most important pathogen
• Widely distributed in environ including soil, plants, decaying vegetation and GIT of over 50 spp animals
• Graow in temp 1-45C and pH of 4.4-9.6. Remarkable resistance to dessication. survives for months in dairy, plants, meats, and soil
• Ingestion primary route of entry
• Facultative intracellular parasitism

Pathogenesis of Listeria

• Attachment, parasite-directed endocytosis, lysis of phagosome, growth in cytoplasm, directed budding/endocytosis into second cell, release into cytoplasm
• Intestinal colonization and translocation
• Replication in the liver and spleen
• T-cell dep resolution or spread
• Tissue invations:
  • Blood-borne bacteria directly invade endothelial cells
  • Monocytes carry and spread bacteria to target cells
  • Oral-phagocyte-facilitated spread to trigeminal axon, retrograde movement to brain stem.
    

Clinical forms of listeriosis

• Zoonotic with incubation period upto 70 days (septicemia, meningitis, abortion)
• Visceral form: septicemia with localization in parenchymous organs (liver and spleen) resulting in focal necrosis (primarily in monogastric species)
  
• Abortion: localizes in placental and fetus (common in cattle and sheep
  
• Neural form: localizes in pons and medulla via sheath of trigeminal nerve or in meninges via bacteremia
  • Most common in ruminants --> circling dz
  • Microabscesses: Perivascular cuffing with infiltrate of leukocytes, focal necrosis
  • Meningitis sporadically occurs in other species

Diagnosis and Treatment

• Susceptible: penicillin/ampicillin, sulfonamides, tetracyclines, chloramphenicol, erythromycin
• Listeriosis very severe: 30% mortality with antibiotic, and 100% in case of meningoencephalitis
• Diagnose:
  • Collect correct tissue specimen
  • Cold enrichment enhancess success of isolation from brain tissue after weeks of incubation
  • Typing to characterize and demonstrate possible epidemiological assoc.

Erysipelothrix rhusiopathiae

• Pleomorphic, small gram-positive rods
• Erysipelas occurs in may spp with swine most freq and severely affected
• Persistent and widespread in environment (Carrier pigs primary reservoire)
• Survives dessication for several months
• Spread by ingestion of contaminated materials

Pathogenesis of Erysipelas

• Following ingestion: invasion, bacteremia, localization in various tissues
• Virulent strains produce high levels of NA; causes vascular damage and thrombus formation
• Articular cartilage damaged by immune response to persisting Ag

Erysipela syndromes in swine

• Acute septicemia
• Urticarial form (Diamond skin dz)
• Vegetative endocarditis (chronic)
• Polyarthritis (chronic

Erysipelas in non-pigs

• Turkeys, geese and other birds (acute septicemia, vegetative endocarditis, arthritis)
• Sheep (polyarthritis
• Dogs (vegetative endocarditis, bacteremia)
• Marine mammals (serious, fatal septicemia
• Humans (Erysipeloid is localized cellulitis)

Treatment and Vaccine for Erysipelas

• Susceptibility: Penicillin, tetracyclines
• 28 serotypes of varying virulence, though surface protective ags essential for immunization and are cross-protective
• Most animals passively protected from naturally occuring dz by hyperimmune antiserum
• Both live attenuated vaccines and bacterins available for pigs and turkeys.

Actinomycetes

• Filamentous, branching, gram-positive rods
• Most are obligate anaerobes or capnophilic
• Present on mucous membranes, often in oral cavity and nasopharynx
• Endogenous infections causing pyogenic or pyogranulomatous reactions
• May form "Sulfur granules" in tissues and exudate (colonies surrounded by calcium phosphate mineral.)
• Some produce L-forms in tissue

Species of Actinomycetes

Actinomyces bovis

Actinomyces viscosus

Actinomyces hordeovulnaris

Actinomyces bovis

• Causes lumpy jaw
• Chronic progressive infection
• principally of cattle
• development of granulomatous, suppurative legions involving bone and soft tissue

Actinomyces viscosus

• Cutaneous pyogranulomas, pyothorax (focal abscess in lungs), osteomyelitis (very hard to treat)

Actinomyces hordeovulnaris

Cutaneous pyogranulomas, pyothorax, osteomyelitis often associated with tissue migrating foxtail awns

Treatment for Actinomycosis

Susceptibility: Trimethoprim/sulfa, penicillin/ampicillin (not for L-forms), tetracyclines

Resistance: aminoglycosides or quinolones (anaerobes!)

