Rabies Flashcards

1
Q

Rabies -definition

A

Rabies virus is in the family of Rhabdoviridae and in the genus Lyssavirus.

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2
Q

Name of the Rabies

A

Rabies is derived from the Latin meaning madness, Lyssa from the Greek word for mad rage.

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3
Q

Type of rabies virus- infection modes and vectors

A

Rabies is a zoonotic infection spread through saliva, usually by biting.

Rabies is present in a variety of mammals, but is extremely uncommon in small rodents (gerbils, chipmunks, guinea pigs, squirrels, rats, mice, rabbits)

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4
Q

Rabies in man

A

In man rabies causes an infection of the brain which is fatal in essentially all cases, making rabies the infectious disease with the highest case fatality rate.

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5
Q

Transmission of Rabies

A

1) from saliva of infected animal by bite or intact skin contact
2) from transplantations of organ or tissue from infected donor
3) * Aerosolization of virus (when working with live virus)

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6
Q

Animal reservoirs of Rabies

A

Racoons, skunks, foxes, coyotes, jackals, farm animals, cats, dogs, and New World bats

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7
Q

Incidence in USA

A

There are 2-3 cases of rabies each year in the U.S., usually related to bat rabies.

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8
Q

Post exposure of Rabies

A

There are many courses of post-exposure rabies vaccination given to individuals either bitten by racoons or following bat “exposure”

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9
Q

Geographic Distribution of Rabies -Exam

A

Worldwide rabies is found in terrestrial animals (mainly dogs), except it is not found in Antarctica, Australia, New Zealand, Japan, parts of Europe and some Caribbean Islands

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10
Q

Geographic Distribution of Rabies

A

Rabies is found in bats only in the New World, but 17 other rabies-like Lyssaviruses have been identified in bats in Africa, Asia, Australia, Europe, Eurasia.

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11
Q

Rabies Virus Structure

A

Bullet shaped
Single stranded (-) RNA
Nucleoprotein
Phosphoprotein
RNA polymerase
Matrix protein
Lipid envelope
Glycoprotein (spike) for attachment, and the target for neutralizing antibodies

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12
Q

Pathogenesis of Rabies: Exam

A
  1. Animal bite
  2. Virus replication
  3. Virus infects peripheral NS by retrograde transport ** Exam
  4. Virus replication in dorsal root ganglion and travels to up spinal cord to brain
  5. Brain infected
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13
Q

CNS disease and Rabies

A

The mechanisms is uncertain, there is NO neuronal
cell death

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14
Q

Upon autopsy some neural disease observed in Rabies

A

At autopsy there is mild cerebral edema, monocytic inflammation about the blood vessels, occasional destruction of nerve cells by phagocytes, and dense, ovoid, intracytoplasmic inclusions (Negri bodies).

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15
Q

Rabies virus entry into neurons and intra-neuronal transport via

A

Retrograde axonal transport ** know the spelling

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16
Q

Retrograde axonal transport

A

1) nAchR located at the postsynaptic muscle membrane
2) nAchR enriches rabies at neuromuscular jux
3) Rabies enters neurons
4) Rabies transport via capsid or vesicle

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17
Q

Axonal Retrograde Transport of Rabies

A

After replicating in the muscle cells at the site of a bite, the virus enters the neuron at the neuromuscular junction (at axon terminal) and uses the axonal transport system present in the neuron to reach the nerve cell body (soma)

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18
Q

Retrograde Transportation

A

This retrograde transportation is along the microtubules in the axon, with the P protein of the virus attaching to the light chain of the dynein motor protein.

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19
Q

Rabies an disease progression

A

1) the inuculum of virus = nature of virus
2) how the bite closer to the brain
3) the # of nerves in bite site
4) clothing - absorb saliva and prevent infection

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20
Q

Rabies and dissemination

A

After the virus infects the brain, it travels along somatic and autonomic nerves to infect the eye, skin of the head and neck, salivary glands, and kidneys.
Viral replication and shedding can occur in the salivary glands.

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21
Q

Incubation of rabies

A

Incubation period:
30-90 days, but can be from several days-many years

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22
Q

Clinical manifestations of Rabies - prodrome : exam

A

Prodrome and then acute
2-10 days
Nausea, vomiting, malaise, fever,
headache, and photophobia

Pain or paresthesias at the bite site; percussion myoedema

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23
Q

Clinical manifestations of Rabies Acute

A

Acute Neurologic Period
● Fever, hydrophobia, pharyngeal spasms, aerophagia, hyperactivity, autonomic instability, paralysis, coma, then death within 2 weeks (Encephalitis rabies, 80%)
● Some have ascending paralysis with eventual involvement of the muscles involved in swallowing and respiration, death (Paralytic rabies, seen 20% cases

24
Q

Lab and Radiological findings in Rabies

A

1) The peripheral WBC may be elevated
2) The CSF shows a lymphocytic pleocytosis (mean 60 cells/uL), normal glucose, elevated protein (under 100 mg/dL)
3) CT may show cerebral edema late.
4) MRI may show increased T2 signal in hippocampus, hypothalamus, brainstem

25
Q

Two types of rabies

A

Encephalitie rabies (80%)
And paralytic rabies (20%

26
Q

Diagnosis of Rabies

A

1) Skin biopsy
2) PCR
3) Antibody in serum
4) CSF antibody

27
Q

Acute Symptoms of Encephalities rabies

A

Fever, hydrophobia, pharyngeal spasms, aerophagia, hyperactivity, autonomic instability, paralysis, coma, then death within 2 weeks

28
Q

Symptoms of Paralytic rabies

A

Some have ascending paralysis with eventual involvement of the muscles involved in swallowing and respiration, death

29
Q

Skin biopsy in rabies

A

Skin biopsy of nape of neck with virus-specific immunofluorescent staining Isolation of virus from saliva by culture

30
Q

PCR test in rabies

A

PCR nape of neck skin biopsy (98 % sensitivity and specificity) or saliva (63% sensitivity, 70% specificity

31
Q

Antibody in serum in rabies

A

Detection of anti-rabies antibody in serum; may be affected by immunization and rabies immune globulin, in which case need rising titer to support diagnosis.

