Endemic Regions

Typhoid fever, caused by Salmonella Typhi (a gram-negative bacterium), is endemic in regions with poor sanitation, limited access to clean water, and inadequate hygiene infrastructure. It’s most prevalent in:

• South Asia: India, Pakistan, Bangladesh, and Nepal bear the highest burden, with India often cited as having the greatest incidence globally.
• Sub-Saharan Africa: Countries like Nigeria, Kenya, and the Democratic Republic of Congo see significant cases, especially in crowded urban slums.
• Southeast Asia: Indonesia, Vietnam, and the Philippines report consistent endemicity.
• Parts of the Middle East and North Africa: Yemen, Egypt, and Morocco have pockets of ongoing transmission.
• Latin America: Though less common, rural areas in Peru, Bolivia, and Haiti still see cases.

The disease thrives where sewage contaminates drinking water or food, often spread via the fecal-oral route. Travelers to these regions are at risk, especially if unvaccinated or consuming untreated water or street food. The World Health Organization estimates 11-21 million cases annually, with 128,000-161,000 deaths, predominantly in these endemic zones.

Presentation

Typhoid fever’s symptoms creep in gradually, typically 6-30 days after exposure, depending on the bacterial load and host immunity. It unfolds in stages:

• Week 1: Low-grade fever starts, often rising stepwise to 39-40°C (102-104°F). Patients feel fatigued, with headache, malaise, and a dry cough. Appetite drops, and abdominal discomfort—like bloating or mild pain—sets in. Constipation is more common in adults, though diarrhea can occur, especially in kids.
• Week 2: Fever plateaus at a high level, sustained rather than spiking. A classic (but not universal) sign is “rose spots”—faint, salmon-colored, blanching rashes on the chest or abdomen. Pulse may be oddly slow relative to the fever (Faget sign). Abdominal issues worsen—distension, tenderness, and sometimes spleen or liver enlargement. Delirium or confusion (“typhoid state”) can emerge in severe cases.
• Week 3: Without treatment, complications peak. Intestinal perforation or bleeding can occur due to Peyer’s patch necrosis in the ileum. Fever persists, and patients may become profoundly weak or toxic.
• Week 4: If untreated, death risk rises (10-20%), but with antibiotics, fever gradually subsides, and recovery begins.

Chronic carriers—about 2-5% of cases—harbor the bacteria in their gallbladder, shedding it in stool without symptoms, famously exemplified by “Typhoid Mary.”

Diagnosis

Diagnosing typhoid fever relies on clinical suspicion and lab confirmation, as symptoms overlap with malaria, dengue, or other fevers. Key methods include:

• Blood Culture: The gold standard, especially in the first week when bacteremia peaks. Sensitivity drops later or with prior antibiotic use (60-80% early on).
• Bone Marrow Culture: More sensitive (80-95%), even after antibiotics, but invasive and rarely done unless critical.
• Stool or Urine Culture: Useful in later stages or to detect carriers, though less reliable early.
• Widal Test: Detects antibodies (O and H antigens) but lacks specificity—cross-reacts with other infections and isn’t great in endemic areas where baseline antibodies are common. It’s cheap but outdated.
• Rapid Serologic Tests: Newer options like Typhidot or Tubex detect IgM/IgG, offering quicker results but variable accuracy.
• PCR: Molecular detection of S. Typhi DNA is emerging but not widely available in endemic settings.

Labs may show leukopenia (low white cell count), mild anemia, or elevated liver enzymes. Imaging (e.g., ultrasound) might reveal splenomegaly. Clinicians in endemic areas often start antibiotics empirically while awaiting culture results, given the disease’s severity.

Treatment typically involves fluoroquinolones (e.g., ciprofloxacin, though resistance is rising), third-generation cephalosporins (e.g., ceftriaxone), or azithromycin. Multidrug-resistant strains complicate things, especially in South Asia.

Disclaimer: NOT MEDICAL ADVICE