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114 Cards in this Set
- Front
- Back
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characteristics of Clostridium botulinum |
1. produces extremely poisonous toxin
2. affects peripheral nervous system (preference for stimulatory motor neurons)
3. requires catalytic cut for cleavage
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what kind of paralysis does Clostridium botulinum produce? |
flacid |
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describe chains of Clostridium botulinum |
1. light chain (A fragment) - molecular weight of 50 kDa
2. heavy chain (B fragment) - molecular weight of 100 kDa |
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what typically causes death in Clostridium botulinum? |
respiratory or cardiac paralysis
*waterfowl die by drowning once they can no longer hold their head up |
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2 ways botulinum toxin can be acquired |
1. ingested pre-form
2. absorbed from contaminated wound or in intestinal tract |
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why can't we develop immunity to botulism? |
the amount of toxin necessary to induce an immune response is lethal |
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species typically affected by Clostridium botulinum |
ruminants, horses and waterfowl
rare in carnivores and swine |
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where is Clostridium tetani found? |
soil - especially heavily-manured soils
intestinal tracts and feces of various animals (considered transient member of normal flora) |
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what kind of paralysis does Clostridium tetani cause? |
muscle spasms |
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describe growth of Clostridium tetani |
unable to germinate and grow in normal tissue/wounds - require necrosis of tissue to grow so they remain localized to the wound |
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describe chains of Clostridium tetani |
single polypeptide chain cleaved extracellularly by bacterial protease into heavy and light chain which remain connected in disulfide bridge |
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what kind of Clostridium tetani is virulent? |
toxins encoded in plasmids |
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relative suceptibility of animals to tetanus toxin |
horse - guinea pig - human - mouse - rabbit - dog - cat - chicken |
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3 agent categories of Clostridium |
(i) neurotoxic
(ii) histotoxic
(iii) enteric |
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the most important cause of clostridial infection in domestic animals
causes.... |
Clostridium perfringens
clostridial myonecrosis (gas gangrene) |
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Clostridium perfringens - alpha toxin |
phospholipase C produced by all animal isolates phospholipid hydrolysis, hemolytic
*critical for necrosis |
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Clostridium perfringens - beta toxin |
leukotoxic and enterotoxic
*similar to S. aureus alpha & gamma toxins |
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Clostridium perfingens - epsilon toxin |
plasmid encoded toxin that targets complex lipids and alters host cell permeability |
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Clostridium perfingens - iota toxin |
dimeric toxin whose active portions ADP-robosylates actin
*dermonecrotic; lethal |
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Clostridium perfingens - entero toxin |
Cpe; present in strains of all toxin types, not a typing toxin |
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Which type of C. perfingens is most associated with infection and where is it found and what does it do? |
type A
soil & intestinal tract
myonecrosis - gangrene |
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how does gas gangrene spread? |
rapid infection of injured muscle in which gas forms fermentation in tissue - the necrotic tissue is excellent place for growth and expansion
*MUST debride and give antibiotics to treat
*spongy and smelly! |
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Clostridium botulinum |
disease - botulism host animal - all site colonization - none type - neurotoxic |
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Clostridium tetani |
disease - tetanus host - all colonization - wound type - neurotoxic |
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Clostridium perfringens, type A (histotoxic) |
disease - gas gangrene host - all colonization - wound type - histotoxic |
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Clostridium chauvoei |
disease - black leg (necrosis) host - cattle; sheep colonization - large muscle type - histotoxic
*not sure how cattle get it - possibly through spores consumed and travel to muscles |
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Clostridium septicum |
disease - malignant edema (more superficial than black leg) host - production animals colonization - multiple type - histotoxic |
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Clostridium haemolyticum |
