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Infectious diseases I & II > Lecture 11 - Rabies, BSE, Scrapie > Flashcards

Lecture 11 - Rabies, BSE, Scrapie Flashcards

1
Q

2 alt. names for Rabies virus (RABV)

A

Hydrofobia, Lyssa

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2
Q

RABIES is a

A

contagious viral disease of mammals, caused by Lyssavirus, characterized by central nervous system (CNS) signs and extremely high fatality.

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3
Q

RABIES is a contagious viral disease of mammals, caused by Lyssavirus, characterized by

A

central nervous system (CNS) signs and extremely high fatality.

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4
Q

Causative agent of rabies.
Genus and family.

A

Rabies virus (RABV) is a Neurotropic virus

Genus Lyssavirus,
family Rhabdoviridae

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5
Q

Describe Rabies strains.

A

Many strains – each has a particular reservoir host (e.g. skunks).

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6
Q

Rabies and rabies-related lyssaviruses are classified into

A

phylogroups.

Phylogroup I, II, III, IV.

Rabies is in phylogroup I.

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7
Q

Stability of RABV.

A

Does not survive long in the environment, not even in dried blood and secretions.

Susceptible to UV radiation.
Rapidly inactivated by sunlight and drying.

Inactivated in pH <3.0 and >11.0
Can be inactivated with many disinfectants (e.g. 45-75% ethanol).

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8
Q

Host range of RABV.

A

Reservoir hosts:
families Canidae (dogs, jackals etc), Mustelidae (e.g. skunks),
Viverridae (e.g. mongooses) and
Procyonidae (raccoons), and
the order Chiroptera (bats).

Each virus strain is maintained in a particular host. Any variant can cause rabies in other species!

NB! ZOONOSIS! All strains are zoonotic.

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9
Q

Morbidity of RABV.

A

All animals exposed to rabies do not become ill.

Humans: 20% of humans bitten by rabid dogs develop rabies.

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10
Q

Mortality of RABV.

A

(<) 100% - very high. Essentially 100% upon presentation of clinical signs.

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11
Q

Distribution of rabies.

A

worldwide

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12
Q

Rabies undergoes 2 epidemiological cycles:

A

the urban cycle
the sylvatic cycle
(sylvatic refer to wild animals)

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13
Q

Describe the urban cycle of rabies.

A

Dogs are the main reservoir host.

Predominates in areas where proportion of unvaccinated and semi-owned or stray dogs is high – Africa, Asia, the Middle East and Latin America.

Virtually eliminated in the U.S., Canada and Europe.

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14
Q

Describe the sylvatic cycle of rabies.

A

Predominant in Europe and North America.

Epidemiology is complex, affected by: viral strain, behavior of the host species, ecology and environmental factors.

Disease pattern in wildlife: relatively stable or a slow moving epidemic.

Maintenance hosts: skunks and bats, raccoons, raccoon dogs, wolves, foxes, mongooses, coyotes, jackals.

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15
Q

Excretion of RABV.

A

Via saliva.

Shedding in 50-90% of infected animals; can begin before the onset of clinical signs.

Main sources of virus: saliva and brain!

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16
Q

Transmission of RABV.

A

Direct contact: route commonly bite wounds

Aerosols – in labs or bat caves

Ingestion – experimentally infected animals

Also: mucous membranes or breaks in the skin (scratches).

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17
Q

IP of RABV.

A

less than 6 months
(dogs and cats: 2 weeks - 3 months)

In humans: few days to several years (typically 1-3 months)

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18
Q

Initial signs of RABV in animals.

A

Are nonspecific

Fearfulness, restlessness, anorexia/increased appetite, vomiting, diarrhea, slight fever, dilation of the pupils, hyperreactivity to stimuli and excessive salivation.

Behavior and temperaments changes, become unusually aggressive or uncharacteristically affectionate.

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19
Q

Forms of RABV. (2)

A

The paralytic (“dumb”) form – progressive paralysis.
- Biting is uncommon!
- Death in 2-6 days (respiratory failure)

The furious form – infection of the limbic system (more common in cats).
- drooling, attacks (fearlessness)
- Progresses to incoordination and ascending paralysis
- Death in 4-8 days after the onset of clinical signs

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20
Q

Clinical signs of RABV in humans.

A

Nonspecific prodromal signs.

Malaise, fever or headache; discomfort, pain, pruritus or other sensory alterations at the site of virus entry.

Later: insomnia, photophobia, hypersalivation, difficulty swallowing (due to laryngeal paralysis), convulsions.

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21
Q

Forms of RABV in humans. (2)

A

Encephalitic (furious) form: hyperexcitability, autonomic dysfunction and hydrophobia.

Paralytic (dumb) form: generalized paralysis.

Death in 2-10 days.
Survival extremely rare.

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22
Q

Post mortem lesions of RABV.

A

No characteristic gross lesions!

Histology of CNS:
Multifocal, mild, polioencephalomyelitis and craniospinal ganglionitis with mononuclear perivascular infiltrates, diffuse glial proliferation, regressive changes in neuronal cells, and glial nodules.

Negri bodies – aggregates of viral material in neurons.