Nocardia

• Aerobic saprophytic soil organisms
• Filamentous, gram positive rod
• PARTIAL ACIDFAST staining differs from Actinomyces
• Causes suppurative and pyogranulomatous reactions in immunosuppressed hosts or compromised tissues
• Rarely produce sulfur granules
• Susceptibility: Trimethoprim/sulfas, tetracyclines (pennicillin NOT ok b/c lipid cell wall is acidfast)

Nocardia asteroides

• Cutaneous granulomas and pyothorax in dogs
• Mastitis in cattle
• Pneumonia in SCID foals

Dermatophilus congolensis

• Pleomorphic, beaded chains (stacked coins), gram-positive
• Reside in foci of infection on carrier animals or within scabs in environment
• Cause sueprficial dermatitis with thick crusts, hair loss in scabs
• Affects cattle, horses, sheep, goats, etc...
• Many names for dermatophilosis: rain-scald, cutaneous streptothricosis, lumpy wool, strawberry footrot
• Susceptibility: penicillins, tetracyclines
• Happens in dirty animals (won't invade further than dermis)

Bacillus

• large, gram-positive, spre-forming, aerobic rods.
• ubiquitous in soil, air, dust, and water
• B. anthracis is the only important pathogen
• Acute, usually septicemic dz, primarily of hervibores
• Often peracute in cattle and sheep, found dead without premonitory signs
• All domestic and wild mammals are susceptible
• Birds are resistant
• Worldwide

Bacillus anthracis

• Broad, gram-positive rods with squared ends, commonly in chains, and within capsules in vivo
• Putrefaction kills vegetative cells within 48-72 hrs
• Most spores form from carcass within 48 hrs
• Requires free oxygen for sporulation
• Temperature 18-46C, tropical/temperate regions
• High humidity allows for fast sporulation

Spores of Bacillus anthracis

• Ca+, moist alkaline environ favors spore survival (long time in graves)
• Spores markedly resistant to extremes of heat, cold, pH, desiccation, chemicals and other adverse conditions
• UV inactivates spores in 4-6 hrs
• Mov't of spores by wind, rain, soil disturbance

Transmission/Pathogenesis of Bacillus Anthracis

• Ingestion of spores while grazing, and legion is necessary for initiation of infection
• Spores phagocytosed by macrophages --> lymph nodes
• Low-level germination at entry site --> local edema, hemorrhage, and necrosis
• Macrophage survival --> multiplication and escape --> extracellular growth --> toxin + virulence factor expression --> macrophage + cytokines --> host symptoms and death --> nutrient depletion --> sporulation in environ.
• Major virulence factors plasmid encoded (antiphagocytic polypeptide capsule --> poor Ab response) (Tripartite toxin = leukocidal, increases vascular permeability, capillary thrombosis --> shock and death)
• Suden death, bleeding from orifices, rigor mortis absent/incomplete, bloating
• Septicemic lesions, subcutaneous hemorrhages, edema, blood fails to clot, splenomegaly
  

Host Range & Disease of Bacillus anthracis

• Ruminants: sudden death, bleeding from orifices, subQ hemorrheages, without prior signs, brief period of fever, edema, blood fails to clot, splenomegaly
• Equids & wild herbivores: Fever, restlessness, dyspnea, agitation
• Pigs, carnivores: local edema, swelling of face, neck, and lymph nodes
• Chronic infections characterized by localized subQ edematous swellings

Diagnosis & Treatment of Anthrax

• Prepare blood smear from superficial body sites
• Look for large, capsulated bacillus withoug spores that are gram +
• Know Bacillus anthracis does not reliably survive more than 24 hrs in carcass
• Diagnostic confirmation: nonmotile, nonhemolytic, pXO1 - toxins, pXO2-capsule-producing, susceptible to gamma phage
• Susceptibility: penicillin, tetracycline, macrolides, quinolones
• Sterne spore vaccine is live "avirulent" (nonencapsulated) strain that produces toxins that are good for cattle but not other spp.
• Disinfect with sporicidal solutions (bleach)
• Incinerate carcasse and MAKE SURE TO REPORT (REPORTABLE DZ)
  