disease - redwater (toxins cause intravascular hemolysis) host - ruminants colonization - liver type - histotoxic (hemolytic)
*necrosis caused by fluke migration |
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Clostridium novyi, type A |
disease - big head (nongaseous, nonhemorrhagic edema) host - sheep (ram) colonization - head type - histotoxic |
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Clostridium novyi, type B |
disease - black disease host - sheep colonization - liver type - histotoxic (hemolytic)
*necrosis caused by fluke migration |
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Clostridium perfringens, type A (enteric) |
disease - necrotizing enterocolitis - colic host - poultry (& others) - horses colonization - intestine - colon type - enterotoxic |
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Clostridium perfringens, type B, C |
disease - lamb dysentery - necrotizing enterocolitis host - sheep - production animals colonization - intestine type - enterotoxin
*lethal beta toxin |
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Clostridium perfringens, type D |
disease- overeating disease; pulpy kidney disease host - sheep colonization - intestine type - enterotoxin (epsilon toxin causes vascular damage) |
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Clostridium difficile |
disease - pseudomembranous colitis - mesocolonic edema - cholic host - humans - swine - horses colonization - colon type - enterotoxic
*toxins A & B |
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what is a granuloma? |
- hypersensitivity reaction (inappropriate immune response)
- pathogens evade immune response - macrophages continue to be recruited |
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granuloma formation |
- central core: necrotic cells & bacteria
- outer capsule of fibrotic tissue
*cannot penetrate capsule to get inside to bacteria, which are doing bad things |
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mycobacterium characteristics |
- aerobic - gram positive (will not stain this way though) - non-motile; non-spore forming - highly variable size - unique cell wall (mycolic acid) - acid fast staining |
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type of Mycobacterium that produces disease in ruminants (important in dairy industry) |
Mycobacterium avium (MAC) - subspecies paratuberculosis |
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Mycobacterium bovis |
cattle, pigs, dogs, cats, primates, cervids, sheep, goats |
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Mycobacterium pathogenesis |
- entry through respiratory or through skin - intracellular pathogen - granuloma formation - dose dependent (compromised immune) - adheres to macrophage and then divides - ingested version is harder to regulate |
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Mycobacterium clinical signs |
- often subclinical - extensive granuloma formation - GI tract (wt loss, anemia, vomiting, D+) - cutaneous granuloma - pulmonary infections (fever, wt loss, cough)
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Mycobacterium avium; subsp. paratuberculosis (MAP) |
- Johne's disease - irreversible wasting of ruminants - rapid wt loss, D+ - typically younger animals - disease doesn't manifest for many years - shed in fetus to utero, feces and colostrum/milk |
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Mycobacterium diagnosis |
- naturally occurs in feces! - acid-fast staining (rapid) - culture (slow) - molecular (PCR - cannot tell if dead or alive) - immunodiagnostics (TB test, serology) |
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Mycobacterium treatment |
- typically start treatment immediately since diagnosis can take a while - food animals - identify and cull - combined antibiotics for a long time |
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Mycobacterium prevention |
- vaccines for humans - use bleach to clean - zoonotic potential is high but is also strain dependent |
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Nocardia characteristics |
- aerobic, gram positive - non-motile; non-spore forming - filamentous (long branching, finely beaded) - acid-fast (cell wall may contain mycolic acid) - unique colony morphology |
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Nocardia species that is most common |
Nocardia asteroides
affects many species |
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Nocardia pathogenesis |
- opportunistic (common soil inhabitant; shed in animal feces) - acquired by inhalation, wound contamination or implantation of foreign material) - typically immunocompromised patients - chronic, progressive, noncontagious - catalase & superoxide dismutase allow it to survive intracellularly |
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Nocardia clinical signs |
- anorexia, fever, lethargy, wt loss - depends on site of entry |
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Nocardia in dogs and cats |
subcutaneous lesions +/- lymph nodes |
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Nocardia in dogs specifically |
thoracic +/- extension into abdominal cavity - abscesses in heart, brain, liver, kidney - gingivitis or oral ulceration - pneumonia |