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23
Q

DDx for rabies.

A

Any suspected mammalian encephalitis and neurological disorder must be considered in the differential diagnosis!

Canine distemper encephalitis,
Aujeszky’s disease
Toxoplasmosis
Neoplasia, trauma
Poisoning (e.g. lead)

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24
Q

Suspect rabies when:

A

behavioral changes and unexplained paralysis

Consider in all cases of unexplained neurological disease!

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25
Q

Material for diagnosis of RABV.

A

brain, saliva

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26
Q

Lab analyses for diagnosis of RABV.

A

Detecting viral antigens (immunofluorescence, immunohistochemistry, ELISA).

RT-PCR – from saliva but note, not all infected animals excrete it via the saliva! False negatives, which is why this method of testing is inadequate.

Histology – nonspecific

Serology (ELISA) – rarely used for clinical cases.

NB! Single negative test does not rule out infection! isolation in cell culture is done concurrently.

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27
Q

Tx of rabies.

A

No Tx once the clinical signs appear.

Humans: post-exposure prophylaxis – wound cleaning, administration of human rabies immunoglobulins and several doses of human rabies vaccine is highly effective if begun soon after exposure but before clinical signs appear.

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28
Q

Prevention of RABV.

A

Vaccination of domestic and wild animals, and humans.

Domestic animals: vax via injections
Wildlife: vax via ingestion

Humans: inactivated vaccines – does NOT eliminate the need for post-exposure prophylaxis but fewer treatments are needed.

Protective clothing;
careful handling of possibly rabid animals.

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29
Q

Control of RABV.

A

Sick animals must be euthanized.

30
Q

BSE, 2 names

A

Bovine spongiform encephalopathy,
Mad cow disease

Prion = PrPres

31
Q

BOVINE SPONGIFORM ENCEPHALOPATHY is

A

a fatal neurodegenerative disease of mammals, cattle as the most affected, caused by a prion.

32
Q

Causative agent of BSE.

A

BSE prion PrPres

Prion = proteinaceous infectious particle

Normal, cellular protein = PrPc
Abnormal, pathogenic BSE protein = PrPres

BSE belongs to the TSEs family.

33
Q

Types of BSE prion. (3)

A

‘Classical’ BSE prion and two atypical BSE prions:
‘H-type’ (H-BSE) and ‘L-type’ (L-BSE)

34
Q

Stability of BSE.

A

Highly resistant to most disinfectants (incl. formalin), heat, UV radiation and ionizing radiation.

Disinfectant that works: e.g. 1-2 N sodium hydroxide solution (lye).

Physical inactivation: autoclaving.

Recommended: combination of chemical and physical decontamination and even then, destruction of all prions is not guaranteed.

35
Q

Name 3 TSEs besides BSE.

A

scrapie
kuru
Creutzfeldt-Jakob (vCJD)

36
Q

Host range of BSE.

A

mammals

Clinical cases: cattle (and exotic ruminants in zoos, various felids).

Very rarely reported in goats.

NB! ZOONOSIS!
In people: variant Creutzfeldt-Jakob disease (vCJD).

37
Q

Morbidity of BSE:

A

Unknown, can only extrapolate based on prevalence.

Prevalence in animals varies widely (UK 1992: 2-3%).

Humans: prevalence of vCJD is unknown.

38
Q

Mortality of BSE.

A

Always fatal once the symptoms appear: 100%.

Humans: always fatal once the symptoms develop: 100%.

39
Q

Distribution of BSE.

A

Worldwide distribution;
but BSE free countries:
Iceland, Australia and New Zealand.

40
Q

Excretion of BSE.

A

no excretion!!

Prion can be found in brain, spinal cord, retina and distal ileum; dorsal root ganglia, peripheral nerves and adrenal glands.

41
Q

Transmission of BSE.

A

Ingestion of tissues containing the BSE prion such as Meat-bone-meal (MBM).

Highest prion concentration in CNS and ileum.

Humans: ingestion and iatrogenic transmission.

Blood transfusion, transplants, contaminated equipment.

In cattle prions can accumulate in the brain as early as 24 months after infection.

42
Q

IP of BSE.

A

Animals: 2-8 years (peak in 4-5 year old animals)

Humans: 11-12 years
Median age of onset: 26 years

43
Q

Clinical signs of BSE.

A
  1. Initial neurologic signs – apprehension, fear, easily startled, depressed
  2. Final stages – Increased excitability, hyperreflexia, hypermetria; ataxia, muscle fasciculations, tremors, and myoclonus.
  3. Terminal state – nonspecific signs.
    Decreased rumination, Weight loss, loss of condition, teeth grinding and decreased milk production. Finally, Recumbency, coma and death.

Symptoms worsen gradually over a few weeks to six months.

44
Q

Clinical signs of BSE in humans.

A

First signs: psychiatric symptoms
- insomnia, anxiety, depression etc.

Frank neurologic signs – appear few months later.
- Gait disturbances, ataxia, incoordination, memory loss, slurring of speech, tremor
- Cognitive function gradually deteriorates

Death in 6 months to 2 years.

45
Q

Post mortem lesions of BSE.

