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BacT - JL > Exam I bacteria > Flashcards

Exam I bacteria Flashcards

1
Q

Actinomyces spp.

A
  • Virulence not well understood
  • Habitat: mucosa of the oropharynx
  • Facutative anaerobic & anaerobic spp. & capnophilic
  • Catalase negative
  • “molar tooth-like”
  • Grow as colonies in center of lesion –> often forms draining tracts
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2
Q

What common diseases are caused by Actinomyces spp.?

A
  • Pyogranulomatous disease
  • Polymicrobial infection within oropharyngeal flora
  • Chronic infections –> bone lysis
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3
Q

Actinomyces bovis

A
  • Causes “Lumpy Jaw” - Pyogranulomatous osteomyelitis
  • Gram-positive, club-shaped rods
  • Localized, chronic, progressive granulomatous abscess in the mandible, maxillae, or bony tissues in the head
  • Introduced via penetrating wounds
  • Facial distortions, loose teeth, dyspnea are commonly found
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4
Q

Actinomyces bovis diagnosis, treatment and control

A

Diagnosis: culture/microscopic exmanation –> must request aerobic and anerobic cultures

Treatment: Susceptible to penicillin G, iodides; long term treatment; surgical removal of froeign bodies

Control: minimize risk of mechanical injury

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5
Q

Dermatophilus congolensis

A
  • Epidermal abscesses with hyperkeratosis
  • Filamentous branching –> divides into “tram-tracks”
  • Aerobic; Catalase positive
  • production of coccoid fragments –> motile zoospores
  • zoospores have chemotaxis for CO2; attracted to moist and damaged skin
  • all animals can be infected: Rain scald in horses; Strawberry footrot in goats; dermatophilosis in reptiles;

Virulence facotrs: chemotaxis of zoospores, keratinolytic activity

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6
Q

Dermatophilus congolensis diagnosis, treatment, and control

A

Diagonsis: microscopic examination of scabs; use of Giemsa stain

Treatment: systemic antibitic treatment - penicillin G and tetracycline

Control: Treat and isolate infected invidiausl; eliminate predisposing factors

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7
Q

Trueperella pyogenes

What’s the significance in Cattle?

A
  • Suppurative infection in ruminant and swine
  • Facultative anerobe; non-spore forming; non-motile; non-capsulated; capnophilic
  • Found on mucous membranes –> most infections are endogenous

In Cattle: involved in most purulent infection of traumatic/opportunistic origin

  • Common location - lung, pericardium, liver, uterus, renal, brain, bones
  • Causes: abortion and summer mastitis (communicable disease among pasutred daily cattle during the dry period)
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8
Q

Actinobaculum suis

A
  • Causes cystitis and pyelonephritis
  • Anaerobic; sexually transmitted pathogen
  • Commensal diphteroid organism in prepucial mucosa of boars
  • Death often follows as a result of renal failure

Virulence factor: UREASE

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9
Q

Staphylococcus spp.

A
  • Facultative anaerobic; catalase positive; cocci

Exceptions: Anaerobic spp: S. sacharolyticus, S. aureus subsp. anaerobius

  • Opportunistic pathogen
  • Habitat: Skin and mucous membranes
  • Suppurative conditions - production of pus

Toxin mediated diseases (superantigens): Staphylococcal toxic shock syndrome (TSST-1); Staphylococcal food poisoning (enterotoxin); Staphylococcal scalded skin syndrome (Exfoliative toxins)

Virulence factor: Protein A - binds FC portion of IgG; Hemolysins; proteases; hyaluronidase; lipases; leukocidin; biofilm formation

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10
Q

What is coagulase? what does it do?

A

Coagulase is an enzyme that is sued to convert fibrinogen to fibrin.

It is often used to differenitate between species

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11
Q

Staphylococci pseudintermedius

A
  • Most common isolate found in dogs
  • Gram positive cocci in clusters
  • Cuases pyoderma and folliculitis

Diagnosis:

  • Direct examination of species
  • Evidence of inflammation with high # neutrophils
  • Culture infection
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12
Q

Staphylococcus hyicus

A
  • Greasy Pig Disease - Exudative epidermitis
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13
Q

Staphylococcus aureus

  • cattle
  • Humans
  • Sheep
  • Birds
A

Cattle - Chronic and acute mastitis/gangrenous mastitis

Humans - Ulcerative pododermatits

Sheep - Cervical lymphadenitis (subsp. anaerobius)

Birds - Bumble Foot

Rodents, humans, horses - Botryomycosis - Chronic pyogranulomatous inflammation

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14
Q

Staphylococcus aureus treatment

A
  • Antimicrobial susceptibility testing is essential
  • Common emergence of multidrug resistant staphylococci
  • inducible Clindamycin resistance in macrolide resistant staphylococcus - isolates which are macrolide resisant is also clindamycin resistant
  • Cephalosporins are first line treatment choice –> quinolones are second line
  • Beta-lactamase-mediated resistance is common; Methicillin resistance becoming a problem (MRSA (zoonotic) & MRSP)
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15
Q

Streptococcus spp.

