🌿 Folk Prescriptions

Typhoid fever is an acute intestinal infectious disease caused by Salmonella typhi, characterized pathologically by persistent bacteremia, involvement of the reticuloendothelial system, formation of microabscesses and ulcers in the distal ileum. Typical clinical manifestations include sustained high fever, abdominal pain, constipation or diarrhea, hepatosplenomegaly, and leukopenia. Some patients exhibit rose spots and bradycardia. Typhoid patients and carriers serve as sources of infection; pathogens are excreted via feces, urine, and vomitus, directly or indirectly contaminating water or food, leading to disease transmission. The disease can occur year-round but is more prevalent in summer and autumn. Immunity after infection is usually long-lasting. This condition falls under the TCM category of "Shi Wen" (Damp-Heat Pestilence).
The causative agent of typhoid is Salmonella typhi. After entering the digestive tract via contaminated food, the bacteria proliferate in the small intestine. They multiply massively in the gallbladder and are continuously excreted into the intestines via bile. Persistent presence in the gallbladder can make patients chronic carriers, often accompanied by chronic cholecystitis, serving as a key source of infection. Some bacteria are excreted in feces, while others re-infect intestinal wall tissues through the intestinal mucosa, causing necrosis and ulceration.
TCM theory holds that the pathogenic factor of damp-heat pestilence enters through the mouth and nose, primarily accumulating in the spleen and stomach, causing damage. In the initial phase, the main pathological change is obstruction of defensive qi by dampness. When damp-heat suppresses the exterior, symptoms include headache, chills, body heaviness, pain, and low-grade fever (Wei stage). Damage to the spleen and stomach impairs digestion and transformation, causing dampness accumulation and obstruction of qi movement, manifesting as chest tightness, epigastric fullness, thick greasy tongue coating (Qi stage). Initially, although dampness contains heat, dampness predominates over heat. Those with pre-existing yang deficiency tend to transform into heat, leading to Yangming stomach involvement; those with pre-existing yang deficiency tend to transform into cold, leading to Taiyin spleen involvement. When in Taiyin, dampness dominates over heat; when in Yangming, heat dominates over dampness. When damp-heat transforms into dryness and fire, it penetrates deeply into the nutritive and blood levels. Blood vessel injury leads to petechiae and bleeding; excessive intestinal bleeding causes collapse of qi with blood loss and depletion of yang energy. Prolonged heat consumption depletes yin fluids, resulting in residual pathogenic factors after the pathogen clears, leaving the body weakened.
(I) Clinical Manifestations
The incubation period is generally 7–15 days. Without treatment, the typical natural course lasts about four weeks and is divided into four phases:
1. Initial Phase: Most patients have insidious onset with gradual progression, presenting with headache, myalgia, loss of appetite, nausea. Initial temperature rises in a fluctuating pattern, then increases gradually by about 1°C per day, paralleling pulse rate. Abdominal dull pain, bloating, and constipation are common. A few patients have mild to moderate diarrhea or epistaxis. By the end of the first week, the liver and spleen may be palpable.
2. Peak Phase: Occurs around days 5–7 post-onset, with sustained high fever at 39–40°C lasting 2–3 weeks, presenting as continuous or remittent fever. Patients appear extremely weak, apathetic, and slow to respond. Delirium, somnolence, frequent diarrhea with possible blood in stool, abdominal distension, abdominal pain or tenderness (most prominent in right lower quadrant) may occur. 30–40% of patients show relative bradycardia. 1/3 to 3/4 have splenomegaly, and hepatomegaly is more common. Some patients develop rose spots—small (2–5 mm), dark red, blanching under pressure, slightly raised above skin surface, numbering fewer than 20, fading in 2–4 days but possibly recurring. Transaminases are often elevated. Mild disseminated intravascular coagulation (DIC) or pseudo-meningitis may occur.
3. Resolution Phase: Temperature begins to decline gradually by the third week, and clinical condition improves.
4. Recovery Phase: After the fourth week, temperature returns to normal, and symptoms and signs disappear. Full recovery of general condition takes about one month.
5. Relapse and Rebound: Relapse refers to reappearance of clinical symptoms 1–2 weeks after resolution, with positive blood cultures again. This is often linked to decreased host resistance, allowing massive proliferation of pathogens in the gallbladder, bone marrow, mesenteric lymph nodes, or macrophages, which re-enter the bloodstream. Rebound refers to a rise in temperature during the second or third week, before normalization, lasting 5–7 days. Blood cultures are typically positive, with mechanisms similar to relapse.
(II) Complications
1. Intestinal Bleeding: Visible blood in stool occurs in 10–20% of cases, but severe bleeding is rare (~2%), mostly occurring in the second or third week, though it may also happen during recovery. Patients often suddenly experience a drop in blood pressure or temperature, increased pulse rate, and passage of blood in stool during otherwise improving general condition. Recent trends show a marked decline in intestinal bleeding incidence.
2. Intestinal Perforation: After antibiotic use, intestinal perforation incidence has dropped to 1–2%, commonly occurring in the terminal ileum, mainly in the second or third week. It often follows abdominal distension, diarrhea, or intestinal bleeding. During perforation, patients suddenly feel severe abdominal pain and signs of peritonitis, such as rigid abdominal muscles. The dullness of the liver may disappear. Abdominal X-ray may reveal free gas.
3. Toxic Myocarditis: Common during peak phase, presenting with tachycardia, low first heart sound, gallop rhythm, and hypotension. Electrocardiogram shows prolonged P-R interval, T-wave changes, and ST-segment shifts indicating myocardial damage.
4. Toxic Encephalopathy: Characterized by coma or semicomatose state, confusion, delirium, or muscle rigidity and tremor paralysis, related to endotoxin interference with basal ganglia neural conduction. More common in the first or second week, but may also occur during recovery or up to two months post-illness.
5. Hemolytic Uremic Syndrome: Typically seen in the first to third weeks. Patients present with anemia, mild jaundice, and dark-colored hemoglobinuria resembling soy sauce. Severe cases may involve shock and acute renal failure. Current understanding attributes its occurrence to abnormal immune status. Others believe it results from endotoxin or immune complexes damaging glomerular endothelium, triggering intravascular coagulation and acute uremia.
6. Toxic Hepatitis: Affects 25–50% of patients. Besides bacterial and endotoxin factors, immune complexes and complement activation are involved. The hallmark of this complication is concurrent hepatitis-like symptoms with hepatomegaly or abnormal liver function, which typically normalize within two weeks as typhoid resolves.