Write a short note on typhoid (enteric) fever.
Aetiology
Enteric fever is a systemic illness caused by *Salmonella enterica* serotype Typhi (typhoid) and serotypes Paratyphi A, B and C (paratyphoid). It is a Gram-negative, flagellated, non-lactose-fermenting bacillus, and humans are the only reservoir — which makes eradication theoretically possible.
Transmission is faeco-oral, through contaminated water and food, and by chronic carriers handling food. It is endemic throughout India, with peaks in the monsoon, and reflects inadequate sanitation and unsafe water.
Pathogenesis
1. Ingested bacilli survive gastric acid (an infective dose of 10⁵–10⁹, lowered by achlorhydria and antacids) and invade the Peyer's patches of the terminal ileum via M cells.
2. They are taken up by macrophages but survive intracellularly, multiplying in mesenteric lymph nodes.
3. Primary bacteraemia seeds the liver, spleen and marrow (the incubation period, 7–14 days).
4. Secondary bacteraemia produces the clinical illness; bacilli re-enter the gut via the gall bladder and bile, causing hyperplasia, necrosis and ulceration of Peyer's patches — the basis of the intestinal complications in the third week.
Clinical Features — the Classic Weekly Progression
| Week | Features |
|---|---|
| Week 1 | "Step-ladder" fever rising progressively each day; headache, malaise, relative bradycardia (Faget's sign), dry cough, constipation more often than diarrhoea in adults, abdominal discomfort |
| Week 2 | Sustained high fever; rose spots — sparse, blanching, 2–4 mm pink macules on the trunk (difficult to see in dark skin); hepatosplenomegaly; abdominal distension; coated tongue with clean red edges; "typhoid state" — apathy, delirium, muttering |
| Week 3 — the dangerous week | COMPLICATIONS: intestinal perforation and haemorrhage; toxaemia; myocarditis; shock |
| Week 4 | Gradual defervescence and recovery, with weakness persisting for weeks |
Complications
- Intestinal perforation (1–3%) — classically in the third week, at the terminal ileum, from necrosis of Peyer's patches. Presents with sudden abdominal pain, guarding, rigidity, loss of liver dullness and free gas under the diaphragm. A surgical emergency with high mortality; in a toxic patient with abdominal pain the signs may be muted, so a high index of suspicion is essential.
- Intestinal haemorrhage — melaena or fresh bleeding from ulcerated Peyer's patches.
- Typhoid encephalopathy — delirium, stupor, coma; the "muttering delirium" of the typhoid state; typhoid meningitis is rare.
- Myocarditis — a leading cause of death; ECG changes, arrhythmia, heart failure.
- Hepatitis and cholecystitis; splenic abscess.
- Osteomyelitis — with a particular association with sickle cell disease.
- Relapse (5–10%) — 1–3 weeks after apparent recovery, usually milder.
- Chronic carrier state (1–4%) — persistent excretion for over a year, usually from the gall bladder (often with gallstones); commoner in women and the elderly. Carriers are the reservoir that sustains transmission.
Investigations
| Test | Timing / yield | Comments |
|---|---|---|
| Blood culture | Week 1 — highest yield (60–80%) | The gold standard. Take a large volume before antibiotics |
| Bone marrow culture | Any week; highest sensitivity (~90%) | Remains positive even after antibiotics; invasive, reserved for difficult cases |
| Stool and urine culture | Weeks 2–3 onwards | Also used to detect carriers |
| Widal test | From the end of week 1; paired samples | Poorly specific — false positives from previous infection, vaccination and other Salmonella; a single titre is of little value and it is over-relied upon in India. A fourfold rise in paired sera is required |
| Typhidot / rapid IgM tests | Early | Convenient but variable performance |
Supporting findings: leucopenia with relative lymphocytosis and eosinopenia (leucocytosis suggests perforation or another diagnosis), anaemia, thrombocytopenia, and mildly raised transaminases. Erect abdominal X-ray or ultrasound/CT for suspected perforation.
Management
- Antibiotics. Choice is dictated entirely by resistance patterns: classical multidrug-resistant strains (resistant to ampicillin, chloramphenicol and co-trimoxazole) are widespread, fluoroquinolone resistance is now very high in India, and extensively drug-resistant (XDR) strains resistant additionally to third-generation cephalosporins have emerged in the subcontinent. Third-generation cephalosporins (ceftriaxone, cefixime) and azithromycin are the current mainstays, guided by local susceptibility data.
- Supportive care: hydration and electrolyte correction, antipyretics, adequate nutrition (a soft, low-residue diet), and monitoring for complications.
- Corticosteroids (dexamethasone) — of proven benefit in severe typhoid with delirium, obtundation, stupor, coma or shock, where they reduce mortality substantially.
- Surgical management of perforation — resuscitation, antibiotics and early laparotomy with closure or resection; delay markedly worsens outcome.
- Chronic carriers: prolonged antibiotic course; cholecystectomy where there are gallstones and eradication fails. Exclude carriers from food handling.
Prevention
- Safe water and sanitation — the definitive answer: chlorination, boiling, protected water supply, safe sewage disposal.
- Food hygiene — hand washing, avoiding raw and street-vended food and untreated water and ice.
- Vaccination — Vi polysaccharide and Vi conjugate vaccines (the conjugate vaccine is effective in young children and gives longer protection) and the oral live Ty21a vaccine; recommended for endemic populations, travellers and outbreak control.
- Identify and treat carriers; notify and investigate outbreaks.
Do not diagnose typhoid on a single Widal test — this is one of the most widespread diagnostic errors in Indian practice, leading to unnecessary antibiotics for what is often dengue, malaria, scrub typhus or a viral fever. Take blood cultures before antibiotics in every suspected case. Conversely, in a patient in the third week with sudden abdominal pain and a rigid abdomen, think perforation immediately, even if the fever appeared to be settling.
Antibiotic choices and durations — resistance patterns in India have shifted substantially and vary regionally; confirm against current local antibiograms and national guidance.
All questions in Infectious Diseases
- Q1Discuss the pathogenesis, clinical features, warning signs, investigations and management of dengue fever. ★
- Q2Discuss the clinical features, complications, investigations and management of severe malaria, including cerebral malaria. ★
- SN1Write a short note on typhoid (enteric) fever.
- SN2Write a short note on COVID-19 and pandemic influenza (H1N1).
- SN3Write a short note on sexually transmitted infections — gonorrhoea and human papillomavirus.
- SN4Write a short note on adult immunisation.
- SN5Write a short note on food poisoning.
- SN6Write a short note on febrile neutropenia.
- SN7Write a short note on varicella (chickenpox) and herpes zoster.
- SN8Write a short note on viral haemorrhagic fevers, including Ebola virus disease.
- SN9Write a short note on leptospirosis.
- SN10Write a short note on scrub typhus and other rickettsial infections.
- SN11Write a short note on visceral leishmaniasis (kala-azar).
- SN12Write a short note on brucellosis.
- SN13Write a short note on rabies, including post-exposure prophylaxis.
- SN14Write a short note on antitubercular therapy, including multidrug-resistant tuberculosis.
- SN15Write a short note on lymphatic filariasis.
- SN16Write a short note on neurocysticercosis.
- SN17Write a short note on chikungunya.