Key Microbial agents causing neurological disease 2 Flashcards

1
Q

What are some features of listeria?

A
  • Gram positive short regular rods
  • Facultatively anaerobic
  • Differentiation to species level not required - Listeria monocytogenes: Main species of veterinary and human pathogenic interest
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2
Q

Where is listeria found?

A
  • Listeria can be isolated from lots of places
     Free living in the environment
     Soil. Silage (organisms multiply when pH rises above 5.5), sewage effluent, decaying vegetation, stream water and over 50 different animal species including ruminants, pigs, horses, dogs, cats and various species of birds
  • Present in animals (and humans) as asymptomatic enteric carriers and are shed in the faeces
  • An important source of infection for humans is food, especially soft cheeses, seafood and meat but also vegetables
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3
Q

How is listeria transmitted?

A
  • Exogenous: Ingestion is the primary route
  • Endogenous: Septicaemia or spread along trigeminal nerves
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4
Q

How does listeria invade cells?

A
  • Bind to cell wall via internalin
  • Escape phagosome with help of haemolysin
  • Multiply in cytoplasm with doubling time of 1 hour
  • Listeriopods invaginate into adjacent cells allowing entry in a double membraned vacuole
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5
Q

What clinical syndromes are associated with listeriosis?

A
  • Visceral form (septicaemia)
  • Abortion
  • Neural form
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6
Q

What clinical signs are associated with the neural form of listeriosis?

A

Neural form presents as meningoencephalitis (circling disease) and is most commonly observed in ruminants with poor quality silage often being tee source.
- Circling in one direction
- Unilateral facial paralysis
- Difficulty swallowing
- Fever
- Blindness
- Keratoconjunctivitis; nystagmus
- Head pressing, head tilt
- Paralysis, recumbency and death
- Sheep and goats can also exhibit star gazing i.e. their heads stretched back due to encapsulated pus in the brain

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7
Q

How does listeria cross the BBB?

A

Listeria crosses the blood-brain barrier either haematogenously or via nerve cells (trigeminal)

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8
Q

Can animals become immune to listeria?

A
  • Facultative intracellular parasite: Cell mediated immunity is important
  • Underlying host immunosuppression especially of the cell mediated immune responses appears to be an important factor in intracellular persistence  clinical listeriosis e.g. decreased cellular immunity occurs with advanced pregnancy
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9
Q

How is listeriosis diagnosed?

A
  • Based on clinical signs
  • Samples obtained from lesions (blood, placenta, aborted foetal tissues or post mortem tissue specimens inc. CNS) -> gram stain/diff quick where you should see gram +ve short rods but may not be present especially in chronic disease
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10
Q

How is listeriosis treated?

A
  • Penicillin
  • most effective in early stages, not effective in chronic cases
  • recovery may be accompanied by permanent neurological damge
  • Trimethoprim/sulfonamides and rifampin combination has been used in cases of listeriosis in dogs
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11
Q

What signs are associated with feline parvovirus?

A
  • Poor motor control
  • Wide based stance
  • Incoordination – very clumsy
  • Intention tremor
  • When asleep = no signs
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12
Q

What can equien herpesvirus 1 cause?

A
  • Late term abortion
  • involved in upper respiratory disease
  • can cause meningoencephalitis (mutant forms of the virus)
  • Horses may present in recumbancy
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13
Q

What is bvoine ephemeral fever?

A
  • Also known as 3 day sickness
  • arthropod borne virus of cattle and water buffalo
  • enzootic in tropical and subtropical regions of africa, asia, middle east and australia
  • epizootics of disease occur when the virus spreads to termperate regions
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14
Q

Describe the pathogenesis of bovine ephemeral fever.

A
  • Virus introduced by arthropod vector (mosquitoes?, midges)
  • Vascular inflammatory response (immune mediated?) -> Synovial membranes, muscles, tendon sheaths and skin
  • Mineral imbalance (hypocalcaemia)
  • Viraemia lasts 4-5 days
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15
Q

What clinical signs are associated with bovine ephemeral fever?

A
  • High morbidity, low mortality (Mortality usually more so to do with recumbency)
  • Sudden onset, sudden recovery (72 hours)
  • Fever (often biphasic)
  • Marked drop in milk production
  • Nasal and ocular discharge
  • Lameness
  • Submandibular oedema
  • May see abortion in 2nd trimester
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16
Q

How is bovine ephemeral fever diagnosed?