A
  • Gram-positive cocci found in pairs/chains
  • Facultative anerobe (aerobic or anaerobic)
  • Catalase negative; haemolytic activity used for classification (beta = pyogenic; alpha = non pyogenic)
  • Some are capsulated

Diseases:

  • Acute suppurative
  • Subacute endocardidits
  • Chronic mastitis

Superantigens:

  • Streptococcal toxic shock syndrdome (STSS)
  • Necrotizing fasciitis and myositis (NFM)
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16
Q

Streptococcous virulence factors

A
  • Capules
  • Peptidoglycan layer with teichoic/lipoteichoic acid
  • M protien*
  • Ig binding proteins
  • Streptokinase
  • Streptococcal pyrogenic exotoxins (superantigens)
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17
Q

Streptococcus pyogenes

A
  • Scarlet fever in humans - Rheumatic fever; kidney disease; skin infection; abscesses of the throat; arthritis
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18
Q

Streptococcus canis

A
  • Commonly infects skin and mucous membranes
  • Embolic lesions in heart and lung; septicemia; skin ulcerations; meningitis; necrotizing fasciitis; toxic shock-like syndrome
  • Kittens and puppies
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19
Q

Streptococcus suis

A
  • gram positive cocci
  • ZOONOTIC
  • Perdominately infection in pigs (type 2 is most common)
  • serositis, meningitis, polyarthritis, endocarditis
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20
Q

Streptococcus iniae

A
  • Infects fish
  • zoonotic
  • Septicemia in fish; central nervous system disruption
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21
Q

Streptococcus procinus

A

Jowl abscess in pigs

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22
Q

Streptococcus pneumoniae

A

Humans - Causes pneumonia, septicemia, and meningitis

Guinea pigs and rodents - pneumonia

Domestic pets - act as carriers

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23
Q

Streptococcous equi

(S. equi subsp. equi)

A

Strangles in horses!!!

  • hyaluronic acid capsule - mucoid appearance
  • Use sugar fermentation test to distinguish between different species
  • All ages are susceptible, average <2 yrs
  • <4 mo are protected by maternal antibodies
  • Enlargement of retropharyngeal lymph nodes
  • HIGHLY contagious - direct transmission or indirect
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24
Q

Streptococcus equi

Virulence factor

A
  • Hyaluronic acid capsule
  • M Proteins
  • IgG Fc binding proteins
  • Peptidoglycan/teichoic acid
  • Streptokinase
  • Hyaluronidase
  • Streptolysin
  • DNAase
  • Exotoxins
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25
Q

Streptococcus equi

Clincal signs

A
  • Fever
  • Purulent nasal discharge
  • Anorexia and dysphagia
  • Moist cough
  • Lymph node abscessation
  • Can survive in pus for 6 - 8 weeks
  • Guttural pouch empyema (pus formation)

Bastard strangles - disseminated infection –> infection of lymph nodes in chest cavity

Purpura haemorrhagica

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26
Q

Streptococcus equi

Recovery

Diagnostic

Treatment

Control

A

Recovery - infected animals usually recover after abscesses mature and rupture

  • 75% deelop immunity after recovery

Diagnostic

  • Culture
  • Serology - ELISA for M protein antibodies

PCR - for M protein

Treatment

  • Most recover spontaneously
  • symptomatic treatment to relieve pain
  • Antibiotics only effective if given soon after exposure

Control

  • REPORTABLE DISEASE
  • apply isolation, hygiene, and disinfection practice
  • Vaccines: Killed –> effetive for pregnant mares and foals to maintain high level of anti-M protein opsonizing antibodies
  • Live –> similar to killed except in all other animals
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27
Q

Enterococcus

A
  • inhibit GI tract
  • nosocomial infection
  • Causes persistant UTI
  • Vancomycin resistance
  • In vivo resistance
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28
Q

Listeria spp.