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Nocardia in horses |
subcutaneous +/- lymph nodes pneumonia & sporadic abortions |
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Nocardia in cattle |
acute or chronic mastits - granulomatous-type lesions & draining fistulous tracts |
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Nocardia diagnosis |
- based on pathology and/or bacteriology - grow well in culture - easy to id - presence of G+, acid-fast & branching filaments - serology is not very effective |
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Nocardia treatment |
- surgical debridement and draining - long term antimicrobial therapy - mastitis is typically chronic - typically cull |
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Nocardia prevention |
- sanitation & wound care - prognosis is guarded with high relapse potential - zoonotic potential is minimal |
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Actinomyces characteristics |
- anaerobic/facultative anaerobic (capnophilic) - gram positive rods - non-spore forming; non-acid fast - distinct colony morphology (pigment production) - harder to grow in lab |
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Actinomyces pathogenesis |
- commensal inhabitant of oral & digestive tract - injury to area inhabited by bacteria - pyogranulomatous response - fimbrial adhesions & enzymatic properties - yellow sulfur colonies |
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Actinomyces bovis |
lumpy jaw - cattle - mandibular granulation & chronic osteomyelitis - suppurative necrosis in esophagus & reticulum - palpable masses
pulmonary infection - cattle & swine
horses - cervical lymphadentitis (like strangles) |
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Actinomyces suis |
opportunistic mammary infection in sows
starts as superficial infection from suckling piglets |
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Actinomyces viscosus |
dogs - cutanoues, noduloulcerative lymphangitis - thoracic & abdominal infections - osteomyelitis
rodents - periodontal disease |
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Actinomyces isralii |
primarily human pathogen
face & neck lesions |
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Actinomyces diagnosis |
- clinically by presence of sulfur granules - wash and crush granules for confirmation - bacteriology methods - don't use serology |
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Actinomyces treatment |
- surgical intervention with drainage - relapses are common - highly susceptible to antibiotics but need one that can penetrate the pus! |
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Actinomyces prevention |
- oral care - no vaccine avialable - zoonotic potential is minimal but it is transmissible via bites |
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Dermatophilus characteristics |
- facultative anaerobes - gram positive - non-acid fast; non-motile - 2 morphologies (filamentous "hyphae" & motile "zoospores") - hemolytic in culture |
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Dermatophilus congolensis |
- obligate parasite in many species - exudative dermatitis in livestock - spread by direct contact or biting insects - tropical and subtropical regions (the moisture is important for causing the initial damage to skin) |
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Dermatophilus pathogenesis |
- zoospores enter through injured skin - spores germinate and hyphae penetrates epidermis - neutrophilic response causes keratinzation - phospholipases & proteolytic enzymes (VF) |
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Dermatophilus clinical signs |
- exudative dermatitis with matting of hair/wool with scab/crust formations - cattle, horses, sheet, goats, deer, rabbits, dogs, cats lizards - horse = rain rot/rain scold; greasy heel - sheep = lumpy wool; strawberry foot rot
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Dermatophilus diagnosis |
pathology, bacteriology or antibody stains
* CAN use serology |
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Dermatophilus treatment |
- remove scabs and wash with soap/water - antibiotics - can be non-responsive to therapy in which case animals can succumb to secondary and systemic infections and die |
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Dermatophilus prevention |
- no vaccine - keep envmt dry and prevent overcrowding - zoonotic potential is rare |
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Rhodococcus characteristics |
- aerobic - gram positive - pleomorphic coccobacillus - non-motile; non-spore forming - may stain partially acid-fast - colonies are mucoid and salmon colored - synergistic hemolysis & positive CAMP test |
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Rhodococcus equi |
- common soil inhabitant - in feces of herbivores |
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Rhodoccus pathogenesis |
- typically via inhalation - swallowing infected sputum can give rise to ulcerative colitis, mesenteric lymphadentitis & D+ - hematogenous dissemination - osteomyelitis - occasionally spread via wound contamination |
