Anthrax

• It is caused by Bacillus anthracis, a spore-

forming, gram-positive rod that is aerobic or
facultatively anaerobic. The name comes from
the Greek word for “coal,” a reference to the
black eschar that eventually forms in the
cutaneous form of in the cutaneous form of
anthraxa.nthrax
• It is primarily a disease of animals, but it has also
been developed in past decades by some nations
as a biowarfare weapon and was used by one or
more unidentified persons as a bioterrorist
weapon in 2001 in the United States. Historical
names that reflect the zoonotic nature of most
human infections include “woolsorter's disease”
and “ragpicker's disease.”
 Transmission

Via contact with Zoonotic source, like goats, sheep,

cattle, antelope, kudu, pigs, horses, zebu and Animal-
related products that can transmit the infection include
meat, wool, hides, bones, and hair . The bacteria get
access to human being from spore containing dirt,
contaminated animal products and tannery waste
waters.
• Incubation period is 2-7 days.
• It is one of the biological terrorism weapon used for
mass destruction because
 Can be easily disseminated or transmitted
person-to-person.
 Cause high mortality.
 Might cause public panic and social disruption.
Require special action for public health preparedness
 The sign and symptom depends on the portal of entry and are
generally Anthrax is classified in to 3 types:

1.Cutaneous Anthrax
• It is infection of skin.
• It is the most common form of the disease(95%).
Naturally occurring cases of cutaneous anthrax develop after
spores of B. anthracis are introduced subcutaneously, often as a
result of contact with infected animals or animal products. Cuts or
abrasions increase susceptibility to cutaneous infection. Spores
vegetate and multiply, and the antiphagocytic capsule facilitates
local spread.
-The incubation period is usually five to seven days.
Sign and symptom
• Over 90 percent of cutaneous anthrax lesions occur in
exposed areas such as the face, neck, arms, and hands. The
disease begins as a small, painless, but often pruritic papule
and quickly enlarges and develops a central vesicle or bulla,
followed by erosion leaving a painless necrotic ulcer with a
black, depressed eschar . Extensive edema of the
surrounding tissues, due to toxin release (edema factor” (EF)
and “lethal factor” (LF), and its antiphagocytic poly-D-
glutamic acid capsule) and is often present along with
regional lymphadenopathy and lymphangitis.
• Systemic symptoms, including fever, malaise, and
headache.
• the case fatality rate is <1 percent with antibiotic
therapy, however, without appropriate therapy,
mortality can be as high as 20 percent.
2. Inhalation anthrax ( Pulmonary Anthrax)

• Inhalation anthrax results from the inhalation into the alveolar

spaces of B. anthracis spore-containing particles aerosolized
through industrial processing, when working with animal products
such as wool, hair, or hides that are contaminated with anthrax
spores, or from intentional release.
• Inhaled airborne particles >5 microns in size are either physically
trapped in the nasopharynx or cleared by the mucociliary escalator
system. In comparison, inhaled particles <5 microns in size can be
deposited on alveolar ducts or alveoli.
• Spores are phagocytosed by alveolar macrophages and
transported to mediastinal lymph nodes. There they
germinate, multiply and release toxins, causing hemorrhagic
necrosis of the thoracic lymph nodes draining the lungs, a
hemorrhagic mediastinitis, and, in occasional cases, a
necrotizing pneumonia at the portal of entry and cause
pleural effusions that are often bloody, can expand rapidly,
recur if drained by thoracentesis rather than by chest tube .
The organisms then become blood-borne, causing
bacteremia and potentially meningitis.
• The incubation period for inhalation anthtaxhrax is estimated to be one to seven
days.
 CLINICAL STAGING SYSTEM FOR INHALATIONAL ANTHRAX

I. EARLY-PRODROMAL STAGE

Nonspecific illness sometimes described as “flulike”

and including any of the following: fever, cough,
headache, chills, nausea, chest pain, or abdominal pain.
Laboratory tests and radiographs are nondiagnostic.
The prognosis for cure is good with appropriate
therapy, but the diagnosis is difficult to confirm acutely
in this stage.
II. INTERMEDIATE-PROGRESSIVE STAGE
Any of the following findings are defining inclusion criteria for this stage:

1. Positive blood cultures (typically positive in <24 hours)

2. Mediastinal adenopathy
3. Pleural effusions: bloody, often large, require drainage,
and may recur

Findings in this stage may include high fever, dyspnea,

confusion or syncope, or increasing nausea and vomiting.
Exclusion criteria for this stage include:
1. Meningitis
2. Respiratory failure requiring intubation and
mechanical ventilation or
3. Shock

Importantly, patients in this “intermediate-progressive”

stage can still be cured with appropriate antibiotics and
drainage of pleural effusions by thoracentesis and/or chest
tube to reduce the adverse mechanical effect on respiration
by large-volume effusions and to remove potentially toxin-
producing Bacillus anthracis from the pleural space.
III. LATE-FULMINANT STAGE

Inclusion criteria include any one of the following findings:

