L 82-83 Viral Hemorrhagic Fevers Flashcards Preview

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Flashcards in L 82-83 Viral Hemorrhagic Fevers Deck (50)
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1
Q

General charactersitics of VHF viruses

A

Enveloped RNA viruses
Animal or arthropod hosts
Transmission generally arthropod vector or contact with rodent excretions
Person-person transmission low
Geographically restricted to where the host species lives
Prevention depends on control of animal/insect host/vector
Treatment is often supportive

2
Q

Shared features among VHF’s

A
Fever and other noon-specific Sx
Hemorrhagic
Thrombocytopenia
Shock
Neuro disturbances

Initial SSx:
Fever, fatigue, dizziness, myalgia, weakness, exhastion

More serious: bleeding under skin, internal organs or from body orifices, coma, delirium, seizures

3
Q

General pathogenesis of VHF’s

A

Virus initially infects macrophages and dendritic cells causing cytokine release. These might include gamma interferon, IL-1,6, TNF-alpha
Cytokines cause inflammatory response and coagulation pathways
Dendritic cells reduce expression of co-stimulatory molecules that are needed for T-cell activation => decreased immune response

4
Q

What is the cause of the bleeding in VHF’s?

A
Multifactorial cause:
Hepatic damage
Coagulation dysregulation
Thrombocytopenia
Increased vascular permeability
5
Q

What are the 4 main virus families in VHF’s?

A

Flaviviridae
Bunyaviridae
Arenaviridae
Filoviridae

6
Q

Flaviviruses features and most common viruses in this group causing hemorrhagic fever

A

Dengue and Yellow fever

(+) sense enveloped RNA

7
Q

Dengue Fever Epidemiology

A

Tends to be in more tropical areas but is spreading
Four serotypes: DENV-1-4, no cross-immunity
Natural host: primates, but humans are now being considered also
Transmission: Aedes aegypti mosquito

8
Q

Dengue clinical features

A

Acute infection
Characterized by high fever and at least 2 of:
Severe headache, eye pain, joint pain, muscle/bone pain, rash, mild bleeding, low WBC or platelets
Resolves in 1-2 weeks

9
Q

Dengue hemorrhagic fever

A

Usually after infection with a second dengue fever

High fever, hemorrhagic manifestations, thrombocytopenia, plasma leaking, pleural effusion, ascites

10
Q

Explain why a second infection from dengue is worse than the first

A

In the first infection, there is production of neutralizing and non-neutralizing antibodies to the virus. The neutralizing antibodies remove the infection and the person recovers.

In the second infection, there is already present many antibodies that are non-neutralizing. They bind to the virus and promote uptake into macrophages and dendritic cells which actually helps the proliferation of the virus.

Enhanced uptake causes the macrophages to release cytokines, and the cells also signal memory T cells to release cytokine => increased vascular permeability

The immune complexes join with platelets and cause coagulation

11
Q

Detection of dengue

A

Viral RNA and NS1 antigen can be detected early

IgM early, IgG later

12
Q

Dengue prevention

A

There is now a vaccine available called Dengvaxia–live-attenuated and tetravalent
Approved for use in other countries

13
Q

Yellow Fever epidemiology

A

Two strains: Dakar and 17D
Africa and South America
Host: primate, but now humans also
Vector: Mosquito–aedes, haemagogus, sabethes

14
Q

Yellow fever clinical manifestations

A

Biphasic disease:
Acute Phase: fever, myalgia with backache, HA, loss of appetite, N/V, red tongue, skin flushing, red eyes, Sx fade in 3-4 days

Toxic Phase: in 15-20% of patients, return of fever, bradycardia, jaundice, GI hemorrhage, abd pain, dissemination to kidneys, heart, vasculature causing widespread hemorrhaging, can be fatal

15
Q

Yellow Fever pathogenesis

A

Similar to Dengue in many ways
Attacks Kupffer cells and hepatocytes
Councilman bodies in liver biopsy

16
Q

Yellow Fever immunity

A

Live-attenuated vaccine against 17D strain, single vaccine sufficient immunity

17
Q

Characteristics of Bunyaviruses

A

Enveloped, (-) sense RNA
Three segments in genome: L, M, S

Viruses causing hemorrhagic fevers:
Phlebovirus
Nairovirus
Hantavirus

18
Q

Rift Valley Fever Epidemiology

A

Eastern and Southern Africa
Mosquito transmission
Also transmitted by contact with infected animal tissues or secretions–livestock

19
Q

Rift Valley Fever clinical features

A

Typically asymptomatic or mild assoc. with fever and liver illness
Can mimic influenza
Can have hemorrhagic manifestations–shock, encephalitis, ocular disease, hepatic necrosis, blindness

20
Q

Rift Valley Fever Pathogenesis

A

Replication in RES cells at site of bite or contact

Viremic spread to other tissues and organs

21
Q

Rift Valley Fever immunity

A

Long-lasting immunity
Vet vaccines available
Not developed for humans

22
Q

Crimean-Congo Hemorrhagic Fever Epidemiology

A

SE Europe, Asia, Africa

Vector and Reservoir: Tick

23
Q

Crimean-Congo Hemorrhagic Fever clinical features

A

Early: fever, HA, severe back, joint, abd pain, vomiting, flushing, red eyes

Later: Hemorrhages–petechia, purpura, ecchymoses, subconjunctival, mucosal membranes; Pulmonary edema and shock, hepatitis, liver and kidney failure

