Introduction
Typhoid fever (enteric fever) is an acute infectious disease most often caused by Salmonella enterica serotype Typhi and sometimes by S. paratyphi. It spreads when food or water contaminated with faeces of an infected person is ingested. Typhoid is common in areas with poor sanitation and unsafe water.
Pathophysiology
After ingestion, bacteria cross the intestinal mucosa (especially through Peyer patches in the distal ileum) and are taken up by macrophages. S. typhi can survive inside macrophages and travel via lymphatics and blood to organs such as liver, spleen and bone marrow. The bacteria multiply, are released into the bloodstream (bacteremia) and re-enter the gut via bile, causing continuous intestinal infection and faecal shedding. S. typhi has a VI capsule that helps it evade early innate responses.
Epidemiology
Typhoid occurs worldwide but is most common in parts of Asia, Africa and Latin America. High-burden countries include India, Pakistan, Bangladesh, Nepal and Indonesia. It mainly affects areas with unsafe water, poor sanitation and crowded living conditions.
Clinical Features
- Incubation: usually 1–3 weeks (can be 3 days to 3 weeks).
- Early symptoms: gradual onset fever, malaise, headache, anorexia and cough.
- Characteristic features: sustained high fever (often ≈40°C), relative bradycardia, abdominal pain, constipation (early) or diarrhea (later), and coated tongue with red edges.
- Rose spots: small faint pink macules on the chest or abdomen (may appear in some patients).
- Splenomegaly and hepatomegaly are common.
- Severe disease: intestinal bleeding, perforation, encephalopathy, sepsis.
Diagnosis
Definite diagnosis is by isolating the organism:
- Blood culture: Most useful in the first week (sensitivity improves with two sets and modern methods).
- Stool culture: May be positive later in illness and for carriers.
- Bone marrow culture: Most sensitive (used when other cultures are negative).
- Widal test: Serologic test detecting anti-O and anti-H antibodies — widely used but has limitations (false positives/negatives) and needs careful interpretation.
Treatment
Early antibiotic therapy reduces mortality to 1–2% from much higher rates seen before antibiotics.
- First-line agents: Use antibiotics per local resistance patterns. Fluoroquinolones (e.g., ciprofloxacin) were widely used but resistance is common in many regions.
- Third-generation cephalosporins: (e.g., ceftriaxone) are commonly used, especially in areas with fluoroquinolone resistance or in pregnancy (IM/IV options available).
- Azithromycin is an oral option in some settings.
- Other options: ampicillin, trimethoprim–sulfamethoxazole (resistance varies).
- Severe complications (perforation, massive bleeding) require surgical management together with antibiotics.
- Supportive care: fluids, antipyretics, nutrition and monitoring for complications.
Complications
- Intestinal haemorrhage and ileal perforation (surgical emergency).
- Sepsis, myocarditis, pancreatitis, hepatitis and acute kidney injury.
- Neuropsychiatric symptoms (delirium, confusion).
- Chronic carriage: some people (especially with gallbladder disease) become carriers and shed bacteria in stool for months.
Prevention
- Safe drinking water and proper sanitation are the most important measures.
- Handwashing with soap after toilet use and before handling food.
- Avoid high-risk foods (raw salads, unpeeled fruits, street foods of uncertain hygiene).
- Vaccination: killed (injectable) and live-attenuated oral vaccines are available and advised for travellers and in some public health programs.
- Prompt diagnosis and treatment of cases and identification/treatment of carriers reduce spread.
Detailed Notes:
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