Page 169 - Concise Pathology for Exam Preparation ( PDFDrive )

154 SECTION I General Pathology

• The three most common forms of plague include
• Bubonic plague (affects the lymphatic system)
• Pneumonic plague (affects the respiratory tract)
• Septicaemic plague (infection of blood)
• Rodents, such as rats, are carriers of the disease and plague accidentally affects humans
when they are bitten by a flea that carries the plague bacteria from an infected rodent.
Rarely, one may get the disease while handling an infected animal. Pneumonic plague
can spread from human-to-human via respiratory droplets.
Morphology
• The distinctive pathological features of plague include protein-rich effusions, marked
tissue swelling, necrosis with haemorrhage and thrombosis and massive neutrophilic
infiltrates.
• Bubonic plague usually initiates on the legs as a small pustule or ulcer. This enlarges to
involve the draining lymph nodes which become soft and pulpy, and may rupture
through the skin.
• Pneumonic plague typically presents with severe necrotizing bronchopneumonia, often
accompanied by haemorrhage and fibrinous pleuritis.
• Disseminated necrotizing lymphadenitis is the histopathological hallmark of septicae-
mic plague. Bacteraemia may induce disseminated intravascular coagulation (DIC) with
the presence of widespread haemorrhages and thrombi.
Plague can be diagnosed by
• Blood culture
• Culture of lymph node aspirate (bubo aspirates)
• Sputum culture (in pneumonic plague)

Typhoid Fever
Also known as ‘enteric’ or ‘bilious fever’, typhoid is caused by the Gram-negative
bacillus, Salmonella typhi. The extent and severity of clinical disease depends on
the bacterial type and its strain. Salmonella possesses protective antigens which
promote host destruction; these include a heat-stable cell wall lipopolysaccharide
(LPS) known as somatic or ‘O’ antigen, flagellar or H antigens derived from struc-
tural proteins and a PS capsular Vi (for virulence) antigen found at the surface of
freshly isolated strains.
Pathogenesis
• Typhoid is transmitted by ingestion of food or water contaminated with faeces from an
infected person.
• After reaching the lumen of intestine, the bacteria multiply by attaching to microvilli of
the intestinal surface. They eventually perforate through the intestinal wall and are
phagocytosed by macrophages. S. typhi alters its structure to resist destruction and
allows it to exist within the macrophage.
• The bacteria localize in the Peyer’s patches in ileum inducing their hyperplasia. Overt
enlargement of the Peyer’s patches causes ulceration of the overlying mucosa. The or-
ganism may spread via lymphatics to get access to reticuloendothelial system and then
disseminate throughout the body.

Clinical Manifestations (Table 7.1)
Typhoid is characterized by a sustained, slowly rising fever accompanied by profuse sweat-
ing, diarrhoea, a rash of flat rose-coloured spots, tender hepatosplenomegaly and elevation
of liver transaminases. Less commonly, there is relative bradycardia, malaise, headache,
cough, rarely epistaxis, abdominal pain and delirium. The illness classically lasts for
3–4 weeks. By the end of third week, recovery commences.

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