A
  • Gram positive facultative anaerobic rods
  • capable of growing in a wide range of temperature (4 - 44C) –> what you find in your fridge!
  • Carried in the GI tract of animals
  • Outbreaks typically seen after feeding poor-quality silage –> winter-spring disease as more silage is fed during this time
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29
Q

Listeria monocytogenes

A
  • Circling disease - neurologic symptom; unilateral facial nerve paralysis
  • Facultative intracellular bacteria –> persists in macrophages (intracellular growth)
  • Outbreak typically occur after feeding poor-quality silage –> winter-spring disease as more silage is fed during thist time
  • Diseases - encephalitis - travels up trigeminal nerve and affects brainstem
  • abortions - focal hepatic necrosis
  • Septicemia - common in monograstrics

Virulence factors - Internalin (adhesion, entry, phagocytosis)

  • Listeriolysin - aids in intracellular multiplication
  • Act A - intracellular movement –> actin filmaent utlized to travel between cells

Lesions:

  • Microabscesses and glial nodules infiltrated by neutrophils; acute vascular fibrinoid necrosis; leptomeningitis; neuronal necrosis;
30
Q

Listeria monocytogenes

Diagnosis

Treatment

Control

A

Diagnosis

  • CNS disease
  • Circling disease
  • Post-mortem - lesions in pons, medullam oblongata, and spinal cord
  • Gram stained CSF short intracellular and extracellular gram positive bacteria

Treatment:

  • Penicillin, ceftiofur, erythromycin
  • high doses are required

Control:

  • No vaccines
  • Avoid high risk food
  • minimize aerosol exposure
31
Q

Erysipelothrix rheusiopathiae

in swine

A
  • Gram-positive facultative anaerobic bacillus
  • Non-sporeforming
  • swine are the most susceptible (30 - 50% of healthy swine are carriers)
  • Causes polyarthritis, vegetative endocarditis, and septicemia

Transmission and virulence factors:

  • Primarily oral transmission –> infection of palatine tonsils

Neuraminidase - adherence to endothelial cells

Heat labile capsule - resistants phagocytosis

32
Q

Erysipelothrix rheusiopathiae

Sheep

Turkey

Marine mammals

Calves

Humans

A

Sheep - Fibrinopurulent polyarthritis and osteomyelitis

Turkeys - cyanotic combs, splenomegaly, haemorrhage, polyarthritis, endocarditis

Marine mammals - septicemia and similar skin lesions

Calves - polyarthritis

Humans - erysipeloid - localized skin lesions

33
Q

Erysipelothrix diagnosis, treatment, and control

A

Diagnosis: culture

Treatment: antimicrobia treatment - penicillin & tetracycline

Control: treat and isolate infected animals

  • vaccination
34
Q

Bacillus spp.

A
  • Large gram positive rods
  • Endospore forming
  • Thickpeptidoglycan layer - teichoic and lipo-teichoic acids
  • Grows very rapidly
  • Aerobic or facultative anerobes
35
Q

Bacillus anthracis

A
  • Koch’s postulate is based on anthrax bacilli
  • Aerobic, non-motile, square-ended gram positive rods in chains
  • non-hemolytic –> meusa head colonies
  • Stains by McFadyean stain

Virulence factors:

  • Capsule - polymers of D glutamic acid; produced in vivo
  • Anthrax toxin: Edema factor = inhibition of neutrophils; lethal factors = cell death; Protective antigen = translocation into cells

**BOTH FACTORS ARE REQUIRED FOR VIRULENCE**

36
Q

What is the pathogensis of Anthrax

A

Exposure to endospore –> endorespores germinate within phagolysosomes of macrophages –> intracellular survival factors allow growth initiation and phospholipase mediates escape from the phagocytic cell –> capsule and edema factor inhibit phagocytosis of vegetative cells –> cells grow rapdily in the body –> complete anthrax toxin causes cell death and affects vascular permeability

37
Q

What are the different forms of anthrax and what animals are susceptible?

A

Ruminants - septicemia

Horses - septicemia

Humans - Wool sorter’s disease - pulmonary distress

Humans - Cutaneous lesions Q

PIgs and dogs - Pharyngeal lesions

Humans, pigs, and horses - Intestinal lesions

38
Q

What are the pre-mortem and post-mortem signs of antrax baclli in…

Cattle/sheep/deer?

Horses?

Swine?

Carnivores?