A

Gross lesions are not found.
Nonspecific signs – emaciation or wasting.

Histopathologic lesions in the CNS:
Cattle: spongiform changes in the gray matter
Usually bilaterally symmetrical
Type L-BSE includes Amyloid plaques

46
Q

DDx for BSE

A

Nervous ketosis
Hypomagnesemia

Listeriosis
Polioencephalomalacia

Rabies
Brain tumor

Lead poisoning
Spinal cord trauma

47
Q

Material for diagnosis of BSE.

A

Brain, medulla, spinal cord, brain stem

The red box indicates the region of the obex, which is the portion of the brain that must be obtained for the diagnosis of BSE and other spongiform encephalopathies such as scrapie and chronic wasting disease.

48
Q

Suspect BSE when:

A

slowly progressive, fatal neurologic dz in cattle

e.g. rabies onset is much faster but otherwise can be similar presentation.

49
Q

Lab analyses for diagnosis of BSE.

A

Detection of prions (PrPres) – immunohistochemistry (IHC) as the gold standard.

Rapid tests: Western blotting, ELISA
NB! Prions cannot usually be detected in the brain until 3-6 months before the onset of clinical disease.

50
Q

Treatment of BSE.

A

No Tx – suspected animals usually euthanized for testing.

51
Q

Prevention of BSE.

A

Do not feed ruminant tissues that may contain prions to susceptible species (MBM/meat bone meal).

Tissues that have high risk of transmitting BSE have been banned from human food in many countries.

There is NO vaccine!

52
Q

Control of BSE.

A

EU: test cattle that are intended for human consumption.

53
Q

Alt. name for Scrapie

A

Tremblante de Mouton

Prion: PrPSc

54
Q

SCRAPIE is

A

a neurodegenerative disease of sheep and goats, caused by a prion.

Prion: PrPSc

55
Q

Causative agent of scrapie.

A

PrPSc

Also atypical scrapie prion: Nor98

Member of TSEs

56
Q

Stability of scrapie.

A

Highly resistant to disinfectants, heat, UV radiation, ionizing radiation and formalin.

Inactivated by autoclaving.

Disinfectant: e.g. sodium hypochlorite.

57
Q

Host range of scrapie.

A

sheep and occasionally goats (rare)

note: doesn’t transmit to humans!

Some genotypes of sheep are more susceptible than others, e.g. sheep with ARR/ARR genotype are highly or completely resistant, sheep with VRQ/VRQ genotypes are most susceptible.

58
Q

Distribution of scrapie.

A

worldwide

59
Q

Morbidity of scrapie.

A

Morbidity: U.S. 2002-2003 overall prevalence 0.20% in mature sheep.

60
Q

Mortality of scrapie.

A

Mortality: always fatal once the symptoms appear.

Annual mortality of affected flock: 3-5% (<20%).

61
Q

Excretion of scrapie.

A

reproductive tract of ewes during pregnancy

Infected ewes can produce either prion-positive or –negative placentas, depending on the genotype of the fetus.

62
Q

Transmission of scrapie.

A

At birth or right after. Direct contact.

Neonates: licking or ingestion of fetal membranes or fluids.

Infected animals carry the prion for life and can transmit the agent even if they remain asymptomatic.

63
Q

IP of scrapie.

A

2-5 years in sheep

2-8 years in goats

64
Q

Clinical signs of scrapie in sheep.

A

First symptoms: behavioral.
Self-isolation, hyperexcitable, high-stepping or hopping gait and/or fixed stare with the head held high.

Later: Ataxia, incoordination, blindness, trembling, convulsions when handled. Weight loss, emaciation. Dry, brittle fleece.

Characteristic sign: nibbling response due to intense pruritus.

Death in 2-6 weeks (up to six months) after the onset of symptoms.

65
Q

Clinical signs of scrapie in goats.

A

Listlessness, weight loss and premature cessation of lactation; behavioral changes.

Prostration and death 1-6 months after the onset of symptoms.

66
Q

Post mortem lesions of scrapie.

A

Carcass: wasted or emaciated

No other gross lesions found

Histopathology: spongiform changes in the gray matter

67
Q

DDx for scrapie.

A

External parasitism
Aujeszky’s disease

Maedi-Visna
Listeriosis

Pregnancy toxemia
Rabies

Abscess/tumor in the brain
Hypomagnesemia

68
Q

Suspect scrapie when:

A

animals develop slowly progressive and fatal neurologic disease (with pruritus!)

69
Q

Material for diagnosis of scrapie.

A

brain, placenta, spleen, LNs

70
Q

Lab analyses for diagnosis of scrapie.

A

Histopathology

Detecting PrPSc in the CNS – immunoblotting, immunohistochemistry (Scrapie-associated fibrils in electron microscopy).

Serology is not useful since no antibodies!

Live animals: third eyelid test (lymphoid tissue biopsy).

71
Q

Prevention & control of scrapie.

A

Closed flock or minimal outside purchases.

Genotyping, use resistant rams.

Quarantines

Removal of fetal membranes and placenta after lambing; bedding change.

No evidence of transmission to humans.

Infectious diseases I & II (33 decks)

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