Typhoid & Paratyphoid Fever Antibodies, Proteins & ELISA Kits

Typhoid fever is caused by a bacteria called Salmonella Typhi (S. Typhi) and paratyphoid fever is caused by S. Paratyphi (A, B and C). Enteric fever is used to describe both typhoid and paratyphoid fever and the pathogens which cause enteric fever are human restricted.

Both typhoid and paratyphoid fever are highly contagious and can be spread in areas of poor sanitation through faeces and urine samples from infected individuals. Enteric fever is commonly observed through contaminated water sources and food which is undercooked. It is estimated that there are between 11-21 million typhoid cases and 5 million paratyphoid cases reported annually.

Antibiotics have been used to treat enteric fever, however, antibiotic resistance is emerging and the misclassification of paratyphoid fever for typhoid fever is increasing the ability of the bacteria to spread antibiotic resistance genes. There are currently live attenuated oral vaccines formulated in capsules and injectable vaccines for typhoid fever. Since typhoid vaccines have been developed and administered to people, there has been a decline in the spread of typhoid fever and there is some evidence of cross protection against S. Paratyphi B. However, paratyphoid fever still persists and researchers are currently trying to create a vaccine in order to stop the spread of infection.

The Vi antigen, typhoid toxin, flagellar H antigen and O liposaccharide antigen which Salmonella species possess are the main virulence components which are responsible for enteric fever pathogenesis. S. Typhi has a Vi antigen which is an antiphagocytic agent overlying the O antigen. Both S. Paratyphi and S. Typhi have an O antigen, typhoid toxin and a H antigen. The H antigen is required for mobility of the bacteria and it is used for adherence to the gut wall mucosa. Hemolysin E (HlyE) is a toxin used for pathogenesis of typhoid fever.

Upon cell entry, bacterial proteins activate host cell Rho GTPases which are able to facilitate the rearrangement of actin to allow uptake of bacterial proteins to the phagosome. In particular, GTPase Rab29 is recruited to vacuoles which contain S. Typhi and S. Paratyphi and it is needed for typhoid toxin transport to the plasma membrane. When humans are infected with these pathogens an antibody response is also elicited whereby IgA, IgG and IgM can be detected against specific S. Typhi and S. Paratyphi antigens.  

The use of metabolomics is becoming a useful tool for identifying biomarkers of infections. Metabolomics analysis in typhoid and paratyphoid fever cases have identified differences in metabolite levels between infected and uninfected individuals. Some of these metabolites are also able to distinguish typhoid from paratyphoid fever such as tryptophan, iron and creatine.

Due to the human specific nature of pathogens causing typhoid and paratyphoid fever there are limited studies using animal models. In order for vaccine and therapeutic approval there needs to be sufficient studies shown with human specific products which illustrate how the immune system reacts to the bacteria and to any therapeutic products developed. Studies have shown that both S. Typhi and S. Paratyphi infections stimulate the production of cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). As well as this, both S. Typhi and S. Paratyphi cause macrophage inflammatory protein-1 beta (MIP-1 beta) chemotactic chemokine to be secreted from macrophages.