A

Cattle/sheep/deer

Pre-mortem:

High fever; blooding from orifices; shock; respiratory distress

Post-mortem:

Dark and unclotted blood; incomplete rigour mortis; splenomegaly

Horses

  • Colic and diarrhea; edema at point of infection

Swine

  • Pharyngeal lesions; ulcerative lesion; lymphadenitis; obstructive edema –> death; ulcerative haemorrhagic enteritis and mesenteric lymphadenitis

Carnivores

  • Similar to swine
39
Q

How do you diagnose Anthrax contamination? how do you treat and control it?

A

REPORTABLE DISEASE

Diagnosis:

  • Blood smear exmaination
  • Aerobic culture and PCR from blood
  • DO NOT CONDUCT FIELD NECROPSY
  • Spleen biopsy
  • Staining with McFadyean’s methylene blue

Treatment

  • can only treat vegetative cells
  • Antimicrobials - penicillin, tetracycline, doxycycline, ciprofloxacin

Control

  • Vaccinate healthy animals
40
Q

Anthrax symptoms/complications in humans

A

Cutaneous anthrax - subcutaneous edema and septicemia (80 - 90 % recover)

Gastrointestinal anthrax - pharyngeal lesions; lymphadenopathy; vomiting blood and bloody diarrhoea (40 - 75 recover)

Pulmonary or inhalation - pulmonary oedema; pneumonia; meningitis (100% fatality)

41
Q

Corynebacterium spp.

A
  • Gram positive pleomorphic caultative anaerobe rods
  • Non-spore forming, non-motile, catalase positive
  • Lipophilic spp - Facultative intracellular bacteria
  • Non-lipophilic spp - pyogenic toxic
42
Q

Corynebacterium renale

A

Contagious Bovine Pyelonephritis - inflammation of the kidney

  • Disease of adult cows
  • Antemortem signs - fever; painful urination; ammoniac odour of urine; acute abdominal pain (colic)

Postmortem signs: Multifocal abscess in kidney; enlarged renal lymph nodes; uremia

43
Q

Corynebacterium pseudotuberculosis

Sheep and Goats

A

Caseous lymphadenitis

  • Effects sheep and goats
  • Gram positive facultative intracellular coccobacillus
  • Abscess formation in or near major peripheral lymph nodes or within internal organs and lymph nodes

Virulence factor:

  • Exotoxin phospholipase D –> damage to endothelial cells and increasing vascular permeability
  • External lipid coat –> provides protection from hydrolytic enzymes from host
  • “onion skin” apperance in the lymph node

Clincal signs:

  • Caseous necrosis of lymph nodes
44
Q

Corynebacterium pseudotuberculosis

Horses

A

Pigeon Fever (Colorado strangles or Dry-lan distemper)

  • Cattle can also be infected
  • Ucerative lymphangitis of lower extremities
  • Abscesses in the pectoral region
  • Found in western and midwestern states
  • Enter through skin abrasions or arthropod vectors
45
Q

Corynebacterium pseudotuberculosis

Diagnosis

Treatment

Control

A

Diagnosis:

  • Culture of purulent materials
  • Synergisitc hemolysin inhibition test (SHI) or you know.. (SHIT) - detects antiboides from phospholipase D exotoxin
  • Positive test indicates: past resolved infection, recent exposure, recent vaccination, or active lesions

Treatment:

  • Not a “curable” disease
  • lancing and draining; surgical excision; systemic antibiotics (penicillin, Rifampin)

Control:

  • Biosecurity practice
  • Culling of infected animals
46
Q

Corynebacterium kutscheri

A
  • Murine pseudotuberculosis (old world rats!)
  • Lung - suppurative pneumonia
  • Lesions in kidney, liver, and heart
  • Subcuticular abscess
  • Lymphoid hyperplasia
47
Q

Corynebacterium bovis

A

dermatitis in MICE!

hyperkertosis

48
Q

Rhodococcus equi

A

Foal Pneumonia (1 - 4 month old; rare in > 8 mo old)

  • gram-positive aerobic rods/cocobacilli
  • Non-spore forming, non-motile, catalse positive
  • Facultative intracellular pathogen
  • unique lipid-rich cell envelope structure rich in mycolic acid (acid fast positive)

Virulence factor:

  • Capsule
  • Virulence associated proteins (VAPs)
  • Mycolic acid, teichoic acid/peptidoglycan
  • Cholesterol oxidase
  • Phospholipase C

Clinical signs:

  • Lung - multiple coalescing firm casenecrotic foci
  • GI - ulcerative enterocolitis over peyer’s patches

Bronchial and mesenteric lymph node - pyogranulomatous lymphadenitis

Bone - Osteomyelitis

49
Q

Rhodococcus equi in..

