CHAPTER ONE

                               INTRODUCTION

1.BACKGROUND OF STUDY

Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.

The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.

S typhi has been a major human pathogen for thousands of years, thriving in conditions of poor sanitation, crowding, and social chaos. It may have responsible for the Great Plague of Athens at the end of the Pelopennesian War. [1] The name S typhi is derived from the ancient Greek typhos, an ethereal smoke or cloud that was believed to cause disease and madness. In the advanced stages of typhoid fever, the patient's level of consciousness is truly clouded. Although antibiotics have markedly reduced the frequency of typhoid fever in the developed world, it remains endemic in developing countries. [2]

S paratyphi causes the same syndrome but appears to be a relative newcomer. It may be taking over the typhi niche, in part, because of immunological naivete among the population and incomplete coverage by vaccines that target typhi.

Note that some writers refer to the typhoid and paratyphoid fever as distinct syndromes caused by the typhi versus paratyphi serovars, while others use the term typhoid fever for a disease caused by either one. We use the latter terminology. We refer to these serovars collectively as typhoidalsalmonel

1.1 RISK FACTORS

Typhoidal salmonella have no nonhuman vectors. An inoculum as small as 100,000 organisms of typhi causes infection in more than 50% of healthy volunteers. [9]Paratyphi requires a much higher inoculum to infect, and it is less endemic in rural areas. Hence, the patterns of transmission are slightly different

The following are modes of transmission of typhoidal salmonella:

·         Oral transmission via food or beverages handled by an often asymptomatic individual—a carrier—who chronically sheds the bacteria through stool or, less commonly, urine

·         Hand-to-mouth transmission after using a contaminated toilet and neglecting hand hygiene

·         Oral transmission via sewage-contaminated water or shellfish (especially in the developing world). [10, 11, 12]

Paratyphi is more commonly transmitted in food from street vendors. It is believed that some such foods provide a friendly environment for the microbe.

Paratyphi is more common among newcomers to urban areas, probably because they tend to be immunologically naïve to it. Also, travellers get little or no protection against paratyphi from the current typhoid vaccines, all of which target typhi. [13, 14]

Typhoidal salmonella are able to survive a stomach pH as low as 1.5. Antacids, histamine-2 receptor antagonists (H2 blockers), proton pump inhibitors, gastrectomy, and achlorhydria decrease stomach acidity and facilitate S typhiinfection. [4]

HIV/AIDS is clearly associated with an increased risk of nontyphoidal Salmonellainfection; however, the data and opinions in the literature as to whether this is true for S typhi or paratyphi infection are conflicting. If an association exists, it is probably minor.

Other risk factors for typhoid fever include various genetic polymorphisms. These risk factors often also predispose to other intracellular pathogens. For instance, PARK2 and PACGR code for a protein aggregate that is essential for breaking down the bacterial signaling molecules that dampen the macrophage response. Polymorphisms in their shared regulatory region are found disproportionately in persons infected with Mycobacterium leprae and S typhi. 

On the other hand, protective host mutations also exist. The fimbriae of S typhi bind in vitro to cystic fibrosis transmembrane conductance receptor (CFTR), which is expressed on the gut membrane. Two to 5% of white persons are heterozygous for the CFTR mutation F508del, which is associated with a decreased susceptibility to typhoid fever, as well as to cholera and tuberculosis. The homozygous F508del mutation in CFTR is associated with cystic fibrosis. Thus, typhoid fever may contribute to evolutionary pressure that maintains a steady occurrence of cystic fibrosis, just as malaria maintains sickle cell disease in Africa. [19, 20]

As the middle class in south Asia grows, some hospitals there are seeing a large number of typhoid fever cases among relatively well-off university students who live in group households with poor hygiene. [21] American clinicians should keep this in mind, as members of this cohort often come to the United States for advanced degrees. The diseases mainly affect those living in poorer regions of the world where sanitation and clean water are lacking. The World Health Organization (2000) estimates that typhoid fever affects 17 million people a year, causing approximately 600,000 deaths. Typhoid fever has a typical case fatality rate of 10%, but this can be reduced to as little as 1% with appropriate antimicrobial therapy. Paratyphoid fever is a similar illness but tends to be milder, with a lower case fatality rate.

1.2 TRANSMISSION

The main reservoir for S. typhi is the human intestinal tract, although people with typhoid fever also carry the bacteria in their bloodstream. In addition, a small number of carriers recover from typhoid fever but continue to carry the bacteria. Both ill people and carriers shed S. typhi in their faeces (Chinn, 2000). Transmission therefore occurs following the ingestion of food or water that has been heavily contaminated by S. typhi (typhoid) or S. paratyphi (paratyphoid).

