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HEMORRHAGIC_FEVERS_SUMMARY

HEMORRHAGIC_FEVERS_SUMMARY

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HEMORRHAGIC FEVERS
\ue000
The viral HF syndrome is a constellation of findings
based on vascular instability and decreased vascular
integrity
\ue000
Cutaneous flushinga nd conjunctival suffusionare
examples of common, observable abnormalities n the
control of local circulation
\ue000
Hemorrhage is inconstant and in most cases an
indication of widespread vascular damage
\ue000
In some viral HF syndromes, specific organs may be
particularly impaired:
\ue000
HF with renal syndromes- Kidney
\ue000
Hantavirus pulmonary syndrome- Lungs
\ue000
Yellow fever- Liver
\ue000
Pathogenesis of HF is poorly understood
\ue000
Acute phase in most cases of HF is associated with
ongoing virus replication andv iremia
\ue000

Exceptions are the Hantavirus and dengue HF/dengue
shock syndrome, in which the immune response plays a
major pathogenic role

\ue000
All begin with abrupt onset of fever and myalgia
\ue000
On initial PE, there is conjunctival suffusion, muscle

or abdominal tenderness to palpation, borderline or
postural hypotension, petechiaea nd periorbital
edema

\ue000
Petechiae is often best visualized in theaxilla
\ue000
Hemoconcentration is most marked in hantavirus
diseases and DHF/DSS
\ue000
Poor prognostic signs:
-
Shock
-
Multifocal bleeding
-
CNS involvement
\ue000
One of the major diagnostic clues is travel to an
endemic area
\ue000
Early recognition is important due to need for virus-
specific therapy and supportive measures including:
-
prompt, atraumatic hospitalization
-
fluid therapy
-
cardiotonic drugs
-
pressors to maintain BP at a level that will
support renal perfusion
-
treatment of secondary bacterial infections
-
replacement of clotting factors and platelets
-
DIC should only be treated if clearly evident
\ue000

Available evidence suggests that HF patients have
decreased cardiac output and respond poorly to fluid
loading

\ue000
Differential Diagnosis:
-
malaria
-
shigellosis
-
typhoid
-
leptospirosis
-
relapsing fever
-
rickettsial diseases
LASSA FEVER
\ue000
Cause endemic and epidemic dsease in Nigeria, Sierra
Leone, Guinea, and Liberia
\ue000
More widely distributed in West Africa
\ue000
Spread to humans via: small particle aerosols from
chronically infected rodents and may be acquired
during capture and eating of these animals
\ue000
Also, thru close person-to-person contact
\ue000

Virus is often present in urine during convalescence and
suspected to be present in seminal fluid early in
recovery

\ue000
Nosocomial spread is uncommon
\ue000
All ages and both sexes are affected
\ue000
Incidence is highest in dry season but transmission
takes place year round
\ue000
Average case has gradual onset (among the HF agents,
only the arenaviruses are typically associated with a
gradual onset) that gives way to more severe
constitutional symptoms and prostration
\ue000
Bleeding is seen in only 15-30% of cases
\ue000
Maculopapular rash is often noted in light skinned
Lassa patients
\ue000
Effusions are common
\ue000
Fetal death rate is 92% in the last trimester
\ue000
WBC are normal or slightly elevated
\ue000
Platelet counts are normal or somewhat low
\ue000
Deafness coincides with clinical improvement in 20% of
cases and is permanent and bilateral in some
\ue000
Fatal outcome if with:
-
high serum conc. Of AST
-
high level viremia
\ue000

Patients with AST level of >150 IU/mL should be treated with IV ribavirin (an antiviral nucleoside analogue)

\ue000
Only major SE of ribavirin is reversible anemia that
doesn\u2019t require transfusion
SOUTH AMERICAN HF SYNDROMES (Argentine, Bolivian,
Venezuelan, and Brazilian)
\ue000
Clinically similar to one another but epidemiology
differs
\ue000
Transmission by: person to person contact or
nosocomial but rare
\ue000

The basic disease resembles Lassa fever with 2 marked
differences:
1.Thrombocytopenia (often marked) is the rule and
quite common
2. CNS dysfunction is much more common than in
Lassa fever and is often manifest by marked confusions,
tremors of upper extremities and tongue and cerebellar
signs

\ue000
Argentine HF is readily treated with convalescent phase
plasma given within the first 8 days of illness
\ue000

In the absence of passive antibody therapy, IV ribavirin
in the dose recommended for Lassa fever is likely
effective in all South American HF syndromes

\ue000
Avoid intimate contacts for several weeks after
recovery
\ue000
A safe, effective, live attenuated vaccine existsfor
Argentine HF
RIFT VALLEY FEVER
\ue000
Mosquito borne Rift Valley fever virus is also a pathogen
of domestic animals
\ue000

Maintained in nature by transovarial transmission in
floodwater Aedes mosquitoes and presumably also has a
vertebrate amplifier

\ue000

Virus is infectious when transmitted by contact with
blood or aerosols from domestic animals or their
abortuses

\ue000
Slaughtered meat is not infectious
\ue000

Anaerobic glycolysis in post mortem tissues results in
an acidic environment that rapidly inactivates the
Bunyaviridae such as Rift Valley Fever virus and
Crimean Congo HF virus

\ue000
Most infections are manifested as the fibrile-myalgic
syndromes
\ue000
No proven therapy
\ue000
Only supportive care need be given
\ue000
Epidemic disease is [revented by vaccination of live
stock
CRIMEAN-CONGO HF
\ue000

This severe syndrome has a wide geographic
distribution, potentially being found wherever
ticks of the genus Hyalomma occur

\ue000

Veterinary serosurveys are the most effective
mechanism of for the surveillance of virus
circulation in a region

