File Name: typhoid fever signs and symptoms .zip
Enteric typhoid fever is a systemic disease characterized by fever and abdominal pain caused by dissemination of Salmonella Typhi or Salmonella Paratyphi type A, B, or C.
NCBI Bookshelf. Jenish Bhandari ; Pawan K. Thada ; Elizabeth DeVos. Authors Jenish Bhandari 1 ; Pawan K. Thada 2 ; Elizabeth DeVos 3. Typhoid fever is an enteric fever characterized by systemic illness along with abdominal pain and fever in a "step-ladder" pattern. The organism responsible for enteric fever is Salmonella typhi. Other serotypes, Salmonella paratyphi A, B, C , also cause similar syndromes but with less clinically significant disease.
This activity reviews the evaluation and management of typhoid fever and highlights the role of the interprofessional team in improving care for patients with this condition. Objectives: Describe the etiology and epidemiology of typhoid fever. Review the appropriate history, physical, and evaluation of typhoid fever. Outline the treatment and management options available for typhoid fever.
Identify interprofessional team strategies for improving care coordination and communication to advance the care for typhoid fever and to improve outcomes. Typhoid fever is also called enteric fever. It is a prospectively, multisystemic illness that has been a public health problem, especially in the developing world. Paratyphoid is clinically indistinct from typhoid fever; thus, enteric and typhoid fever are used mutually.
Typhoid fever is one of the major causes of mortality and morbidity in overcrowded and unhygienic areas though comprehensive research and public health interventions have decreased the occurrence. The disease course ranges from early gastrointestinal distress to nonspecific systemic illness but ultimately may lead to multiple complications.
Salmonella is said to spread by the 'four Fs" flies, fingers, feces, fomites. Fever characteristically comes in a step-wise pattern i. Nontyphoidal salmonella NTS is more typical in children and is mostly limited to gastroenteritis.
Salmonella is transmitted by the fecal-oral route through contaminated water, undercooked foods, fomites of infected patients, and is more common in areas with overcrowding, social chaos, and poor sanitation. It is only transmitted from an infected person to another person, as humans are its only host. Major sources of salmonella are poultry, eggs, and rarely turtles.
Normal flora of the gut is protective against the infection. The use of antibiotics such as streptomycin destroys the normal flora, which heightens its invasion. Malnutrition decreases normal gut flora and thus increases the susceptibility to this infection as well.
While the United States reports only about culture-confirmed cases of typhoid fever and fewer than paratyphi A cases each year since , enteric fever remains an important cause of illness worldwide. Approximately , deaths result from over 26 million cases of typhoid fever and 5 million cases of paratyphoid infection each year worldwide.
Most cases in developed countries are carried by travelers returning from endemic areas and travelers visiting relatives and friends that are at heightened risk due to their likelihood to be less cautious with sources of food and water.
Those less likely to seek vaccination and pretravel consultation are also at heightened risk. Typhoid fever is more prevalent in temperate and tropical climates. It is directly associated with sanitation, sewage, and water treatment system. The number of new cases of typhoid fever has been increasing worldwide due to rapid increases in population, pollution, and shortages of pure drinking water.
Still, death rates have decreased due to extensive research, changes in treatment modalities, and the invention of new drugs despite growing multidrug-resistance.
In the era of routine antibiotics, classic presentations are not always seen. These patients remain asymptomatic after their acute treatment, but they may excrete Salmonella for up to 1 year in their stool, or less frequently their urine.
Blood group antigens may also be linked to susceptibility to S. The pathogenesis of typhoid fever depends upon a number of factors, including infectious species, virulence, host's immunity, and infectious dose. The larger the infectious dose, the shorter the incubation period, and the higher the attack rate. Typhoid fever is more severe in debilitated and immunocompromised patients such as those with HIV mainly paratyphi , those on glucocorticoid therapy, and those with altered phagocyte function i.
Salmonella is an acid-sensitive bacteria except for a few resistant strains, so typically it is destroyed in the stomach by gastric acid unless a large dose is ingested. Food and beverages also act as buffers against gastric acid that facilitates bacteria reaching the small gut. The virulence of Salmonella is determined by typhoid toxin, Vi antigen polysaccharide capsule , liposaccharide O antigen, and flagellar H antigen.
