Biomedical Engineering Reference
In-Depth Information
lungs, or by invading abraded or lacerated skin.
There is neither available vaccine nor dependable
therapy [5,11].
4.8.3 Diagnosis
Gram stain of lesion exudates reveals small Gram-
negative bacteria.
B. mallei
grows slowly on ordi-
nary nutrient agar, and special growth media may
be used to enhance isolation. Agglutination tests
are not positive for 7-10 days, and a high back-
ground titer in normal sera (1:320 to 1:640) makes
interpretation difficult. Complement fixation tests
are more specific and are considered positive if
the titer is equal to, or exceeds 1:20. Cultures of
autopsy nodules in septicemic cases will usually
establish the presence of
B. mallei
[5,11].
4.8.2 Clinical Features
Glanders may occur in an acute localized form,
as a septicemic rapidly fatal illness, or as an
acute pulmonary infection. Combinations of these
syndromes commonly occur in human cases. A
chronic cutaneous form with lymphangitis and
regional adenopathy is also frequent. Aerosol
infection produced by a
B. mallei
could produce
any of these syndromes. The incubation period
ranges from 10-14 days, depending on the inhaled
dose and agent virulence. The septicemic form
begins rapidly with fever, rigors, sweats, myalgia,
pleuritic chest pain, photophobia, lacrimation,
and diarrhea. Physical examination may reveal
fever, tachycardia, cervical adenopathy, and mild
splenomegaly. Blood cultures are usually negative
until the patient is moribund. Mild leukocytosis
with a shift to the left or leukopenia may occur.
The pulmonary form may follow inhalation or
occur by hematogenous spread. Systemic symp-
toms as described for the septicemic form occur.
Chest radiographs may show miliary nodules
(0.5-1.0 cm) and/or a bilateral bronchopneumonia,
segmental, or lobar pneumonia and necrotizing
nodular lesions.
Acute infection of the oral, nasal and/or conjunc-
tival mucosa can cause mucopurulent, blood-
streaked discharge from the nose, associated with
septal and turbinate nodules and ulcerations. If
systemic invasion occurs from mucosal or cuta-
neous lesions then a papular and/ or pustular rash
may occur that can be mistaken for smallpox
(another possible BW agent).
The chronic form is unlikely to be present within
14 days after an aerosol exposure, and is character-
ized by cutaneous and intramuscular abscesses on
the legs and arms. These lesions are associated with
enlargement and induration of the regional lymph
channels and nodes. Recovery from chronic glan-
ders may occur or the disease may erupt into an
acute septicemic illness. Nasal discharge and ulcer-
ation are present in 50% of chronic cases [5,11].
4.8.4 Medical Management
Standard Precautions should be used to prevent
person-to-person transmission in proven or
suspected cases. Sulfadiazine 100mg/kg per day
in divided doses for 3 weeks has been found
to be effective. Various isolates have markedly
different antibiotic sensitivities, so that each isolate
should be tested for its own individual resistance
pattern [5,11].
4.8.5 Prophylaxis
There is no vaccine available for human use. PEP
may be tried with TMP-SMX [5,11].
4.9 Disease: Q Fever
4.9.1 Causative Agent
Coxiella burnetii
, the causative agent of Q fever, is
a Gram-negative coccobacillus, is resistant to heat
and desiccation and is highly infectious by aerosol
exposure [5].
4.9.2 Clinical Description
The incubation period for Q fever is between
10-40 days. There are a variety of Q Fever clin-
ical syndromes. Flu-like symptoms occur as soon
as 10 days after exposure. Q fever is usually
a self-limiting febrile illness lasting 2-14 days.
Patients usually present with headaches, fatigue,
chills, sweats, and myalgias. Infections range from
asymptomatic to severe. Severe headache is present
in about 75% of patients. Pneumonia occurs in