Cattle

Sheep

Goats

Pigs

Cats

Humans

A

Cattle - Metritis, lymphadenitis, pneumonia

Sheep - Caseous bronchial lymphadenitis

Goats - Pyogranulomatous lesions in liver and lungs; osteomyelitis of the vertebra and skull; entercolitis

Pigs - Tubercuolosis-like lesions in submaxillary and cervical lymph nodes

Cats - Pyogranulomatous skin lesions

Humans - zoonotic in immunocompromised inidividuals

50
Q

Rhodococcus equi in humans

A

Lung - Pyogranulomatous pneumonia (alveoli filled with abundant macrophages); septal necrosis and atelectasis

Intestine - pyogranulomatous inflammation of lymphoid tissue

Lymph nodes - pyogranulomatous lymphdenitis

51
Q

Rhodococcus equi

Diagnosis

Treatment

Control

A

Diagnosis:

  • Evalulte the entire premise
  • Screen for early detetion of disease
  • Serology tests - Culture or PCR on transtracheal aspirate; cytologic evidence of sepsis
  • Smears of affected tissue, transtracheal aspirates, bronchoalveolar lavages

Treatment:

  • Prolonged treatment –> expensive and adverse effects
  • Combination of macrolide and rifampin
  • Hyperimmune plasma and NSAID

Contorl:

  • Hyper immune plasma can prevent penumonia
  • Early detection, treatment, and environmental management
52
Q

Norcardia asteroides

A
  • Gram positive pleomorphic facultative intracellular bacterium
  • Non-motile and non-sporeforming
  • Appears as rods, cocci, or coccobacilli –> long branching filaments
  • AEROBIC
  • most commonly isolated in species in dogs and cats (more ind ogs than cats)
  • Opportunistic, noncontagious, pygranulomatous –> suppurative disease
53
Q

Norcardia asteroides

Horses

Cattle

Sheep

Swine

Humans

A

Horses - N. asteroides and N. braziliensis cause fibinopurulent pneumonia and pyothroax

Cattle - Bovine farcy - cutaneous nocardiosis –> lymphangitis and lymphadenitis

Humans - defects with T cell mediated immunity

Horses, cattle, sheep, and swine - abortions

54
Q

Norcardia asteroides

Diagnosis

Treatment

Control

A

Diagnosis

  • Culture –> acid fast strain –> ID

Treatment:

  • aminoglycoside + carbapenem

Control:

  • Difficult –> sporadic disease
55
Q

Clostridium spp.

A
  • Neurotoxic - binds to nerves and causes neuronal damage
  • Histotoxic and invasive - invade tissues and causes damage
  • Enteric/enterotoxigenic - infects the GI tract and produces toxins

Virulence factors:

  • All clostridia produce one or more bacterial protein toxins or etracellular enzyme
  • Requirement of anaerobic environment = necrosis as a predisposing factor
56
Q

Clostridium tetani

A

TETANUS - “wooden horse syndrome”

  • Anaerobic gram positive Rod
  • Terminal endospores –> grows in contaminated wounds
  • Produces neurotoxin –> spastic paralysis

Pathogensis:

wound infected with C. tetani –> toxin produced –> toxins enter nearest motor nerve –> retrograde transport –> neuromusclar ending –> prevents release of neurotransmitters –> spastic paralysis

57
Q

Clostridium tetani

Diagnosis

Treatment

Control

A

Diagnosis:

  • Culture is often unrewarding –> takes too long
  • Serolog is not very useful
  • look for clinical signs: locked jaw + straightened and stiff limbs

Treatment:

  • Antitoxin
  • Anti-tetanus equine serum (IV or IM)
  • Antimicrobial treatment –> only stops production of toxin
  • Supportive care

Control:

  • Toxoid immunization
  • Post exposure prophylaxis
  • Prompt wound management
58
Q

Clostridium botulinum

A

BOTULISM

  • Botulinum neurotoxin –> inhibits neurotransmitter release
  • Food intoxication (vegetable and meats) –> toxin absorbed and distributed in bloodstream
  • Occasional toxico-infectious forms –> wounds in intestine
  • Commonly seen in babies given raw honey –> honey is a good source of C. botulinum spores
  • one gram of dried flesh can have enough botulinum to kill a cow

Clinical signs:

