Exam 2 Flashcards
What is the most common c/s of listeriosis?
Circling disease
What pathogen is the cause of circling disease?
Localized ascending asymmetric infection of the brain stem of ruminants
-Listeria monocytogenes
What nerves are damaged?
Cranial nerves V, VII, and VIII.
C/S:
-Unilateral facial paralysis
-Meningoencephalitis
Tx:
-High dosages of antimicrobials effective if early
What are the characteristics of listeria monocytogenes?
Monocytogenes Most pathogenic
- Small rod
- hemolytic colonies in blood agar
- Gram positive
- Non-spore forming
- Grows on non-enriched media
- Facultative anaerobe
- Catalase-positive
- Oxidase negative
- Hydrolyses esculin
- Environmental saprophytes (GI of carrier, oral-fecal route)
- *Outbreaks = bad silage**
Tolerates
- 4 to 45 Celsius
- pH 5.5 to 9.6
What disease or C/S does Listeria ivanovii cause?
What animals are affected?
- Less pathogenic than Monocytogenes
- Sheep cattle
- Causes abortion
What disease or C/S does Listeria innocua cause?
What animals are affected?
- Meningoencephalitis
- Sheep
What are the three major forms of listeriosis in ruminants?
How long is the incubation period?
What are the lesions and clinical signs?
- Neural: circling disease, silage disease, meningoencephalitis
- Visceral: septicemia, seen in neonates, specially calves and piglets
- Abortions: sporadic abortions
Incubation: 14- 40 days
Lesions:
- Neural: micro abscesses and perivascular lymphocytic cuffing
- Depression, drooping ears, protrusion of the tongue, salivation, paralysis of the face.
- Death within days
Clinical signs
- Abortion no signs for 12 days
- Septicemic: 2-3 days incubation, micro abscesses of the heart, kidney, liver
- Cattle and sheep: keratoconjunctivitis and iritis (ocular listeriosis)
Pathogenesis of Listeriosis
Transmission
- Ingestion of contaminated silage
- Organisms penetrate M cells in Peyer’s patches in the intestine
- Lymph and blood spread
- Pregnancy = transmission transplacental
- Mucosal invasion through the dental pulp, followed by trigeminal nerve infection with axonal transport to the brain, midbrain, pons and medulla oblongata.
Transmission
- Temperate or colder climates high incidence of intestinal carriers worldwide
- Natural reservoir = soil and mammalian GI tract (monocytogenes) which contaminate vegetation
- Animal to animal via fecal-oral route
- Primary winter-spring feedlot animals
- less acidic pH of spoiled silage = pathogen multiplication
- Remove or change Silage
Virulence factors
Diagnosis
Treatment
Control
- Invades epithelial cells or phagocytic cells
- Listeriolysin = hemolysin breaks down phagosome membrane. Once in cytoplasm, it begins replication
- Actin tails = spread intracellular
Dx
- Clinical signs, spoiled feed
- Lab specimens: CSF, cotyledon (abortion), fetal abomasal contents, uterine discharges.
Pathogen test
- Small colonies, smooth, flat, BLUE-GREEN color when illuminated obliquely
- Narrow zone of complete hemolysis
- CAMP test positive
- Catalase positive
- Tumbling motility at 25 C
Tx and control
- Penicillin
- Ceftiofur
- Erythromycin
- Trimethoprim/sulfonamide
- High doses required
Outbreak
- animals segregation
- corn ensiled before too mature = acidic pH
Zoonotic Potential
- Raw milk
- Fetal material handling
- Raw vegetables
Tetanus and Botulism
- Both affect the nervous system
- Both are caused by genus Clostridium
What are the characteristic c/s of Tetanus?
-CNS: spasmodic, tonic muscular contractions
What are the characteristic c/s of Botulism?
-Neuromuscular junction, flaccid paralysis
Clostridium spp.
- Gram-positive
- Obligate anaerobe
- Spore-forming rods
- Found in soil and GI of some animals
- Produce potent exotoxins
How is C. tetani introduced into body?
Tx, Dx, c/s
- Deep puncture wounds: dehorning, traumatic wound, castration in cattle.
- Toxin causes generalized muscular spastic paralysis
Tx
- Supportive care
- Injection of antitoxin
- Tetanus toxoid vaccine
C. tetani
- Lacks oxidase, superoxidase, dismutase
- Susceptible to oxygen
- Drum-stick appearance rod
- Tissue necrosis due to soil or foreign object contributes to multiplication
- Other bacteria that take up the oxygen contributor
Spread of Tetanus toxin
- Tetanospasmin: causes spasmodic, tonic contractions by interfering with release of inhibitory neurotransmitter from presynaptic nerve ending
- Descending tetanus when toxin excess is carried by lymph to bloodstream arriving at CNS
- Can be severe = bone fractures
- Respiratory failure, cardiac arrhythmias, tachycardia, hypertension
C/S or findings
- Lockjaw
- sawhorse stance
- Profuse sweating in horses, saliva accumulation
- Sensitivity to touch
- Respiratory failure may occur
Dx
- Clinical signs, history of trauma
- Tetanus toxin in serum
- Gram stain smears
- Anaerobic culture
- PCR on wound material
Tx
- Antitoxin: specific antibody to a toxin
- Toxoid: vaccine
- Large doses of penicillin; metronidazole
- Quiet and dark environment
- IV therapy sedatives, tranquilizers
- Surgical debridement of wound
What animals are most and less susceptible to C. tetani?