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Rhodoccus virulence factors |
- facultative intracellular pathogen - plasmid is essential - specifically targeted to macrophages by CR3 receptor (cell death) - large influx of nutraphils (granulation formation) |
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Rhodococcus clinical signs |
- foals: pyogranulomatous bronchopneumonia > abdominal abcesses; peritonitis; adhesions - pigs: granulomatous lesions > less virulent and localized > +/- plasmid |
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Rhodococcus diagnosis |
- difficult based on clinical signs - culture is definitive - cytology shows intracellular G+ rods - serology cannot differentiate |
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Rhodococcus treatment |
- minimize stress (respiratory distress) - antibiotics must be able to penetrate plasmid - prolonged drug therapy - good prognosis with medication - no long term effects |
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Rhodococcus prevention |
- good immunity - no vaccines - remove manure frequently; good husbandry - public health concern is minimal |
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Corynebacterium characteristics |
- facultative anaerobe - gram positive - pleomorphic rods (club shape; chinese letter) - non-spore forming; non-motile - not acid-fast |
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major pathogens of Corynbacterium |
C. pseudotuberculosis - horses & small ruminants
C. renale - cattle
C. diptheriae - humans |
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Corynbacterium pseudotuberculosis |
- positive CAMP reaction - VF: lipid rich cell wall &toxic phospholipase D - enters through skin wounds, multiplies & undergoes phagocytosis - cell death increases spread - transmitted from evmt, arthropods & fomites |
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Corynbacterium pseudotuberculosis clinical signs |
- caseous lymhadenitis (CLA) - sheep & goats - ulcerative lymphangitis and ventral abcesses in horses (pigeon fever) - abscesses and mastitis in cattle - edema, fever, non-healing wounds, lameness, wt. loss, anorexia, depression |
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Corynbacterium pseudotuberculosis diagnosis |
- bacterial culture > abscess contents (not fastidious) - ELISA (internal abscesses) - ultrasonography to determine extent of internal abscesses |
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Corynbacterium pseudotuberculosis treatment |
- lance/flush external abscesses **collect contents - contaminate envmt - antimicrobial tx depends on severity - prognosis for sheep/goats is poor but horses are much less likely to develop internal infection |
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Corynbacterium pseudotuberculosis prevention |
- sanitation, fly control, proper wound care - disinfect sheering blades between sheep - combination vaccine for ruminants - minimal public health concern |
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Corynbacterium renale pathogenesis |
- normal flora of lower urinary tract in ruminants - opportunistic pathogen - pilus-mediated attachment - urease positive (ammonia production) - grow readily in urine and spread - not sure of VF |
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Corynbacterium renale clinical signs |
- typically females - fever, anorexia, arched back, urinate small amounts frequently - urine has albumin, leukocytes, fibrin & small blood clots - cystitis, ureteritis, pyelonephritis - sheep: posthitis (pizzle rot) - high protein diet is predisposing factor |
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Corynbacterium renale diagnosis, treatment & prevention |
- bacteriology tests (u/a) - role of immunity is unknown - antibiotic tx - reduce protein in diet - zoonotic potential is minimal |
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Arcanobacterium/Trueperella characteristics |
- gram positive - short rods - facultative anaerobes - non-motile; non-spore forming - no unique cell envelope structure - very small colonies (narrow, distinct zone of hemolysis) |
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4 animal pathogens in Arcanobacterium/Trueperella |
A. hippocoleae - equine vaginitis
A. phocae - seal septicemia
A. pluranimalium - deer lung abscess; porpoise splenic abscess
T. pyogenes*** |
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Truperella pyogenes pathogenesis |
- opportunistic (typically secondary pathogen) - inhabitant of mucous membranes - physical damage allows it to get in and spread - skin, viscera, mammary gland, repro tract, joints - VF: pyolysin (PLO) exotoxin lyses RBC; adhesion proteins; exoenzymes Dnase, neuraminidase, protease |
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Truperella pyogenes clinical signs |
- abscesses - mostly localized; common in domestic ruminants; liver abscess in cattle - suppurative mastitis (teat injury; seasonal - flies) - septic arthritis in swine - umbilical infections, foot rot, traumatic reticulitis in calves; can cause abortion in cattle |
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Truperella pyogenes diagnosis, treatment & prevention |