  • Symmetrical flaccid paralysis
  • Cranial nerve impariment (double vision, dysphagia)
  • Hind limb paralysis
  • Respiratory failure

HUGE problem in aquatic birds

  • Maggots can carry C. botulinum –> infect aquatic birds during feeding
59
Q

Clostridium botulinum

Diagnosis

Treatment

Control

A

Diagonsis:

  • Demonstration of toxin in serum, food/stomach contents

Treatment:

  • IV or IM antitoxin –> only use if toxin is still being absorbed
  • Therapeutic drugs to enchance cholinergic neurotransmitters

Control:

  • Toxoid immunization in high risk animals
  • Avoid feeding suspected food
60
Q

Features of histotoxic clostridial diseases

A
  • mechanical injury –> wounds –> anaerobic environment –> endospore growth
  • Toxins cause tissue destruction –> fermentation of msucle glycogen –> gase accumulation
  • Deposited endospores may remain dormant in the body for extended periods
61
Q

What is necrotic myositis?

A

Necrosis of skeletal muscles

62
Q

Clostridum chauvoei

A

BLACK LEG - Necrotic myositis - emphysematous swelling

  • Cattle and sheep
  • Lesions appear haemorrhagic
  • Sudden death is common (100% fatality) –> myocardium and diaphragm effected

Clinical signs:

  • Fever, anorexia, depression, lameness
63
Q

Clostridum novyi

A

Spores in intestine and reach liver –> traumatic damage by liver fluke provides anaerobic conditions –> germination of spores

64
Q

Clostridium septicum

What does it cause in all species?

What does it cause specfically in sheep?

A

Malignant edema

  • Fatal toxemia affect in all species of animals
  • Local exotoxins = inflammation –> edema, necrosis and gangrene

BRAXY in sheep

  • Highly fatal infection
  • Toxemia and inflammation of the abomasal wall
65
Q

Clostridium chauvoei, septicum, novyi

Diagnosis

Treatment

Control

A

Diagnosis:

  • Direct fluorescent antibody staining test (DFA)

Treatment:

  • antimicrobial treatment (penicillin)
  • Hyperbaric oxygen

Control:

  • Routine vaccination
66
Q

Clostridium perfringens

A

Necrotizing haemorrhagic enteritis

  • Enteric clostridium
  • Five types of toxins - Type D is more commonly found in small ruminants

Type D enterotoxemia - similar symptoms as listeria! - Edema and malacia

67
Q

Clostridium difficile

A

Enterocolitis

  • Affects humans, horses, pigs dogs, cats, laboratory rodents
  • Risk factors: recent antibiotic use, increased age, hospitalization
  • neonates are resistant
  • Dysbiosis - disruption of normal flora –> pseudomembraneous colitis

Tox A - Enterotoxin, fluid loss

*Tox B - Cytotoxin, destroys cells rapidly

68
Q

Clostridium difficile

Diagnosis

Treatment

Control

A

Diagnosis:

  • Culture - obligate anaerobe –> requires anaerobic median
  • Direct toxin detection - antigen for Tox A and B

Treatment:

  • Stop antibiotics
  • Clindamycin should NOT be used in horses
  • give probiotics
  • avoid anti-diarrhoeal medication –> accumulates toxin
69
Q

Clostridum spiroforme

A
  • Found in rabbits (4 - 8 weeks old)
  • Entertoxemia –> explosive diarrhoea
  • Do not use lincomycin, clindamycin, and erythromycin –> induces clostridium related enterotoxemia
70
Q

Clostridium piliforme

A

Tyzzer’s Disease

  • GRAM NEGATIVE
  • Focal liver necrosis –> fatal diarrheal
71
Q

Non-sporeforming anaerobes

A
  • usually infects mucous membranes and skin
  • require high levels of Vit K, hemin, and growth factors
  • Endogenous origin

Virulence factors:

  • Catalase and superoxide dismutase –> protection from oxygen

Clinical signs:

  • Foul smelling discharge (from necrotic tissue)
  • Gas in tissues or discharge
  • Pyogranulomatous lesions
  • Infetions do NOT repsond to aminoglycosides
72
Q

Fusobacterium necrophorum

A

Foot Rot and Liver abscess

  • Extensive necrosis and keratinolysis in severe cases

Diagnosis:

  • Culture and PCR

Treatment:

  • Remove necrotic tissue
  • Oxygenation
  • Antimicrobials (penicillin, metronidazole, clindamycin chloramphenicol, doxycycline)

Control:

  • Very difficult

BacT - JL (3 decks)

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