24
Q

Crimean-Congo Hemorrhagic Fever pathogenesis

A

Similar to Dengue in replication at bite site and spread to other organs and tissues

25
Q

Hantaan virus Epidemiology

A

Considered an old world virus
China, E. Russia, Korea
Causes Korean hemorrhagic fever or Hemorrhagic Fever with Renal Syndrome
Reservoir: striped field mouse
Infection: contact with infected rodent tissues or secretions

26
Q

Hantaan (HFRS) clinical features

A

Early: F/C, HA, flushing, low back pain, abd pain, N/V/D, blurred vision, hemorrhages–petechia, purpura, subconjunctival, thrombocytopenia

Later: Low BP, vascular leakage, edema, renal dysfunction, shock

27
Q

Hantaan (HFRS) Pathogenesis

A

Virus replicates similar to RVF in RES cells and spreads throughout body, especially to the kidneys

28
Q

Hantavirus Epidemiology

A

New world virus–Americas
Causes Hantavirus Pulmonary Syndrome (HPS)
Sin Nombre Virus (many others exist)
Host: deer mouse
Infection: by contact with rodent secretions–stool, urine, saliva
Also from eating foods contaminated by infected mice

29
Q

Hantavirus (HPS) Clinical Features

A

Early: 1-5 weeks after infection, fever, fatigue, muscle aches, HA, dizziness, chills, abd Sx

More serious: cough, SOB, tachycardia, tachypnea, pulmonary edema=ards

30
Q

Sin nombre virus Pathogenesis

A

Infection through respiration of airborne particles from infected rodents
Does not cause hemorrhagic symptoms

31
Q

Characteristics of Arenavirus

A

Enveloped ambisense ssRNA viruses
Segmented genome–2: L and S
Many viruses, cover Lassa virus here

32
Q

Lassa virus epidemiology

A

First seen in Nigeria
Reservoir: rat
Transmitted: ingestion of contaminated urine or feces, or direct contact with rat, can transfer person-person

33
Q

Lassa clinical features

A

Initially: insidious onset, fever, malaise, myalgia, retrosternal pain, cough, sore throat, severe headache, nausea vomiting

Severe: exhaustion, facial edema, neuro–tremors, seizures, coma, deafness; hemorrhagic in skin and mucous membranes, multiple organ necrosis, shock

34
Q

Lassa Pathogenesis

A

Acquired through inoculation, inhalation, ingestion from infected rat
Virus infects endothelial cells and macrophages causing cellular and vascular damage as well as release of inflammatory mediators

35
Q

Characteristics of Filoviruses

A

Single genome, filamentous looking virion
Includes Ebolavirus, Marburgvirus
Both cause severe and often fatal hemorrhagic fevers
Sx similar for both

36
Q

Marburg epidemiology

A

Endemic to Africa
Fruit bats likely reservoir
Transmission: likely contact with secretions or tissues, human to human possible

37
Q

Ebola epidemiology

A

Endemic to Africa
Five subtypes
Reservoir: fruit bat
Transmission: likely contact with secretions or tissues, human to human possible

38
Q

Filovirus clinical features

A

Severe to fatal hemorrhagic fever
Early: HA, fatigue, fever, myalgia,

Later: sudden high fever, vomiting blood, passive behavior, bruising, brain damage, bleeding nose and mouth, LOC, seizures, massive internal bleeding, death within week of onset of symptoms

Bleeding form thrombocytopenia and vascular damage

39
Q

Filovirus Pathogenesis

A

Virus replicates rapidly in blood stream causing extensive necrosis in liver, adrenal, spleen, lymph, lungs, endothelium, etc.

Macrophages release mediators that mimic shock causing widespread hemorrhage => DIC, edema, hypovolemic shock

40
Q

Diagnosis of VHF and HPS

A

Geographic
Serology
PCR
Lab findings

41
Q

Treatment of VHF and HPS

A

Supportive care
Ribavirin shown to be helpful in some
ZMapp for Ebola

42
Q

Preventing VHF and HPS

A

Vaccines for Yellow Fever and Dengue, patient isolation, rodent control

43
Q

Patient has been to Korea, contact with a striped field mouse, and has renal dysfunction
Disease?

A

Hemorrhagic fever with renal syndrome (HFRS)

Hantaan virus

44
Q

Patient from E/S Africa, bit by mosquito that has been feeding on livestock, ends up with blindness
Disease?

A

Rift Valley Fever

45
Q

Patient from SE Europe, is bitten by a tick

Disease?

A

CCHF

Crimean-Congo Hemorrhagic Fever

46
Q

Patient bit by mosquito that has been feeding on monkeys, found to have the NS1 antigen, has hemorrhagic symptoms, and can progress to shock

A

Dengue fever

47
Q

Patient in africa or south america, bit by mosquito after feeding on monkeys, jaundice, black vomit and councilman bodies found

A

Yellow Fever

48
Q

Patient in Africa

Contacted fruit bat secretions, rapid course, extensive tissue necrosis

A

Marburg or Ebola

49
Q

Patient in West Africa, disease from a rat, causes cough, sore throat, deafness

A

Lassa virus

50
Q

Patient in North America, deer mouse infection, pulmonary edema, ARDS, no hemorrhagic manifestations

A

Sin nombre virus

Hantavirus Pulmonary Syndrome