- Most susceptible: horses
- Least susceptible: birds
- Humans after horses, dogs less
Clostridium botulinum
Characteristics
- Gram-positive rod
- Forms spores
- Saprophyte in soil and transient in feces
- Obligate anaerobe
- Botulinum toxin potent
- Susceptibility (most to least): Water birds, poultry, horses, human, cattle, dogs, cats, pig.
- 8 different strains: B = horses, A, E = humans, C alpha = Waterfowl, C beta = Cattle, horses, humans, D = cattle, sheep.
Entry
- Exotoxin mediated, not bacteria itself
- Different than tetanus (bacteria enters and produces toxin)
- Toxin is sufficient to cause disease
- Toxins can enter via:
1. INGESTION of PREFORMED TOXIN via contaminated food - Example: feed contaminated with animal carcasses or bird droppings
2. TOXICOINFECTIONS (less common) bacteria multiply in intestinal tract, possibly ulcers, produce toxin which is absorbed systematically - Floppy baby syndrome
- Shaker foal syndrome (wound botulism)
3. Wound botulism: (rare) toxin absorbed through wound, multiplying in wound
Multiplication and spread
-following entry, toxin is distributed via bloodstream to neuromuscular junction. Multiplication doesn’t always apply because the toxin is all that is needed to cause disease.
Tetanus vs botulin toxin
- In botulism toxin prevents synaptic release of acetylcholine at the neurotransmitter junction at peripheral nerve endings, leading to muscular blockage and flaccid paralysis.
- Tetanus toxin inhibits inhibitory transmitter in CNS which leads to continuous stimulation
Botulism Tx and prevention
- Antitoxin: type specific or combined. Only inactivates toxin not yet bound. Amount needed depends on how much was absorbed
- Antibiotics: not always applicable bc no bacteria present; however, helps to prevent secondary bacterial infection
- Supportive care
- Prognosis: grave, recovery may take weeks to months
- Immunization with toxoid. Cattle (C+D) horse (B).
- Toxin typing necessary
* *Most potent toxins: 1 g kill 10 million people or 400,000 cows
Glasser’s disease
What animals are affected?
What pathogen causes it?
- It affects pigs
- Haemophilus parasuis
Characteristics of Haemophilus parasuis
- Gram-negative rods
- Small motile
- Fastidious: some species require X and V factors in chocolate agar to grow
- 5-10% oxygen optimal growth
- Facultative anaerobes
- Commensals on mucous membranes
What pathogen causes thrombotic meningoencephalitis (TME) in cattle?
Histophilus somni and it causes septicemia
Histophilus somni
Haemophilus parasuis
Avibacterium paragallinarum
- Coccobacillary and may form short filaments
- Do not grow in MacConkey Agar
- Fastidious growth: specific and picky
- Transparent, dewdrop-like colonies
- H. parasuis (Catalase +, Oxidase -) and Avibacterium paragallinarum require Factor V (NAD)
- H. somni does not require factor X and V. Catalase negative, and oxidase positive.
Pathogenicity and pathogenesis
Histophilus somni
Haemophilus parasuis
- Opportunistic due to predisposing factors
- Young or naive
- environment and other factors contribute
Virulence factors Histophilus somni
- endotoxin
- Phase variation Lipo-oligosaccharide and evasion of immune response
- LOS apoptosis of endothelial cells and leukocytes
- Production of transferrin and immunoglobulin-binding proteins
- Immunoglobulin-binding proteins Fc portion of IgG2 resistance to complement mediated killing in serum
- Biofilm formation = exopolysaccharide and filamentous haemagglutinin proteins
Dx
- Specimen need to be frozen in dry ice to lab within 24 hours
- Chocolate agar or blood agar inoculated with a streak of S. aureus. 5-10% CO2, 37C for 2-3 days in moist atmosphere
Identification criteria
- Small, dewdrop-like colonies after 1-2 days
- Requirement V and X growth factor
- Biochemical profile
- PCR
Infections Histophilus somni in cattle
- Part of normal flora in male and female genital tracts. It can also colonize the respiratory tract
- Environmental Stress contributor
- Direct contact or aerosol
- More resistant in the environment than Haemophilus spp.
C/S
- Septicemia
- TME: thrombotic meningoencephalitis young cattle recently introduced to feedlots
- High fever, depression, blindness, ataxia, lameness.
- Sudden death due to myocarditis
- Arthritis after acute phase survival
- H. somni isolated from enzootic calf pneumonia complex
Dx
- Neurological signs
- Multiple foci of hemorrhagic necrosis affected brains at post-mortem
- Histologically: vasculitis, thrombosis, and hemorrhage in brain, heart and other parenchymatous organs
- Confirmation by isolation and identification from CSF
Tx
- Isolation
- Oxytetracycline
- Penicillin, erythromycin, potentiated sulfonamides
- Bacterins may reduce morbidity and mortality