A

Based on clinical signs or serology

17
Q

How is bovine ephemeral fever controlled?

A
  • Avoidance of vectors not practical
  • effective vaccines are available (may be routine in endemic areas)
18
Q

What is the source of cryptococcus?

A
  • Exogenous: Inhalation of basidiospores from environment
  • Opportunistic
  • Environmental
19
Q

Describe the characteristics assoicated with cryptococcosis

A
  • Dimorphic, basidiomycetous fungi
  • Source dependent on species e.g. bird guana (C. neoformans) vs dead plant material in eucalyptus hollows (C. gatii)
  • Most common systemic mycosis in animals in Australia
20
Q

What is the pathogenesis of cryptococcosis?

A
  • Based on the small size of basidiospores, the lung is primary site of infection in humans and horses
  • In cats, dogs, and koalas, the nasal cavity may be the primary site
  • Cryptococcal rhinitis (URT pathogen)
  • Chorioretinitis
  • Haematogenous dissemination
  • Cutaneous lesions
  • CNS involvement
21
Q

How is cryptococcisis diagnosed?

A
  • Nasal flush - Cytology
  • Histology of lesions
  • Crypto-latex agglutination test (LCAT) – blood test -> Shows cryptococcal antigen if anywhere in the body AND Used for diagnosis but also for treatment monitoring
22
Q

What is this?

A

Cryptococcus -> causes cryptococcosis

23
Q

What is the most common disease presentation of FIP?

A

Pleural effusion or ascites

24
Q

What is FIP?

A
  • Fatal inflammatory disease of domestic and non-domestic cats
  • Induced by Feline Infectious Peritonitis virus (a mutant form of feline coronavirus)
  • Feline coronavirus (Enveloped RNA virus, usually causes mild gastrointestinal disease)
  • Imbalance of the immune system: Inflammation in the blood vessels, serosal surfaces and several body organs AND/OR dysregulation of immune system leading to profound T cell depletion and hypergammaglobulinemia
25
Q

How does FIP occur?

A
  • FIP occurs when avirulent enteric biotype (FECV) mutates to virulent biotype (FIPV) within an individual cat, causing it to lose its tropism for intestinal cells while gaining greater macrophage tropism
  • FIP requires:
     Systemic infection with FIPV
     Sustainable replication of FIPV in monocytes
     Activation of these FIPV-infected monocytes
  • Ultimate target cell is not just any macrophage, but a distinct population seen in the lining of blood vessels in the membranes covering the lungs, abdominal organs, brain and eyes
  • Infected monocytes mediate a granulomatous phlebitis and periphlebitis through interaction with endothelial cells
  • Cytokines and adhesion moecules produced by the activated macrophages cause systemic damage to vascular endothelium
  • FIPV infection also results in depletion of some other white blood cells, natural killer cells and regulatory T cells usually involved in stopping infection
26
Q

How would a cat with feline immunodeficiency virus (FIV) present?

A
  • Leukocytopaenias -> chronic, recurrent or opportunistic infections
  • Weight loss and recurrent GIT disease
  • Neurological disease (direct effect on CNS): Damages astrocytes and microglia cells
27
Q

What is the pathogenesis of FIV?

A
  • Long term disease
  • Disease associations difficult to investigate with FIV infection due to long asymptomatic phase
  • Lymphoid depletion and severe immunodeficiency and neoplasia
28
Q

What is the link between lymphosarcoma and FIV?

A
  • 50% of cats in Sydney with lymphosarcoma were FIV positive
  • Multiple anatomical sites
  • Often involve abdominal structures
  • B cell lymphosarcoma
29
Q

What is caprine arthritis-encephalitis virus (CAEV)?

A
  • Disease of goats that occurs worldwide including Australia
  • Transmission is via colostrum or milk during neonatal period but can occur via respiratory route
30
Q

What are the clinical signs assocated with CAEV?

A

o Younger animals -> Ataxia and cerebral depression
o Older animals -> arthritis

31
Q

Treatment of CAEV?

A

Euthanasia

32
Q

Control of CAEV?

A

Rate of infection in newborn goats can be reduced by removing kids after birth and providing them with colostrum heated for 1 hour at 56oC, feeding them pasteurised milk and isolating them from infected goats