Page 168 - Concise Pathology for Exam Preparation ( PDFDrive )
P. 168
7 Infections 153
Clinical Manifestations
• C. diphtheriae infection may be asymptomatic or manifest as clinical diphtheria. The
latter may be classified as nasopharyngeal or cutaneous depending on the area of
involvement.
• Pharyngeal diphtheria has a wide spectrum of clinical manifestations ranging from
mild pharyngitis to airway obstruction due to the formation of a pseudomembrane. The
bacteria induce the formation of an intense fibrinosuppurative exudate, the coagulation
of which creates a tough, dirty, grey membrane, which eventually leads to asphyxiation.
Accompanying cervical lymphadenitis causes marked swelling of the neck (also called
bull neck diphtheria). Released toxins can cause loss of motor function leading to seri-
ous complications, eg, inability to swallow and congestive heart failure (also attributed
to direct action of diphtheria toxin on the myocardium).
• Infection of chronic wounds is a common manifestation of cutaneous diphtheria. The skin
lesions are also covered by a grey-brown pseudomembrane like the pharyngeal lesions.
Morphology
Histological sections typically show abundant neutrophils, vascular congestion, interstitial
oedema and fibrin exudation. The release of exotoxins induces generalized hyperplasia of
the reticuloendothelial system, degeneration of myelin sheaths of nerves, fatty change and
necroses of multiple organs such as the myocardium, liver, kidneys and adrenals.
Anthrax
Anthrax is a zoonotic infection caused by Bacillus anthracis, which is a spore-forming,
Gram-positive, rod-shaped bacterium. It occurs in animals that have contact with soil
contaminated with B. anthracis spores. Anthrax spores can be ground to a fine powder
which makes them a potential weapon for bioterrorism. B. anthracis produces potent tox-
ins and has a polyglutamyl capsule, which is antiphagocytic. There are three major anthrax
syndromes:
1. Cutaneous anthrax: Responsible for 95% cases of anthrax, cutaneous anthrax begins
as a painless itchy papule which eventually transforms into a vesicle. The cutaneous
lesion is accompanied by regional lymphadenopathy. The vesicle ruptures to form an
ulcer that gets covered with dead tissue (eschar). Shedding of the eschar is a sign of
recovery. Bacteraemia is rarely seen. Histopathology of anthrax skin lesions shows oe-
dema, necrosis and lymphocytic infiltration. No suppuration is seen. Gram’s staining
demonstrates bacilli in the subcutaneous tissue.
2. Inhalational anthrax: Occurs due to inhalation of anthrax spores, which then travel
to the regional lymph nodes via macrophages. The anthrax spores germinate in the
lymphatics and release toxins. This results in high-grade fever, cough, chest pain,
breathlessness, excessive sweating, shock and frequently death. Histopathology
shows necrotizing haemorrhagic pneumonitis, submucosal haemorrhages in the re-
spiratory passages, with haemorrhage and necrosis of peribronchial lymph nodes.
Gastrointestinal and meningeal lesions may occur as a result of haematogenous
spread.
3. Gastrointestinal anthrax: This is the least common form of anthrax. It is introduced
into a human via contaminated undercooked meat. Manifestations include flu-like
symptoms (fever, fatigue and sore throat); neck swelling, difficulty in swallowing, ab-
dominal pain, vomiting and diarrhoea (both of which may be bloody). Microscopy
reveals massive oedema, lymphocytic infiltrate and necrosis at infected sites. Gram’s
staining of peritoneal fluid may demonstrate gram-positive bacilli.
Plague
• It is a zoonotic infection caused by Yersinia pestis, a Gram-negative, facultative, intracel-
lular bacterium, transmitted by fleabites or aerosols. It has an incubation period of
2–7 days. The disease is frequently fatal (thus named ‘Black Death’).
mebooksfree.com