Strains positive for Vi antigen have an attack rate twice that of Vi negative strains, even for the same dose of micro-organisms.
The main role of the Vi antigen is to act as an antiphagocytic agent preventing the action of macrophages, thus shielding the O antigen from antibodies that confer the serum resistance. The flagellar H antigen provides bacterial mobility and adherence upon the gut wall mucosa. Invasion of the gut wall is assisted by flagella, and the type III secretion system is capable of transferring bacterial protein into enterocytes and M cells specialized epithelial cells that serve as antigen-presenting cells in gut mucosa or lymphoid tissue or by direct penetration of mucosa.
Bacteria attached to M cells are absorbed by pinched off cytoplasm containing bacteria and extruded into the luminal space. In this process, M cells are damaged, and the basal lamina is exposed. It provides easy access to pathogens for the invasion, which worsens the condition. This special characteristic of the bacteria helps them to remain viable in a pool of host immunity.
Salmonella also produces a molecule that stimulates the epithelial release of chemoattractant eicosanoid, which sequesters neutrophils into the lumen and potentiates mucosal damage. Bacteria induce proliferation of Payer patches via recruitment of lymphocytes and mononuclear cells and induce necrosis and eventually, ulceration that complicates the symptoms.
Pathogens reach the reticuloendothelial system via both lymphatic system and bloodstream, including other multiple organs, most commonly gallbladder in almost all cases.
The early bacteremic phase 24 hours to 72 hours is asymptomatic and transient as these bacteria are phagocytosed by macrophages and monocytes in the reticuloendothelial system called primary bacteremia.
The capacity of pathogens to grow in these immune cells makes them characteristic, and intracellular multiplication of bacteria in the reticuloendothelial system enforces them to re-enter the bloodstream causing continuous bacteremia for several days and weeks known as secondary bacteremia.
Secondary bacteremia is the phase in which disease symptoms manifest. The lipopolysaccharide induces the shock-like reaction, and endotoxemia leads to vascular hyperactivity and catecholamine release, which causes focal necrosis and hemorrhage.
Clinical presentations of both Salmonella typhoid and Salmonella paratyphoid are similar, though arthralgia is more common with typhoid.
Obtaining a history of permanent residence, travel history travel to endemic and outbreak areas , immunization, socioeconomic status, lifestyle, onset and duration of illness, drug history chemoprophylaxis of malaria, dose, and interval of the drug are important to pave the way for diagnosis.
Exposure history and related activities like impure drinking water, animal contact, insect bites, accommodations, undercooked food aid in excluding other infectious diseases.
Typhoid is an infectious disease that presents with nonspecific symptoms. Patients complain of enterocolitis after 12 hours to 48 hours of inoculation.
Symptoms of enterocolitis generally last a few days and are self-limited without the need for medical intervention except in the old and very young. Abdominal distress is frequently seen in typhoid fever. Due to the hypertrophy of Payer patches, constipation may predominate over diarrhea in some cases.
Physical examination findings can be nonspecific. In the first week, a documented fever may be accompanied by a decreased heart rate. In the second week, findings are more common, including abdominal distention. When typhoid is complicated by ileal perforation, tenderness, rigidity, and guarding of the abdomen may be present. Visible rose spots rose-colored macules on the abdomen are associated with typhoid fever but occur only rarely. The patient looks pale, mildly distressed, and dehydrated with sunken eyes, dry skin, and lethargy.
If the diagnosis is delayed until the third week, the patient is more toxic, anorexic, and with notable weight loss.
Chances of bowel perforation increase with time, which worsens abdominal distension and peritonitis. The patient becomes tachypneic with crackles over the lung base on auscultation. Signs of metastatic complications appear. Dry cough due to pneumonia can also be present as well as neck rigidity due to meningitis, or rarely, chest pain due to myocarditis and pericarditis. Patients of endemic areas like India and Africa have more frequent neurologic manifestations like delirium, psychosis, insomnia, confusion, apathy, and in extremely rare cases, parkinsonism.