S. typhi can be passed in the faeces of patients who are acutely ill with typhoid fever or are chronic carriers. The bacteria may then enter the food chain and water supply if personal and food hygiene and/or sanitation measures are poor. Direct faecal-oral transmission may occur if vegetables fertilised with human waste are eaten raw, while shellfish that have been harvested from sewage-contaminated beds, and milk products contaminated by workers’ hands all may result in typhoid infection (Connor and Schwarz, 2005).

In countries where the enteric fevers are endemic, risk factors for contracting them include eating or drinking contaminated food or water, inadequate sanitation and living conditions, poor personal hygiene and close contact with those infected with S. typhi or S. paratyphi (Ericsson, 2003).

The risk of contracting typhoid fever is highest for travellers to the Indian sub-continent (India, Pakistan and Bangladesh), South East Asia and parts of Latin America and Africa. In these region, the attack rate for travellers has been estimated at 10 per 100,000. The risk of typhoid and paratyphoid fevers in resource-rich countries such as Europe, North America and Australia is less than one case per million visits (Lee and Leese, 2001).

1.3 SIGNS AND SYMPTOMS

Typhoid fever is a systemic disease that varies in severity, but nearly all patients experience fever and headache. Some young children will experience a mild illness that is treatable with antibiotics, but they may also suffer from severe disease.

The incubation period for typhoid fever is usually 7-14 days, but this can be shorter or longer depending on how many bacteria are ingested. Symptoms include:

- Low-grade fever (which typically becomes higher as the illness progresses)

- Chills;

- Headache;

- Myalgia;

- Malaise;

- Anorexia;

- Nausea.

Patients may also experience abdominal discomfort and constipation, and diarrhoea may occur early in the course of the illness. Moderate enlargement of the liver and/or spleen occurs in about of 50% of patients, while in some, rose spots appear on their trunk, although these may be difficult to see in dark-skinned patients (Chinn, 2000).

Paratyphoid fever is clinically similar, but the disease is usually milder and of shorter duration. It often manifests as acute gastroenteritis (Steffan et al, 2003).

Primary healthcare professionals play a key role in preventing enteric fevers by offering typhoid vaccination and hygiene advice to travellers, and managing people who become infected.

1.4 COMPLICATIONS

Complications occur in 10-15% of all patients and are more likely in those who are untreated and present late in the course of the illness. They include:

- Intestinal haemorrhage and perforation;

- Toxic myocarditis;

- Pneumonia;

- Seizures;

- Typhoid encephalopathy and meningitis (usually in young children).

The fatality rate is usually less than 1% with prompt antibiotic therapy, but may be as high as 20% in untreated patients.

All patients with typhoid and paratyphoid fevers excrete the organisms at some stage during their illness. About 10% of patients with typhoid fever excrete S. typhi for at least three months following the acute illness, and 2-5% become long-term carriers (more than one year).

The likelihood of becoming a chronic carrier increases with age, especially in females and those with biliary tract abnormality. Chronic carriers require prolonged courses of antibiotics to clear the organism (HPA, 2005a; 2005b)

1.4 ROLE OF THE FAMILY IN HOSPITAL CARE

Although it is recognized that the family plays a role in the care of ill family members around the world, this role is more extensive and institutionalized in some countries. In many low-resourced Sub-Saharan African countries, care in hospitals, including food and medication, is supplied by the family and a family member stays with the patient most of the time. Managing medication, a typical nursing role, is also ascribed to the relatives who buy prescribed medication and administer it to the patient. This may be by default rather than design, but nevertheless, it reflects the reality for many nurses in Sub-Saharan Africa. The nurses actually oversee any aspect of care contribution by the family

1.5 STATEMENT OF PROBLEM

The annual mortality rate per 100,000 people from typhoid fever in Nigeria has increased by 7.0% since 1990, an average of 0.3% a year.

Though this has been the trend overall, adjust the filters at the top of the visualization to see how the mortality rate for typhoid fever has changed over time for men and women of specific age groups in Nigeria. For men, the deadliness of typhoid fever in Nigeria peaks at age 1-4. It kills men at the lowest rate at age 50-54.

Women are killed at the highest rate from typhoid fever in Nigeria at age 1-4. It was least deadly to women at age 40-44. At 5.5 deaths per 100,000 women in 2013, the peak mortality rate for women was higher than that of men, which was 4.3 percent

1.5 RESEARCH OBJECTIVES

The ultimate aim of this research is to conduct a study of typhoid fever in west Africa in order to target the affected region for public health interventions. The specific objectives are to:

 • Understand the knowledge, attitudes and practices of west Africa concerning typhoid .

 • Understand effectively the role of nurses in managing and treating typhoid fever

. • Disseminate information that will lead to the implementation of effective preventive interventions and public health policies

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