Typhoid Fever in Children - Essay Example

Typhoid Fever in Children by 0 DEFINITION Typhoid fever is defined as “a systemic infection caused by Salmonella enterica serotype typhi (S typhi)” (Bahn et al., 2005). Typhoid fever is known to have a fatality damage of 216,500 deaths worldwide in the year 2000, and 21,600,000 illnesses in that year alone (Bhan et al., 2005). Much later data, however, point out to approximately 600,000 deaths every year worldwide (Beig et al., 2010). The disease has a high incidence particularly in Southeast Asia, South-Central Asia, and Southern Africa. However, in Western countries like the United States alone, typhoid fever accounts for as few as 300 cases a year due to a good access in vaccination and other preventive factors (Lynch et al., 2009). Moreover, typhoid fever usually hits children and young adults aged 5-19 years, although the age range can be much younger to much older (Bhan et al., 2005). Paratyphoid fever, which is a related disease, accounts for 5.4 million sick people worldwide (Crump & Mintz, 2010). Thus, one can see the severity of typhoid fever and paratyphoid fever and the fatalities that they bring. Unless, therefore, there are measures to prevent typhoid fever, there is no way that the situation can be improved. 2.0 HISTORY The Salmonella enteric bacterium has evolved beginning 50,000 years ago and has been known for its “remarkable mechanisms for persistence” in the human host (Bahn et al., 2005). By the early 20th century in Europe and the United States, the disease has greatly declined because of the improvement in the water supply as well as in the sewage systems. Nevertheless, the disease remained a serious health concern for the public. It was the introduction of chloramphenicol treatment that somehow made typhoid fever a manageable infection and not anymore a fatal disease. Nevertheless, in 1972, some chloramphenicol-resistant typhoid fever emerged. This was then countered with new antibiotics – ampicillin, amoxicillin and co-trimoxazole. In the 1980s and the 1990s, some new resistant strains once more emerged and this time they are resistant to chloramphenicol, ampicillin, amoxicillin and co-trimoxazole. The current treatment is now third-generation cephalosporins and fluoroquinolones, although there have also been reported decrease in susceptibility (Bahn et al. 2005). 3.0 SALMONELLA ENTERICA, DIFFERENCE BETWEEN TYPHOID, NON TYPHOID SALMONELLAE AND S. PARATYPHI IN TERMS OF GEOGRAPHIC DISTRIBUTION Typhoid salmonellae involve the invasion of the gut mucosa located in the terminal ileum either through the M-cells that serve as the epithelium of all gut tissue or through the enterocytes. Through the epithelial receptor called cystic fibrosis transmembrane conductance regulator protein, the typhoid Salmonellae adhere to the intestinal mucosa in the terminal ileum. On the other hand, non-typhoidal Salmonella leads to the invasion of the non-phagocytic epithelial cells and eventually the peripheral blood leucocytes and the lamina propia. The non-typhoidal Salmonellae then reach the intestinal lymphoid tissue, the mesenteric nodes, the thoracic duct until it causes bacteremia that infects the vital organs of the body within 24 hours. The affected parts could be the spleen, the liver, the bone marrow, as well as other parts of the reticuloendothelial system (Bhan et al., 2005). Typhoid fever is found in India, Indonesia and Vietnam, as well as in Bangladesh and Nepal. Paratyphoid fever, which is less prevalent than typhoid, occurs in India and Nepal (Bhan et al., 2005). 4.0 HOW DOES THE BACTERIA CAUSE A DISEASE? S. typhi causes the disease through the invasion of the gut mucosa in the terminal ileum. Then it enters the mucosa through the M-cells or through the enterocytes (Bhan et al., 2005). As the mucosal barrier is overcome, what follows is bacteremia. Then there is exudative inflammation in the terminal ileum and colon, thus causing diarrhea. What further takes place is interstitial inflammation and decrease in the number of neutrophils. Moreover, as proven by two studies, there has been a corresponding elevation of the tumor necrosis factor in the sera of those with typhoid fever. There is also a corresponding increase in infection among those with Gram-negative sepsis. There is also a corresponding decrease in the oxygen consumption of neutrophils, thus it is possible that S. typhi can indeed evade the body’s natural immune responses (Raffatellu et al., 2008). 5.0 SYMPTOMS AND COMPLICATIONS According to Bhan et al. (2005), typhoid fever is characterized by a range of symptoms, from low fever to marked toxemia. There could also be non-specific symptoms for patients in areas endemic to the disease such as vomiting, diarrhea and respiratory symptoms. Nevertheless, the average symptoms of typhoid fever include the following: prolonged low-grade fever, body malaise, dull frontal headache, myalgia, a dry bronchitic cough, nausea, and anorexia. Other symptoms include lethargy, bradycardia, coated tongue, altered bowel habits ranging from constipation to diarrhea, hepatomegaly, abdomen, splenomegaly, erythematosus maculopapular lesions on the arms, legs and back. In the case of neonates, there is fever, diarrhea, vomiting and distension of the abdomen, there are also seizures, jaundice and hepatomegaly (Bhan et al., 2005). In short, almost the whole body suffers from typhoid fever and is even the worst when it comes to children who do not have any vaccine available for them (Kumar et al., 2010). Care should therefore be taken to ensure that new forms of vaccines can be developed so that very young children can be spared from it. Moreover, around 10-15% develop severe forms of typhoid fever, with complications that range from intestinal perforation, gastrointestinal bleeding, and typhoid encephalopathy. Other rare and serious complications include intestinal perforation that account for 1-3% of the cases, insomnia, and intermittent confusion. Neuropsychiatric symptoms are also prevalent and may include muttering delirium, picking at imaginary objects and coma vigil. Deep coma, encephalomyelitis, typhoid meningitis, Guillain-Barre syndrome as well as peripheral or cranial forms of neuritis may also be accounted for among the relatively more serious symptoms. Complications also include convulsions, sever pneumonia, hemorrhages, intravascular coagulation, multiple organ dysfunction syndrome, granulomas of the bone marrow, spleen and liver, abscesses of the spleen and liver, hemtophagocytic syndrome, pylonephritis, pericarditis, endocardits, glumerolonephritis, pseudotomor cerebri, and hemolytic uraemic syndrome. Still, in a few rare cases, there is cardiogenic shock, toxic myocarditis, and arrythmia (Bhan et al., 2005). 