Other unusual presentations are severe epigastric pain radiating to the back due to pancreatitis, bone pain because of osteomyelitis, and abscesses, which can occur anywhere in the body. The approach to typhoid patients should be clinical. Patients residing in areas with poor sanitation or impure drinking water or history of travel from endemic areas presenting with febrile illness for more than three days along with gastrointestinal manifestations pain, constipation, or diarrhea are highly suspicious.
Diagnosis in the first week is difficult, but a variety of laboratory studies assist in making the diagnosis.
It is widely available and the most commonly performed test, as it is not expensive or technically difficult.
The efficacy of the blood culture is increased when high volume samples are taken. Blood cultures done during secondary bacteremia i. Stool culture is diagnostic in the second and third weeks. Chronic carriers intermittently pass pathogens in the fecal matter for a long time so, several samples should be taken. Additional metabolite biomarkers are under investigation. It is more sensitive than blood cultures due to the larger number of micro-organisms present in the bone marrow.
An antibody titer of greater than and greater than for anti-H antigen and anti-O antigen respectively are considered as cut off levels to predict recent infection of typhoid fever in an endemic area. When the convalescent titer is four times greater than the acute titer, the study is considered positive.
Endemic areas will require higher titers to make the diagnosis and are still limited in that they may represent prior infection. The Widal test is not reliable due to its common false-negative and false-positive results, poor agreement with blood culture, and poor performance. This testing is also cost-prohibitive in many low resource settings. Liver function testing may show a pattern of viral hepatitis, and though nonspecific C-reactive protein may be elevated. When obtained, cerebrospinal fluid studies may reveal mild pleocytosis less than 35cells , though most are unremarkable.
Antibiotic therapy is the mainstay of treatment. The treatment has been complicated by multidrug resistance strains developed in many endemic areas, especially in India and south-east Asia.
The author is deeply grateful to the following: Brigadier W. Hamilton, O. Sugden , T. Lee , R. McManners , R.
Typhoid fever with classical features presents no difficulty in recognition. However, when it presents atypically in the guise of one of its rare complications, diagnosis becomes difficult and appropriate treatment is delayed. Typhoid glomerulonephritis is one such rare complication. Mesangial proliferative glomerulonephritis, IgA nephropathy, acute diffuse proliferative glomerulonephritis and crescentic IgA nephropathy have been reported in the past. We report a year-old boy presenting with high grade fever, hematuria, proteinuria and Salmonella typhi bacteremia.
Back to Health A to Z. Typhoid fever is a bacterial infection that can spread throughout the body, affecting many organs. Without prompt treatment, it can cause serious complications and can be fatal. It's caused by a bacterium called Salmonella typhi, which is related to the bacteria that cause salmonella food poisoning. Typhoid fever is highly contagious.
Learn more about the symptoms, cause and treatment of this serious intestinal illness. Typhoid fever is caused by Salmonella typhi bacteria.
Typhoid fever , also known as typhoid , is a disease caused by Salmonella serotype Typhi bacteria. The cause is the bacterium Salmonella enterica subsp. In , Typhus is a different disease. The name typhoid means "resembling typhus".
Typhoid fever is endemic in Pakistan. This document is intended to guide all physicians regarding the appropriate management of typhoid in the setting of high antimicrobial resistance. Paratyphi causes a less severe illness. Typhoid fever is an acute, life-threatening, febrile illness. Typhoid fever begins days after ingestion of the organism.
Typhoid fever is caused by Salmonella typhi bacteria. Typhoid fever is rare in developed countries. It is still a serious health threat in the developing world, especially for children.
NCBI Bookshelf. Jenish Bhandari ; Pawan K. Thada ; Elizabeth DeVos. Authors Jenish Bhandari 1 ; Pawan K.
The only way to know for sure if an illness is typhoid fever or paratyphoid fever is to have a sample of blood or stool poop tested for Salmonella Typhi or Salmonella Paratyphi. If you have a fever and feel very ill, see a doctor immediately.
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