1.Meningitis
2.Respiratory failure requiring intubation and
mechanical ventilation or
3.Shock :end-organ hypoperfusion
Findings in this stage may also include any of
those from previous stages, so there are no
exclusion criteria. The probability of survival is
lowest in this stage. Novel therapeutics that
safely and effectively neutralize toxin may be
needed to increase survival.
• Early clinical symptoms of inhalation anthrax are
nonspecific i.e. myalgia, fever, and malaise mimicking
those of influenza. Two to three days later, infected
patients become dramatically sicker with the
development of respiratory symptoms, including
severe dyspnea and hypoxemia.Untreated case end
up in death. Hematogenous spread can result in
lesions in other organ systems, including
hemorrhagic meningitis and submucosal
gastrointestinal lesions
3.Gastrointestinal anthrax
• It presents in two clinical forms, oropharyngeal and
intestinal.
• It develops following the consumption of
undercooked infected meat from animals with
anthrax, and tends to occur in family clusters or
point source outbreaks. The incubation period is
estimated to be one to six days and the case fatality
rate is estimated to range from 25 to 60 %
• Following ingestion, the spores infect the
gastrointestinal tract epithelium. Extensive
edema of the infected intestinal segment
and mesentery can develop, and lesions
may become necrotic and ulcerated. The
mesenteric lymph nodes may be enlarged
and infected
 Clinical symptoms

• Symptoms may include fever, nausea and

vomiting, anorexia, abdominal pain and
tenderness, and progress to hematemesis and
bloody diarrhea. Abdominal distension with
voluminous, hemorrhagic ascites may be
present. The disease may progress to toxemia,
cyanosis, shock, and death.
• The oropharyngeal form develops following
infection of the oropharyngeal epithelium with
consumption of undercooked, contaminated meat.
Edematous lesions develop, which progress to
necrotic ulcers covered with a pseudomembrane.
Edema and swelling develop in the oropharynx and
neck, accompanied with cervical lymphadenopathy,
pharyngitis, and fever.
 Diagnosis
• Hx and P/E
Investigations
• CBC,CXR ( specially in inhalational anthrax)
• Culture from- blood, skin lesion exudates,
cerebrospinal fluid (CSF), pleural fluid, sputum,
and feces.
• Non-culture detection of B. anthracis-PCR,
Serology (ELISA) antibody response against the
anthrax toxin protein, protective antigen (PA),
 Treatment

• Anthrax is a reportable disease and

immediate notification should be made to
the local or state health department and
public health laboratory following clinical
or laboratory suspicion of anthrax or
exposure to B. anthracis.
• chloramphenicol 500mg,or Ampicilin 500mg IV QID

for 7-10days or, tetracycline 500mg po QID for 7-10

days, erythromycin 500mg ,po QID for 7-10

days,Ciprofloxacin 500mg IV or PO BID for 7-10 days

NB-B. anthracis is not susceptible to cephalosporins or

trimethoprim-sulfamethoxazole; these antibiotics should

not be used for the treatment of anthrax.

• Pleural effusion drainage-use of chest tubes
or thoracentesis to drain pleural effusions as
adjunctive treatment.
• Corticosteroids-In patients with
meningoencephalitis and patients with
cutaneous anthrax with extensive edema
involving the head and neck.
• Antipain-Diclofenac 75 mg im prn
• Fluid and electrolyte replacement.
 PREVENTION

• Prevention of naturally-occurring anthrax in

humans is primarily dependent on the
control of the disease in animals, especially
livestock.
Cough Reflex
• It is one of the primary defense mechanism of
the respiratory system.
• It protects the lung from accumulation of
secretions and from entry of irritating and
destructive substances.
• It is initiated by receptors located on the
tracheobronchial wall. They are Extremly
sensitive to irritating substances and to
presence of excess secretions.
• Receptors →Afferent impulse→ Respiratory
Centers in Pons and medulla.
Differential diagnosis of COUGH

• Disease processes which cause cough

1. Infectious 2.Non-Infectios
• Common cold. • Asthma.
• Tonsilopharengitis • Chronic bronchitis.
• Sinusitis. • Bronchiectasis.
• pneumonia. • Interstitial lung diseases
• Tuberculosis. e.g. pneumoconiosis.
• Bronchitis. • Bronchogenic Cancer.
• Epiglotitis. • Pulmonary edema.
• Foreign body in lung.
Differential diagnosis of Chest pain
 It is ranged from simple myalgia to life threatening
myocardial infarction.
NB-There is little correlation between the severity of
chest pain and gravity of its cause.
 There is poor correlation between geography of
chest pain and its source.
 A patient may have more than one disease process
occurring simultaneously.
1.Cardiovascular origin

chest pain

• Ischemic heart diseases

• Pericarditis.

• Aneurysm of Aorta

(dissecting type).

• Aortic Stenosis.
2.Pulmonary disease
• Pleursy.
• Pneumonia and other inflammatory condition
of lung parenchyma.
• Spontaneous pneumothorax.
• Massive pleural effusion and or heamothorax.
• Pulmonary embolism.
• Lung cancer-primary or secondary.
• Collapse of lung.
3.Gastrointestinal disorders

A.Esophagial

 Reflux esophagitis.

 Malory weiss syndrome.

 Carcinoma of esophagus

B. Peptic Ulcer disease

C.Cholecystitis and cholilithiasis.

D.Pancreatitis and cancer of pancreas.

4. Causes in thoracic wall
A. skin
• Herpes Zoster
• Soft tissue injury.
• Mastitis.
B. Musceles
• Myalgia
C.Skeletal
• osteoarthritis.
• Fracture (vertebral bone, ribs
fracture).
Approach to chest pain
• Site
• Character-burning,squeezing,piercing…
• Radiation-e.g. MI to left shoulder,jaw,arm…
• Duration-e.g. MI ( short) ,Bronchogenic ca
( prolonged time..)
• Aggravating and relieving factors-Food,
exercise…
• Associated symptoms