\ue000
Human infection acquired via a tick bite or during
the crushing of an infected tick
\ue000
Domestic animals don\u2019t become ill but do develop
viremia
\ue000
Thus, there s danger of the infection at the time
of slaughter
\ue000
Causes extensive liver damage
\ue000
Clinical lab values show:
-
DIC
-
Elevated AST, CPK, and bilirubin
\ue000
Patients with fatal cases develop leukocytosis
\ue000
Thrombocytopenia is more marked
\ue000
Clinical experience showsribav irin is efficacious
and should be used
HF with renal syndrome
\ue000
First to be identified as an HF
\ue000
Widely distributed in Europe and Asia
\ue000
In Europe, most often caused by Puumala virus (rodent
reservoir, the bank vole)
\ue000
In Asia, by Hantaan virus (rodent reservoir, the striped
field mouse)
\ue000
Most cases occur in rural residents andvacationer s,
exception is the Seoul virus diseases
\ue000
Human infections is acquired primarily through
aerosols of rodent urine
\ue000
Patients with Hantavirus diseases are not infectious
\ue000
HF with renal syndrome is the most important form of
HF today
\ue000
Severe classic Hantaan disease has 4 stages:F-HOP
\ue000
FEBRILE period: abrupt onset of fever, headache,
myalgia, thirst
\ue000
HYPOTENSIVE phase: falling BP; relative bradycardia;

lab findings include leukocytosis with a left shift,
atypical lymphocytosis, proteinuria, vascular leakage
causing hemoconcentration, and renal tubular necrosis;
kinin activation is marked; rising hematocrit levels
reflects increasing vascular leakage

\ue000
OLIGURIC phase: continuing hemorrhage; oliguria
persisting for 3-10 days before renal function returns
\ue000
POLYURIC stage: As renal function returns, there is
danger of dehydration and electrolyte abnormalities
\ue000

Mainstays of therapy are management of shock,
reliance on pressors, modest crystalloid infusion, IV
use of human serum albumin, and treatment of renal
failure with prompt dialysis

\ue000
IV ribavirin has reduced mortality and morbidity in
severe cases
\ue000
Puumala virus, the most common cause of HF with
renal syndrome (former name\u2014nephropathia
epidemica)
\ue000

Dominant features of infections with Puumala viruses
are: fever, abdominal pain, proteinuria, mild oliguria,
and sometimes blurring of vision or glaucoma ff. by
polyuria and hyposthenuria in recovery

\ue000
Diagnosis is readily made by IgM-capture ELISA
HANTAVIRUS PULMONARY SYNDROME
\ue000

Causative viruses are hantaviruses of a distinct
phylogenetic lineage that is associated with the rodent
subfamilySigmo dontinae

\ue000
Sin nombre virus chronically infects the deer mouse
and is the most important virus causing Hantavirus
pulmonary syndrome in the United States
\ue000

Disease is linked to rodent exposure and particularly
affects rural residents in dwellings permeable to
rodent entry

CLINICAL FINDINGS:
\ue000

Prodrome: (3-4 days; range 1-11 days) fever, myalgia, dizziness, vertigo, malaise, nausea, vomiting, abdominal pain

\ue000
Patients are usually recognized as the
cardiopulmonary phase begins
\ue000
Cardiopulmonary phase: tachycardia, hypotension,
tachypnea, early signs of pulmonary edema
\ue000

Final phase: rapid decompensation with
hypoxemia, resp. failure, low cardiac output,
myocardial depression, increased pulmonary
vascular permeability, shock

\ue000

Goal of management is to prevent severe hypoxemia by oxygen therapy, and if needed, intubation and intensive respiratory management

LAB FINDINGS:
\ue000
Thrombocytopenia (important early clue), atypical

lymphocytes, and a left shift, often with
lymphocytosis; hemoconcentration; hypoalbuminemia;
and proteinuria

\ue000
IgM testing of acute phase serum can yield positive
results, even during the prodromal stage
\ue000
RT_PCR of blood clots or tissue usually gives a positive
result in the first 7-9 days of illness
PROGNOSIS:
\ue000
Most pts who survive for 48 hrs recover with residua
\ue000
Mortality rates are approx. 30-40% despite optimal
management
YELLOW FEVER
\ue000
Causes a typical HF syndrome with prominent hepatic
necrosis
\ue000
Pts are viremic for 3-4 days and can have jaundice,
hemorrhage, black vomit, anuria, and terminal delirium
\ue000
Albuminuria is usually noted and may be marked
\ue000
Urban yellow fever can be prevented by control of the
mosquito vector Aedes aegypti
\ue000
The continuing sylvatic cycle requires vaccination of all
visitors to areas of potential transmission
DENGUE HEMORRHAGIC FEVER/DENGUE SHOCK SYNDROME
\ue000

Previous infection with a heterologous dengue virus
serotype may elicit nonprotective antibodies and
enhanced disease if pts are reinfected

\ue000
DHF is marked by bleeding tendencies
\ue000
DSS is more serious because of vascular permeability
leading toshock
\ue000

Period of shock lasts only 1-2 days and most patients
respond promptly to close monitoring, oxygen
administration, and infusion of crystalloid or\u2014in severe
cases--colloid

\ue000

In severe cases, frank shock occurs with cyanosis,
hepatomegaly, ascites and pleural effusions, and GI
bleeding

\ue000
Control of Aedes aegypti, the mosquito vector, is key
to control disease
\ue000
Macrophage or monocyte infection is central to
pathogenesis of dengue fever and to the origin of
DHF/DSS
\ue000
Induction of vascular permeability and shock depends
on multiple factors, include the ff:
-
presence of enhancing or neutralizing
antibodies

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