In New Zealand, paratyphoid Fever is managed by infectious diseases. Paratyphoid fever is a systemic febrile illness caused by Salmonella enterica serovars Paratyphi A, B, and C — clinically similar to typhoid fever but generally milder and increasingly common across South Asia. Together with typhoid fever, it is called enteric fever.
Paratyphoid fever (ICD-10: A01.1-A01.4) is enteric fever caused by Salmonella enterica subspecies enterica serovars Paratyphi A, Paratyphi B, or Paratyphi C — three closely related Gram-negative bacilli that are restricted to humans and produce a clinical syndrome similar to typhoid fever. After ingestion of contaminated food or water, the bacteria survive gastric acid, invade the small intestinal mucosa through M cells over Peyer's patches, are taken up by macrophages where they survive and replicate, and disseminate through the lymphatic system and bloodstream. The bacteria preferentially seed the liver, spleen, bone marrow, and gallbladder, producing the characteristic prolonged bacteremia that defines enteric fever. Clinical features include 5-30 day incubation, then stepwise rising fever to 39-40°C over the first week, relative bradycardia (Faget sign), abdominal pain (often right lower quadrant), constipation more often than diarrhea in adults (the reverse in children), hepatosplenomegaly, and occasionally the salmon-colored 'rose spot' rash on the trunk.
The key symptoms of Paratyphoid Fever are: Stepwise rising fever to 39-40°C over the first week, reaching a sustained plateau in week two — the hallmark of enteric fever as opposed to abrupt-onset bacterial enterocolitis., Profound malaise, fatigue, headache, and anorexia accompanying the fever — patients describe weakness disproportionate to a typical viral illness., Abdominal pain often localized to the right lower quadrant and exacerbated by palpation; constipation more common in adults, diarrhea more common in children (Crump 2015)., Relative bradycardia for the degree of fever (Faget sign) — pulse rate lower than expected for the temperature, a classical though imperfect clinical clue., Hepatosplenomegaly developing in the second week of illness in 30-50% of cases, contributing to abdominal discomfort., Salmon-colored maculopapular 'rose spot' rash on the trunk in 5-30% of paratyphoid patients, transient and easily missed., Dry cough, particularly in the first week, and sometimes pharyngitis — a non-specific finding that can lead to initial misdiagnosis as viral upper respiratory infection..
Paratyphoid fever is suspected on the basis of compatible clinical features — sustained fever with malaise, abdominal pain, hepatosplenomegaly — in a patient with relevant travel or contact history, and is confirmed microbiologically. Blood culture is the gold-standard test, with sensitivity 40-80% in the first week of illness, falling thereafter. At least 10-15 mL of blood (proportional to weight in children) should be drawn into both aerobic and anaerobic bottles before any antibiotics are given. Bone marrow culture has higher sensitivity (over 90%) at any stage and is used in patients pretreated with antibiotics or when blood cultures are negative despite high clinical suspicion, though it is rarely performed in routine practice. Stool culture is positive in only 30-50% of cases and tends to be positive later in the illness; it is most useful for detecting chronic carriers. Urine culture has limited sensitivity. Modern molecular methods (PCR on blood) are increasingly available in reference laboratories and can detect Salmonella nucleic acid even after antibiotics have started, but are not yet standard of care. The Widal test — historical serologic test detecting antibodies to O and H antigens — has poor sensitivity and specificity, with high false-positive rates in endemic regions due to prior exposure, and is now discouraged by WHO and CDC. The newer Typhidot and TUBEX rapid tests have improved performance but are still inferior to blood culture. After diagnosis, all isolates should undergo antibiotic susceptibility testing, particularly for fluoroquinolone resistance (assessed by ciprofloxacin MIC and nalidixic acid screening; many South Asian isolates carry gyrA mutations), ceftriaxone susceptibility, and azithromycin susceptibility. The differential diagnosis is broad — malaria, dengue, leptospirosis, rickettsial infections, viral hepatitis, brucellosis, and amebic liver abscess all overlap clinically — so endemic-region fever workup includes thick and thin blood films for malaria, dengue NS1 antigen, leptospirosis serology, and abdominal imaging as appropriate.
With prompt diagnosis and appropriate antibiotic therapy, paratyphoid fever has an excellent prognosis. Defervescence typically occurs within 3-5 days of starting effective antibiotics; complete recovery within 2-4 weeks. Case-fatality is under 1% in adequately treated paratyphoid, compared with 10-20% in untreated cases in historical series. Mortality is higher in pregnancy, extremes of age, immunocompromise, and complicated disease (perforation, hemorrhage, severe sepsis). Relapse occurs in approximately 5-10% of treated cases, more common with shorter antibiotic courses; relapse responds to a repeat course. Chronic biliary carriage develops in 1-5% of cases, more frequently in women, older patients, and those with gallstones — carriers can shed organisms for years and serve as community sources. The major prognostic concern is antibiotic resistance: fluoroquinolone resistance exceeds 70% in many South Asian Paratyphi A isolates, and extensively drug-resistant strains are emerging. Each case prompts public health investigation to identify carriers and prevent secondary spread. Vaccination provides minimal direct protection against Paratyphi (existing typhoid vaccines do not cover Paratyphi A well) but reduces overall enteric fever burden. Long-term sequelae are uncommon in adequately treated cases.
Refer to infectious disease or tropical medicine specialist for any confirmed or strongly suspected paratyphoid, particularly in travelers returning from South Asia where antibiotic resistance is widespread. Hospitalization with specialist input is warranted for severe disease, complications, suspected drug resistance, immunocompromise, pregnancy, and pediatric cases. Chronic carriers should be managed by infectious disease physicians with experience in prolonged antibiotic regimens.
Find specialists →Defervescence within 3-5 days of starting effective antibiotics for sensitive isolates. Full clinical recovery within 2-3 weeks for uncomplicated disease. Complicated disease (perforation, hemorrhage, severe sepsis) extends hospital stay to 3-6 weeks. Stool cultures should be repeated at 4-6 weeks post-treatment to detect carrier state. Return to work or school is typically permitted at 1-2 weeks if symptoms have resolved, but food handlers and healthcare workers require documented stool clearance. Carrier eradication takes 4-6 weeks of prolonged antibiotic therapy, sometimes combined with cholecystectomy.
Strict bed rest is recommended during the febrile phase. Light activity may resume after defervescence and full clinical recovery, typically 2-3 weeks into treatment. Avoid abdominal strain (heavy lifting, contact sports) for 4-6 weeks because intestinal ulcers heal slowly and rare late perforations are described. Return to full athletic activity once asymptomatic and at least 4 weeks post-treatment.
Look for centers with access to rapid blood culture systems, full susceptibility testing including fluoroquinolone MIC and ESBL screening, and IV antibiotic options for severe disease. In endemic countries, specialty infectious disease departments and government hospitals routinely manage high case volumes. Travel medicine clinics provide pre-travel counseling and post-travel evaluation.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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