6.0 DIAGNOSIS IN GENERAL (PROBLEMS WITH WIDAL TEST AND CONSEQUENCE, DIFFERENTIAL DIAGNOSIS, TREATMENT IN CHILDREN AND RESISTANCE According to Bhutta (2006), the standard diagnostic requirement for typhoid fever is a positive blood culture, or a bone marrow culture. However, the test is positive only in around 40-60% of the cases. Stool as well as urine cultures are not sensitive to the test as they may become positive only one week after the infection. The problem is that antibiotic use may also interfere with the sensitivity of blood cultures. Bone marrow cultures are actually more sensitive compared to blood cultures but the former are difficult to obtain (Bhutta, 2006). There are also other hematological investigations for the diagnosis of typhoid fever and one of these is blood leucocyte counts, which are usually low due to fever and toxicity. Leucocytosis is also common among children. Other relatively less common diagnostic determinants may include the presence of thrombocytopenia or significant hepatic dysfunction as a result of liver function tests (Bhutta, 2006). The classic Widal test is also useful in measuring antibodies directed against the O and H antigens of S. typhi. However, this over-100-year-old test actually lacks sensitivity as well as specificity. Thus, reliance on the Widal test results may merely result in overdiagnosis (Bhutta, 2006). Nevertheless, one good thing about the Widal test is that it is relatively easier to administer, and it resulted in the successful identification of typhoid fever as distinguished from malaria. However, the big problem is that the Widal test cannot distinguish S. typhi infections from those of other Salmonella types like S. typhimurium and non-typhoidal strains like S. paratyphi (Ammah et al., 1999). This data, however, was taken from a 1999 study, which may perhaps mean that nowadays, with the advent of new and more precise diagnostic tests, the Widal test may have already severely declined in terms of popularity. Some relatively newer diagnostic tests like Typhidot or Tubex are relatively more useful as they may directly, more specifically and more precisely detect IgM antibodies as compared with other host-specific antigens of S. typhi. Nevertheless, this specialized function of these diagnostic tests has not been sufficiently effective in large community settings (Bhutta, 2006). In fact, the Typhidot M test as well as the relatively new Diazo tests are actually good replacements for the Widal test. However, although the Typhidot M test is relatively more superior to the Diazo, the latter remains more suitable and practical compared the first. The reasons for this include the ease in using it and the fact that it is actually relatively economical (Beig et al., 2010). Some very sensitive and very specific methods of diagnosis for typhoid fever include polymerase chain reaction and nested polymerase chain reaction. These molecular diagnostic tests, especially the latter, may actually replace blood culture as the “gold standard” of diagnosing typhoid fever (Bhutta, 2006). The problem of diagnosing typhoid fever actually lies on the fact that typhoid fever may actually mimic many similar or related diseases and physiological conditions such as enteric fever, acute gastroenteritis, bronchopneumonia, bronchitis, sepsis involving other bacterial pathogens, malaria, intracellular organism infections like tuberculosis, leptospirosis, brucellosis, tularemia, and forms of rickettsial diseases. Moreover, viral infections like acute hepatitis, dengue fever and infectious mononucleosis may also be mistaken as typhoid fever because of similarity in symptoms and physiological conditions (Bhutta, 2006). This is the reason why there is a need for a very sensitive diagnostic test. 7.0 PREVENTION According to Kantele et al., (2012), non-typhoid Salmonella, or popularly known by the acronym NTS, is actually one of the leading causes of illnesses derived from infected food, and is somehow developing antimicrobial resistance as time goes by. Therefore, because of this, there is a need to develop a vaccine that is resistant enough to the pathogen in the years to come. The Ty21a oral vaccine is seemingly ideal to this kind of situation knowing that this type of vaccine naturally elicits intestinal immune responses that can cross-react with strains of NTS, as long as the NTS strains share O-antigens with the vaccine. Thus, the Ty21a oral vaccine is extremely effective against common NTS, Salmonella Enteriditis and Salmonella typhimurium. Thus, this very promising vaccine, whose advantages have only been proven in the laboratory, is believed to have cross-protective efficacy against not only typhoidal but also the non-typhoidal types of the disease (Kantele et al., 2012). Although the proof for the efficacy of the Ty21a oral vaccine, such data still serves as immunological evidence and therefore serves to support claims for its introduction into the world. According to Guzman et al. (2006), there are three major existing vaccines and where one of these can be administered to children. Still, however, based on experimental data, the Ty21a vaccine is the one that is considered better than the other two. One reason for this is that the Ty21a vaccine has Read More