Biomedical Engineering Reference
In-Depth Information
develops pulmonary edema or adult respiratory
distress syndrome (ARDS), there may be a cough
with frothy sputum. Fever may last 2-5 days,
and cough may persist for up to 4 weeks. Toxin
ingestion leads to acute salivation, nausea, and
vomiting followed by abdominal cramps and diar-
rhea. Fever and respiratory involvement are not
seen in foodborne SEB intoxication. Higher expo-
sure can lead to septic shock and death if left
untreated. Physical examination is often unremark-
able. Postural hypotension may be present, partic-
ularly with ingestion of SEB, due to fluid loss.
Conjunctivitis and rales may be present [5].
4.10.4 Differential Diagnosis
For inhalational exposure, similar symptoms
in large numbers of patients might suggest
several respiratory pathogens. Influenza, Q fever,
tularemia, plague, and respiratory illnesses due to
exposure to SEB and chemical agents such as phos-
gene should be included in the differential diag-
nosis. SEB intoxication would likely have a more
rapid onset and lower mortality. Acute lung injury
induced by phosgene would progress much faster
than that caused by ricin. Nerve agent intoxication
would be characterized by acute onset of cholin-
ergic crisis with dyspnea and profuse secretions.
The differential diagnosis for patients who have
ingested ricin would include disease due to all the
major enteric pathogens. These should be ruled out
with culture [5].
4.11.3 Diagnosis
A diagnosis may be made by the detection of
antibodies via an ELISA assay. Toxin accumu-
lates in urine and may be detected via ELISA for
several hours after exposure. PCR may be helpful
in demonstrating the presence of toxin in environ-
mental specimens [5].
4.10.5 Treatment
Management of patients is supportive. Aceta-
minophen for fever, and cough suppressants may
make the patient more comfortable. Management
of ricin-intoxicated patients depends on the route
of exposure. Patients with pulmonary intoxica-
tion are managed by appropriate treatment for
pulmonary edema and respiratory support as indi-
cated. Gastrointestinal intoxication is best managed
by vigorous gastric decontamination with super-
activated charcoal, followed by use of cathartics
such as magnesium citrate. Volume replacement of
GI fluid losses is important [5,12].
4.11.4 Differential Diagnosis
Influenza, adenovirus, parainfluenza, or myco-
plasma infection could cause fever, non-productive
cough, myalgias, and headache in large numbers
of people in a short time. Early clinical mani-
festations of SEB may be similar to those of
inhalation anthrax, tularemia, plague, or Q fever.
However, the rapid progression of respiratory signs
and symptoms to a stable state differentiates SEB
intoxication. Chemical agents, such as mustard
gas, would show marked vessiculation of the
skin as well as pulmonary injury. During 6-12
hours following exposure, clinical tests may detect
toxin, including blood samples, urine nasal swabs,
and induced respiratory secretions. Most patients
develop a significant antibody response after 6 days
following exposure. Acute and convalescent sera
should be drawn for immunological testing [5,12].
4.11 Disease: Staphylococcal
Enterotoxin B Intoxication
4.11.1 Causative Agent
Staphylococcal enterotoxin B (SEB) is one of
several exotoxins produced by the Gram-positive
bacilli
Staphylococcus aureus
[5].
4.11.2 Clinical Description
From 3-12 hours after aerosol exposure, fever,
chills, headache, myalgia and non-productive
cough may appear. Shortness of breath and
retrosternal chest pain may develop. If the patient
4.11.5 Medical Management
Supportive care with close attention to oxygena-
tion and hydration. In severe cases, ventilation
is provided, with positive-end-expiratory pressure