Human threat to Bacillus anthracis

• Cutaneous form: black scab and edema. Fatality rate of 10-20% if untreated
• Inhalational form: pulmonary edema and hemorrhagic pneumonia, septicemia; nearly 100% fatal
• Intestinal anthrax of consumption of diseased meat. Highly fatal
• Not contageous-age resistance in youngsters
• Antimicrobial: ciprofloxacin (quinolone), doxycycline, amoxicillin

Clostridium

• Large gram-positive rodes, obligate anaerobes, spore-forming (resistant to drying, heat, irradiation, and disinfectants)
• Wide distribution in soil (major habitat), freshwater, marine sediments, and intestinal tract of animals and humans. (some types only present in localized areas)
• Infection acquired by wound contamination, ingestion (including indigenous flora)
• Most pathoogetic types produce potent exotoxins with variable invasive ability.

Pathogenic types of clostridia:

• Neurotoxic: potent exotoxins, limited colonization or invasiveness (C. tetani and C. botulinum)
• Histotoxic: Invasive and potent exotoxin producers resulting in acute necrosis of tissues (wounds, mm, liver). Includes gas gangrene (C. chauvoei, C. septicum, C. novyi, C. sordelli, C. perfringens)
• Enterocolitis: Produce exotoxins active within intestinal tract causing necrosis, food poisoning, diarrhea. May also be histotoxic (c. perfringens, C. difficile)

Clostridium botulinum

• Widely but unevenly distributed in soils and aquatic environ
• Growth and toxin production in anaerobic environ (contaminated meat, fish, veggies, carcasses, rottin gvegetation etc...)
• Only time colonization occurs is wound and infant botulism
• Toxin ingested, absorbed, and distributed to myoneural junctions and release of ACh suppressed via hydrolysis of SNARE proteins --> flaccid paralysis
• Most common in water birds (limber neck), ruminants, horses, mink and poultry. Carnivores relatively resistant
• Limited serotype-specific vaccine and diagnostic reagents
  

Clostridium tetani

• Natural habitat is soil, esp contaminated by animal feces; transient in intestines
• Endospores enter traumatized tissue/wounds (castration, docking, umbilicus, parturition, etc...)
• Local bacterial growth and production of tetanus toxin
• Tetox travels retrograde through motor neurons at nueromuscular jxn to spinal cord + medulla in inhibitory neurons and prevents NT release by hydrolyzing SNARE proteins --> uninhibited ACh release in neuromuscular junction
• Susceptibility: humans + horses > pigs > cattle and sheep > dogs, cats, poultry resistant
• Toxoid used as vaccine. Antitoxin= hyperimmune serum w/ Abs vs tetox
  

Histotoxic clostridia

• Inhabit soil and intestinal tract
• May enter wounds or spores may be absorbed and carried to mm or liver
• Damage to tissue reduces oxygenation and enhances growth (emphysema in tissues due to fermentation)
• Produce potent exotoxins, proteases, lecithinases (causes extensive necrosis, hemorrhage, emphyseme in tissues)
• May progress to toxemia, septic shock and death
• Antitoxin immunity is essential for resistance

Histotoxic Clostridia Spp

Clostridium chauvoei

Clostridium septicum

Clostridium perfringens

Clostridium sordellii

Clostridium novyi

Clostridium haemolyticum

Clostridium chauvoei

• Causes blackleg in ruminants (primarily cattle)
• Spore ingested, carried to mm, growth facilitated by anaerobic conditions
• vaccination 98-99% effective
• Usually results in sudden death

Clostridium septicum

• 2nd most common
• Causes malignant edema  in ruminants, pigs, and horses.
• Causes sudden death in ruminants and pigs
• Causes massive area of necrosis and sloughing in horses, but survive
• Primarily enters and grows in wounds