32
Q

CSF antibody in rabies

A

CSF antibody is diagnostic regardless of immunization history

33
Q

Differentiation from rabies

A

Herpes simplex encephalitis,
VZV encephalitis,
flavivirus infection (Japanese encephalitis, West Nile),
Enteroviral 71 infection,
adenoviral infection,
Nipah,
CMV, and E

34
Q

Vaccines for Rabies : Exam

A

Post-exposure prophylaxis worked because of the long incubation period of rabies.

35
Q

Treatment for rabies

A

There have been a few survivors of rabies, mostly in those who were partially immunized in the past, and with many with neurologic deficits.

Palliative care with sedatives and analgesics is provided to many patients, depending on the age, clinical presentation, patient and family preferences

36
Q

Post-exposure Prophylaxis Against Rabies

A

Post-exposure prophylaxis is given each year in the U.S. to 16,000-34,000 patients with contact with potentially rabid animals.
Rabies immune globulin (RIG) is given if there is no prior vaccine history at 20 ug/kg, with as much injected into the wound site as possible and the rest IM. It is derived from pooled plasma from hyperimmunized human donors

37
Q

Treatment rabies for young patients

A

Aggressive approach may be indicated for patients who are young, lack co-morbidities, have received at least one dose of rabies vaccine prior to symptom onset, are infected with a bat strain, are negative for rabies RNA and positive for neutralizing antibody.

38
Q

Treatment rabies and ICU

A

Treatment involves ICU care, administration of rabies vaccine if not given (but any efficacy once symptoms are present is unknown), The antivirals interferon-alpha (intrathecal), ribavirin (intrathecal), favipiravir (a viral RNA polymerase inhibitor) might be considered, but efficacy is not at all established in man.

39
Q

T/F
Rabies can infect CNS by causing neuronal cell death

A

False
The mechanisms is uncertain, there is NO neuronal
cell death

40
Q

Encephalitis rabies

A

Fever, hydrophobia, pharyngeal spasms, aerophagia, hyperactivity, autonomic instability, paralysis, coma, then death within 2 weeks

80% case

41
Q

Paralytic rabies

A

Some have ascending paralysis with eventual involvement of the muscles involved in swallowing and respiration, death
20% cases

42
Q

T/F
CSF antibody is diagnostic with Rabies regardless of immunization history

A

True

Cf. Detection of anti-rabies antibody in serum; may be affected by immunization and rabies immune globulin, in which case need rising titer to support diagnosis.

43
Q

T/F
Post-exposure prophylaxis worked because of the long incubation period of rabies.

A

True

44
Q

T/F

There have been a few survivors of rabies, mostly in those who were partially immunized in the past, and with many with neurologic deficits.

A

True

45
Q

Which Ig will be given to person without Rabies vaccine.?

A

Rabies immune globulin (RIG) is given if there is no prior vaccine history at 20 ug/kg, with as much injected into the wound site as possible and the rest IM. It is derived from pooled plasma from hyperimmunized human donors

46
Q

T/F

If at continuous risk, the rabies neutralizing antibody titer should be checked every two years, with a 1:5 dilution of the serum able to neutralize the virus, otherwise a booster is needed.

A

True

47
Q

Negri Bodies in the Neurons of Cerebellar Tissue

A

Negri bodies are composed of granular and filamentous material, representing viral ribonucleoprotein, and peripheral, fully formed virions budding into the surrounding endoplasmic reticulum.

Rabies Vaccine
In 1885 Louis Pasteur found he could use air-dried rabid rabbit spinal cord tissue to inj

48
Q

Differential diagnosis of Rabies

A

Differential diagnosis: Herpes simplex encephalitis, VZV encephalitis, flavivirus infection (Japanese encephalitis, West Nile), Enteroviral 71 infection, adenoviral infection, Nipah, CMV, and EBV

49
Q

In Rabies patient, the CT will show edema late.

A
50
Q

In Rabies patient the MRI will show

A

Increased T2 signals in hippocampus,hypothlalamus, brainstem

51
Q

Incubation period of Rabies

A

30-90 days, but can be from several days-many years

52
Q

Prodrome of Rabies

A

2-10 days
● Nausea, vomiting, malaise, fever, headache, and photophobia
● Pain or paresthesias at the bite site; percussion myoedema

53
Q

Acute Neurologic Period

A

Fever, hydrophobia, pharyngeal spasms, aerophagia, hyperactivity, autonomic instability, paralysis, coma, then death within 2 weeks (Encephalitis rabies, 80%)
● Some have ascending paralysis with eventual involvement of the muscles involved in swallowing and respiration, death (Paralytic rabies, seen 20% cases)

Patients with Rabies

54
Q

Dissemination of the Virus

A

After the virus infects the brain, it travels along somatic and autonomic nerves to infect the eye, skin of the head and neck, salivary glands, and kidneys.

55
Q

T/F
Viral replication and shedding can occur in the salivary glands.

A

True

56
Q

This retrograde transportation is along the microtubules in the axon, with the P protein of the virus attaching to the light chain of the dynein motor protein.

A
57
Q

Once the virus reaches the cell body it can replicate and then travel to the brain from the spinal cord, initially infecting the diencephalon, hippocampus, and brainstem.

A

Retrograde axona, transport