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Typhoid Fever

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Typhoid Fever

 

Pathogenesis

Pathogenesis means the mechanism through which the cause operates to produce the pathological and clinical manifestations. Infection is induced by the infection of salmonella organisms derived directly or indirectly from a human source (Gibani, Britto, & Pollard, 2018). For a healthy person, a large number of organisms should be swallowed for one to be symptomatic. For the immunocompromised ones even, a small amount causes symptomatic infection. After ingestion, salmonella gets to the stomach where they can be killed due to the gastric acid and low ph. A few that survive then passes to the small intestine where they multiply. The bile in the small intestines presents an excellent medium. They multiply in the lymphoid tissues of the Peyers Patches and mesenteric lymph nodes and eventually pass into the bloodstream via the thoracic duct and disseminate in the livers, spleen, and reticuloendothelial systems (Upadhyay et al., 2015). The process takes eight days to 3 weeks, depending on the dose and virulence of organisms ingested. As bacteremia develops, the clinical onset of the disease occurs, and the excretion of salmonella with the bile takes place where they multiply and reenter the intestinal tract for the second time (Veeraraghavan, Pragasam, Bakthavatchalam, & Ralph, 2018). This heavy reinfection of the lymphoid tissue is responsible for major pathological changes in the various organs such as the small intestines, lungs, heart, gallbladder, among others (Gibani, Britto, & Pollard, 2018).  Other factors which determine the outcome of ingestion of salmonella include a physical barrier to epithelial penetrations imposed by intestinal mucus, the cleansing effects of intestinal motility, lysozyme present in the secretions, the bacteriostatic activity of the lactoferrin present in the stomach and the gut, and the nutritional state of the individual exposed to salmonella.

 

Etiology

Etiology is the cause of a disease. Typhoid is commonly caused by salmonella typhi, Salmonella paratyphi A, B, and C. Direct or indirect involvement with an acute case is necessary for infection. Direct causes may include:  when one takes contaminated food or water, close proximity to a person who is suffering from the disease or is a chronic carrier, drinking water supplies contaminated with sewages, food handlers, especially the typhoid carriers, are a major source of the spread. For example, Mary Mallow [ typhoid Mary) is one of the outstanding stories. She was a cook for families in and around the city of New York and was a typhoid carrier who caused several deaths. Contact with personal things and even on typhoid patients may spread the infection.  The direct oral-fecal route is the primary way of spread especially in children who come in contact with the feces, urine, and secretions from an infected individual (Gibani, Britto, & Pollard, 2018). Indirect transmission of the disease includes administration of the organisms in the intravenous route by platelet transfusion, the transmission of organisms by inadequately sterilized fiber optic instruments, and rarely through the airborne way. Man is the only reservoir of this infection.

Diagnosis

One of the tests is through the laboratory diagnosis, which is done in two ways, which include isolation of the causative organism from specimens such as blood, bone marrow, urine, aspirate, and tool. Secondly, through the detection of salmonella typhi antigens by the Widal test (Gibani, Britto, & Pollard, 2018). Since typhoid is known to present in several odd forms, no distinctive clinical signs and symptoms are usually present, and the initial clinical diagnosis will mostly depend on a high risk of suspicion. A careful history may reveal a patient had fever sometimes during the preceding two to three weeks. It’s the most constant feature, and its absence negates a diagnosis of enteric fever. Chills is the other sign used, but when excessive, malaria might be co-existing.   A dull frontal or diffuse headache is often present, and it is associated with general malaise, aches, and pain systems (Upadhyay et al., 2015). Bradycardia may be common in the first week, but, in case of toxemia, tachycardia may occur.  Rose spots may appear though their exact etiology is not known. Dry cough may also manifest due to hypostatic congestion of the lung. Abdominal pain, mild to moderate in intensity with tenderness in all quadrants, may present during the first week. Anorexia, diarrhea, nausea, vomiting, constipation and abdominal discomfort also presents

Treatment/ prognosis

Supportive measures are important in the management of typhoid fever and may include: oral or intravenous hydration, the use of antipyretics, appropriate nutrition, and blood transfusion if necessary.  When selecting the first line of treatment, efficacy, availability, and cost are critical criteria to consider. The fluoroquinolones are an optimal treatment for typhoid, especially in adults. They are relatively cheap, more rapidly, and effective than the former first- line of choice, which included amoxicillin, chloramphenicol, ampicillin, and trimethoprim-sulfamethoxazole ((Veeraraghavan et al., 2018). The fluoroquinolones attain excellent tissue penetrations, kills the salmonella typhi in its intracellular stationary stage in monocytes/ macrophages, and achieve higher drug levels in the gall bladder than any other drug. They produce a high therapeutic response, such as the clearance of fever and symptoms in three to five days. It has very low rates of post-treatment carriage.  The emergence of multi-drug resistance has reduced the choice of antibiotics. There are two types of resistance: resistance to antibiotics and resistance to fluoroquinolone drugs. Resistance to the fluoroquinolones may be total or partial. Prognosis is the determination of the recurrence of a disease. Nalidixic-acid resistant S.typhi is a marker proof reduced susceptibility to fluoroquinolones compared to reduced nalidixic acid and thus determines which one between the two is worse than the other. There is a significant number of multi-drug resistant strains from the Indian subcontinent and some other Asian countries (Bhutta, 2006).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

References

Bhutta, Z. A. (2006). Current concepts in the diagnosis and treatment of typhoid fever. Bmj333(7558), 78-82.

Gibani, M. M., Britto, C., & Pollard, A. J. (2018). Typhoid and paratyphoid fever: a call to action. Current opinion in infectious diseases31(5), 440.

Upadhyay, R., Nadkar, M. Y., Muruganathan, A., Tiwaskar, M., Amarapurkar, D., Banka, N. H., … & Sathyaprakash, B. S. (2015). API recommendations for the management of typhoid fever. J Assoc Physicians India63(11), 77-96.

Veeraraghavan, B., Pragasam, A. K., Bakthavatchalam, Y. D., & Ralph, R. (2018). Typhoid fever: issues in laboratory detection, treatment options & concerns in management in developing countries. Future science OA4(6), FSO312.

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