Clostridium perfringens

Causes wound infection and gas gangrene in all species

Clostridium sordelli

Similar to C. septicum (wound infections and edema

Clostridium novyi

• Big head in rams (subQ lesion in head) - type A
• Black disease (infectious necrotic hepatitis) - type B

Clostridium haemolyticum

• Causes bacillary hemoglobinuria (redwater)
• Predominantly in mountain valleys of western US, esp wherever liver flukes occur.
• Death by lysis of erythrocytes

Antimicrobials for Clostridium

• Susceptibility: penicillin/ampicillin, tetracyclines, chloramphenicol, macrolides, lincosamides
• Resistance: aminoglycosides, quinolones, sulfonamides

Clostridial spp for Neurotoxic Clostridia

Clostridium tetani

Clostridium botulinum

Spp for Enterocolitis

Clostridium perfringens

Clostridium difficile

Clostridium perfringens

• Enterotoxemia. Potent lethal toxins produce din intestine by overgrowth (over eating dz)
• Locally may cause necrotizing hemorrhagic enteritis
• Absorbed --> toxemia-->septic shock and death
• Enterotoxin produced in large intestine when bacteria convert to spores, causing diarrhea
• Hemorrhagic bowel syndrome in cattle prob multifactorial
• Occurs in dogs too

Clostridium difficile

• Enterocolitis and diarrhea in horses, pigs, and dogs
• Fibrin and plasma leakage --> hemorrhage too
• Important nosocomial problem, some strains with increased virulence
• Difficult to isolate, not all strains are toxigenic - test for toxins
• No vaccine
• Spores hard to rid of --> nosocomial problems

Clostridium piliform

• aka Bacillus piliformis, Tyzzer's bacillus
• Tyzzer's dz: acute fatal infection causing focal necrotic hepatitis, enteritis and colitis
• Lab mice, foals and other animals
• Reservoire is probably infestine of rodents

Non-spore-forming obligate anaerobes

• Large grp of gram-pos and gram-neg bacteria that exist primarily as commensals (normal flora) of mucous membranes.
• Commonly found (35%) in necrotic and suppurative infections, usually in mixed infections
• Lowered redox potential req for growth (trauma, necrosis, ischemia, parasitic invasion, or concomitant growth of facultative anaerobes)
• Infection occurs by extension of normal flora into compromised tissues
• Virulence factors: capsules, pili, exotoxins, LPS, leukotoxins, and other metabolic byproducts
• Typically foul-smelling, pyonecrotic lesions

Spp of non-spore-forming obligate anaerobes

Fusobacterium spp

Bacteroides spp

Porphyromonas spp

Prevotella spp

Periodontal dz

• Periodontal dz begins as reversible gingivitis
  • normal flora in mouth interact with nutrients
  • form plaque which mineralize to form calculus on teeth
• Calculus blocks oxygen diffusion (Porphyromonas spp proliferate in biofilms and produce toxins destructive to the tissue)
• Inflammatory rxn releases enzymes in subgingival space and periodontal pockets
• non-reversible destruction of periodontal lig, bone loss, eventually leading to tooth loss

Porphyromonas vaccine

• An aid to preventing periodontitis in dogs
• Bacterin contains P. denticanis, P. gulae and P. salivosa
• Duration of immunity, efficacy, potency unknown
• Circulating IgG Abs supposedly prevent dz by opsonizing Porphyromonas bacteria to reduce biofilm (calculus) formation and to prevent release of toxins

Dichelobacter nodosus

• Non-spore-forming obligate anaerobe
• Contagious footrot: infection of interdigital skin of ovine feet (progressively spreads inside the inner wall of hoof, across sole, causing separation of horny layer of hoof)
• Pili mediate adherence
• Serine proteases digest horn promoting separation

Treatment/Diagnosis of Non-spore-forming anaerobes

• Suseptibility: penicillin/ampicillin, tetracyclines, macrolides, chroramphenicol
• Resistance: aminoglycosides, quinolones, sulfonamides
• When isolating: protect from O2 exposure. specimen collected from sites that normally possess anaerobic flora NOT appropirate for anaerobic culture. culturing and ID not very helpful anyway.