Define Enteric Fever. Describe its pathogenesis, clinical features, investigations and management.

Definition

• Enteric fever is a systemic infection caused by Salmonella enterica serotype Typhi (and Paratyphi A/B).
• It is transmitted by the faeco-oral route through contaminated food and water, and is common where sanitation is poor.

Pathogenesis

Ingestion of the organism → Invasion via Peyer's patches of the ileum → Spread to mesenteric lymph nodes → bacteraemia → Seeding of the reticulo-endothelial system (liver, spleen, marrow) → Secondary bacteraemia → clinical illness

Clinical Features (BY Week)

• Week 1 — stepladder (rising) fever, headache, malaise, relative bradycardia (Faget sign), coated tongue, constipation or diarrhoea.
• Week 2 — sustained high fever, rose spots (blanching pink macules on the trunk), hepatosplenomegaly, abdominal distension, toxaemia.
• Week 3 — complications (intestinal perforation/haemorrhage from Peyer's-patch ulceration), 'typhoid state' (apathy, delirium).

Investigations

• Blood culture — the gold standard (highest yield in the first week).
• Widal test — rising O and H agglutinin titres (positive from week 2; has limitations/false results).
• Bone-marrow culture — the most sensitive (unaffected by prior antibiotics); stool/urine culture positive later.
• Typhidot (IgM); CBC — leucopenia with aneosinophilia.

Management

• Antibiotics — ceftriaxone is the usual drug of choice for hospitalised/severe cases; cefixime or azithromycin for uncomplicated outpatient treatment (fluoroquinolone resistance is now common).
• Supportive care — hydration, antipyretics, and adequate nutrition (soft diet).
• Dexamethasone for severe disease with shock, delirium or encephalopathy.
• Monitor for and manage complications (surgery for perforation).

Differential Diagnosis of Prolonged Fever

• Malaria, tuberculosis, urinary tract infection, and other bacteraemias.
• Viral infections (dengue), abscess, and (less commonly) malignancy/connective-tissue disease.

The Chronic Carrier State

• A small proportion continue to excrete the organism for > 1 year (usually from chronic gallbladder carriage, sometimes with gallstones).
• Carriers are an important source of transmission and may need prolonged antibiotics or cholecystectomy.

Paratyphoid Fever

Salmonella Paratyphi A/B causes a clinically similar but generally milder illness ('paratyphoid'); together with typhoid it constitutes 'enteric fever'.

Epidemiology

• Endemic where sanitation and safe water are lacking; humans are the only reservoir.
• Spread by the faeco-oral route via contaminated food/water and by carriers handling food.

Clinical Course & Monitoring

• Defervescence usually occurs within 3–5 days of effective antibiotics; slow response suggests resistance or complication.
• Monitor for the third-week complications (perforation, haemorrhage) and for relapse after apparent recovery.

Pathology (WHY the Third Week Is Dangerous)

The organism proliferates in the Peyer's patches of the terminal ileum, which undergo hyperplasia, necrosis and ulceration; these ulcers can perforate or bleed in the third week — the classic surgical emergencies of typhoid.

Antimicrobial Resistance

• Multidrug-resistant (MDR) typhoid (to older first-line drugs) and widespread fluoroquinolone resistance now guide empirical therapy toward ceftriaxone/azithromycin.
• Culture with sensitivity testing directs definitive treatment; de-escalate once results are available.

Dietary & Supportive Care

• Maintain hydration and a soft, easily digestible, high-calorie diet during the febrile illness.
• Antipyretics for comfort; monitor closely for abdominal signs heralding perforation/bleeding.

Complications

• Intestinal perforation and haemorrhage (3rd week — the most feared).
• Myocarditis, hepatitis, encephalopathy, nephritis.
• Relapse and a chronic carrier state (persistent gallbladder carriage).

Prevention

• Typhoid conjugate vaccine (TCV).
• Safe drinking water, sanitation, hand hygiene and food safety; identification and treatment of carriers.

WHY the Third Week Is the Dangerous One

• A concept that determines vigilance is understanding why the complications of typhoid — which are the things that kill — occur in the third week, just as the family thinks the child is recovering.
• The organism multiplies within the PEYER'S patches of the terminal ileum — the lymphoid aggregates of the gut wall.
• Over the first two weeks these become progressively hyperplastic, then necrotic, and then they ulcerate.
• By the third week, these ulcers have eroded deeply into the bowel wall — and it is now that they reach the blood vessels (causing intestinal haemorrhage) or perforate the wall entirely (causing perforation and peritonitis).
• Both are catastrophic, and perforation carries a high mortality.
• And here is the trap: by week three the fever may be settling and the child appearing better — so the sudden appearance of severe abdominal pain, distension, rigidity or shock may be dismissed or attributed to something else.
• Hence: watch for haemorrhage and perforation in the third week, and treat any sudden deterioration with acute abdominal pain as a perforation until proved otherwise.
• The other complications are encephalopathy ('typhoid state'), myocarditis and the chronic carrier state.