Biomedical Engineering Reference
In-Depth Information
with serologic evidence of infection in a patient
with a compatible clinical syndrome. Tularemia
can be diagnosed by recovery of
F. tularensis
from clinical specimens, although cultivation is
difficult and slow. Blood smears can be stained
with specific fluorescent antibody. Hemagglutinins
appear
fever, myalgia, and prostration. Physical exam-
ination may reveal conjunctival injection, mild
hypotension, flushing, and petechial hemorrhages.
Illness may progress to shock, with general-
ized mucous membrane hemorrhage, and is often
accompanied by neurological, pulmonary, and
hematopoietic involvement. Renal insufficiency
is usually proportional to cardiovascular compro-
mise. Mortality can be substantial (50-90% among
Ebola victims) [5,14].
in 10-12 days; a rising titer
is diag-
nostic [5,6].
4.5.5 Medical Management
Patients with tularemia who do not receive appro-
priate antibiotic treatment may have a prolonged
illness characterized by malaise, weakness, weight
loss, and other symptoms that last for months.
Streptomycin 15mg/kg IM q12h for 10-14 days,
or gentamicin 3-5mg/kg IV qd (2.5mg/kg IV q8h
in children) for 10-14 days are generally consid-
ered the treatments of choice. Doxycycline and
ciprofloxacin may also be used in doses equal to
those given for plague. Doxycycline 100mg po
q12h (2.2mg/kg po q12h in children) for 14 days,
or tetracycline 500mg po qid for 14 days may be
given as PEP [5,6,10,11].
4.6.3 Diagnosis
A general clinical diagnosis of “viral hemorrhagic
fever” can be made in febrile patients with a
bleeding diathesis. Definitive diagnosis relies on
viral isolation or on the detection of viral antigen
in acute phase serum by immunoassay [5].
4.6.4 Differential Diagnosis
VHF can be suspected in any patient presenting
with a severe febrile illness and evidence
of vascular involvement (postural hypotension,
petechiae, easy bleeding, flushing of the face
or chest, non-dependent edema) who has trav-
eled to an area where the virus is known to
occur, or a bioterrorism threat is suspected. Signs
and symptoms suggesting additional organ system
involvement are common (headache, photophobia,
pharyngitis, cough, nausea or vomiting, diar-
rhea, constipation, abdominal pain, hyperesthesia,
dizziness, confusion, tremor).
Definitive diagnosis is made by specific viral
identification. Other clinical tests can be useful,
e.g., thrombocytopenia and leukopenia will be
seen in the filoviruses, but not with Lassa
virus; proteinuria and/or hematuria are common.
Malaria is the major disease to be considered
in the differential diagnosis of naturally acquired
VHF. Others include typhoid fever, non-typhoidal
salmonellosis, leptospirosis, rickettsial infections,
shigellosis, relapsing fever, fulminant hepatitis,
meningococcemia, acute leukemia, lupus erythe-
matosus, idiopathic or thrombotic thrombocy-
topenic purpura, hemolytic uremic syndrome, and
the many other causes of disseminated intravas-
cular coagulation [5].
4.6 Disease: Viral Hemorrhagic Fever
4.6.1 Causative Agent
The viral hemorrhagic fever (VHF) viruses include
filoviruses [e.g., Ebola, Marburg], arenaviruses
[e.g., Lassa, Machupo], bunyaviruses [e.g.,
Hantaviruses], and flaviviruses [e.g., Dengue and
Yellow Fever]. They may cause clinical hemor-
rhagic fever, where the target organ is the vascular
bed, and the dominant clinical features are often
due to microvascular damage and changes in
vascular permeability [5,14].
4.6.2 Clinical Description
These viruses cause febrile illnesses that can
feature flushing of the face and chest, petechiae,
bleeding, edema, hypotension, and shock. Malaise,
myalgia, headache, vomiting and diarrhea may
also occur. Disseminated intravascular coagula-
tion and coagulopathy occur to varying degrees
with various VHFs. Common symptoms include