- positive culture from abscess material (48hrs) - highly susceptible to antibiotics in vitro but in vivo it has to get through capsule & pus - treatment is often not practical - vaccination is unsuccessful - zoonotic potential is minimal |
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Erysipelothrix rhusiopathiae characteristics |
- slender, gram positive rod - non acid-fast - facultative anaerobe - small clear colonies - narrow zone of incomplete hemolysis - produces coagulase |
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Erysipelothrix rhysiopathiae disease |
- carried asymptomatically in tonsils of swine - non humans: erysipelas - acute septicemia - swine & poultry industry concerns - access blood stream via GI tract, trauma or biting insects - vaccination is effective |
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3 stages of E. rhysiopathiae in swine |
1. acute - septicemia (6-12 mo old)
2. subacute - diamond skin disease
3. chronic - arthritis & vegetative endocarditis |
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E. rhysiopathiae pathogenesis |
*poorly understood - capsule (required for virulence) - neuraminidase - cleaves sialic acid residue on endothelial cells - diamond lesions - hyaluronidase & coagulase - levels do not correlate with virulence |
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Listeria monocytogenes characteristics |
- gram positive - facultative anaerobes - motile - narrow zone of clear hemolysis - naturally resistant to nalidixic acid - can be isolated from soil, animal feed, feces and tissues |
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Listeria monocytogenes health concern |
- common contaminant of food - grow very well at cooler temps (refrigeration) - latest outbreak in 2002 with 7 deaths |
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clinical manifestations of Listeria monocytogenes |
1. contaminated food source - oral entry 2. colonization of intestine 3. intestinal translocation 4. replication in liver & spleen 5. resolution or spread to other organs
*often don't show signs until stage 5 in animals |
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sequelae of Listeria monocytogenes |
- abortion in pregnant animals
- invasion of CNS: facial paralysis, circling disease in ruminants (sheep) , meningitis, meningoencephalitis
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pathways for Listeria monocytogenes to cross blood brain barrier |
1. direct hematogenous contact with endothelial cells of blood/brain
2. entry of bacteria between cells via infected phagocytes
3. entry into neurites following consumption of contaminated food & nonhematogenous transit to the brain |
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listerial cellular pathogenesis factors |
1. entry - internalin A (inlA) & inlB 2. escape from uptake vacuole - listeriolysin O (LLO): pore forming cytolysin 3. cytosolic replication and mvmt - surface protein ActA 4 cell-to-cell spread - 2 phospholipases |
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Bacillus anthracis |
anthrax - domesticated and wild animals - humans |
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Bacillus cereus |
food poisoning
infrequently causes abortion and mastitis in cattle |
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Bacillus thuringiensis |
insect control |
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Bacillus characteristics |
- large, gram-positive - spore forming rod form oval spores located centrally in nonswollen "sporangium" - lab & serological tests can differentiate species |
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Bacillus anthracis pathogenesis |
- initiated by uptake of spores by macrophages - germinating spores escape uptake vacuole and are released by macrophages - sepsis - vegetative bacteria synthesize an antiphagocytic capsule - release toxins |
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Bacillus anthracis toxins |
1. edema factor (EF) - adenylylcyclase causing edema via altering intracellular cAMP conc. 2. lethal factor (LF) - metalloprotease causing cell death through unknown mechanism 3. protective antigen (PA) - protein subunit associates with EF & LF to promote their entry into cells |
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Bacillus anthracis transmission |
- spores live in soil but vegetative form is ONLY inside hosts - do NOT open up animal that may have died of anthrax - aerobic envmt will allow to get back into soil - spores are resistant to boiling but not incineration |
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Anthrax in medical & vet importance |
humans - GI from consumption of affected meat - highly fatal inhalation (bioterror) - cutaneous proliferation (most common) herbivores - GI route (death in 2-3 days) pigs - relatively resistant - acute septicemia or edema of face and neck dogs - edema of face and neck |
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signs of anthrax related death |
- acute/peracute death - rigor mortis does not set in - dark blood oozing from mouth, anus, nostril - lack of clotting - hemorrhages along GI tract mucosa - ulcers - meningitis |
