Aetiology is the study and establishment of causes. Aetiological agents are pathogens (bacteria, viruses, parasites, fungi) or toxins that cause disease. There are also environmental and non-infectious factors involved in the aetiology of disease. Virulence is a pathogen’s ability to infect a host and the degree of damage it causes, also described as pathogenicity. This can be influenced by virulence factors which affect the progression of the disease. Diseases must be rapidly identified to minimise harm to the host. Due to recent advances in technology a multitude of methodologies for identifying a wide range of diseases has been developed which aids health care professionals in efficiently and effectively treating disease (1).
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Respiratory tract infections are grouped according to their anatomic involvement and symptomatology. Infections can occur in the upper respiratory tract (e.g. pharyngitis) or lower respiratory tract (e.g. bronchitis). Pharyngitis is an inflammation of lymphoid tissues of the lateral pharyngeal bands and posterior pharynx, most often referred to as a ‘sore throat’. It is one of the most common reasons for doctor visits (2). There are numerous viral and bacterial agents that can cause pharyngitis. Group A β-haemolytic streptococcus is a bacterial agent most frequently isolated (5-36%) and infection is specifically referred to as ‘strept throat’. The majority of infections (up to 40%) are caused by viruses such as the rhinovirus and adenovirus (3). A proportion of cases have non-infectious aetiologies such as smoking, shouting, pollution or humidity. The effect of the cause of infection on the course of the infection is shown in figure 1.
Figure 1 – A diagram to represent how the course of a sore throat (pharyngitis) can change with infectious and non-infectious aetiology and with a change in stimuli (3)
Virulence factors of group A streptococci include a hyaluronic acid capsule that inhibits phagocytosis, lipoteichoic acid and M protein for attachment, streptokinase and other extracellular factors which increase the bacteria’s ability to infect a host cell. Virulence factors for rhinovirus include two proteases; 2Apro and 3Cpro which are responsible for the damage to host cells which results in symptoms of pharyngitis (4). Diagnostic testing for pharyngitis is based on routine throat cultures and collecting clinical specimens with pharyngeal swabs. Serological methods using fluorescent-antibody staining are very quick and can identify group A streptococci (5).
Genitourinary infections are usually grouped into two main categories; infections caused by sexually transmitted pathogens or infections due to resident flora. Infections occur in any part of urinary system including the kidneys, ureters, bladder and urethra. Sexually transmitted aetiological agents include bacteria such as Treponema pallidum which cause syphilis and viruses such as herpes simplex virus (HSV) which cause herpes (6). Treponema pallidum attacks intact mucosa and enters the lymphatic system to reach any organ in the body. The pathologic hallmark of syphilis is inflammation of the inner lining of an artery resulting in occlusion of the lumen (obliterative endarteritis). Motility is a virulence factor for T. Palladium as it rotates itself around a longitudinal axis allowing it to easily migrate through gel-like materials such as the mucosa which would otherwise hinder other organisms. T. pallidum cannot be cultured in vitro. Therefore, identification of infection is made by microscopic examination of ulcer material or smears from lesions for spirochetes (spiral-shaped bacteria) and serological detection of an antibody response are used to make a diagnosis (6).
Figure 2 – T. Pallidum is a spirochete bacterium and has a flat and wavy structure with a cytoplasmic
and outer membrane. Detection of the bacteria can be difficult, and diagnosis is usually based on clinical
presentation, microscopy and serological tests (7).
Virulence of HSV is associated with the ability of the virus to replicate in epithelial cells which can then spread. HSV has viral gene products that maintain thymidine kinase and ribonucleotide reductase required to maintain replication. Furthermore, other gene products destabilise cellular mRNA to aid the virus in shutting off host protein synthesis. Virulence is also associated with the virus’ ability to avoid host defences. Several proteins expressed by HSV during lytic infections affect the hosts ability to recognise and destroy virus infected cells (8). HSV is usually fastidious and difficult to culture which makes microbiological diagnosis difficult (9). Direct testing for HSV includes obtaining samples from a vesicular lesion, isolating the virus and detecting the antigen. More recently, HSV DNA can be detected using molecular diagnostic techniques. Type-specific HSV serology is being developed (10).
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Gastrointestinal tract infections (GTIs) cause gastroenteritis (inflammation of gastrointestinal tract and small intestine). This can lead to many conditions, most commonly diarrhoeal diseases. They are the third most infectious disease causing 2.2 million deaths worldwide, affecting mainly children under 5. The most common viral causes of diarrhoeal diseases can be the Norovirus and rotavirus and bacterial causes include Salmonella, Cholera, E. Coli, Shigella and Campylobacter (11). Non-typical Salmonella causes the most hospitalisations and deaths in the US (12). Cholera is an acute bacterial disease characterised by excess loss of water through diarrhoea caused by the gram-negative Vibrio Cholerae. Virulence factors for V. Cholerae include toxins which facilitate pathogenicity such as toxin coregulated pilus (TCP) which is linked to the production of cholerae toxin (CT). These toxins aid colonisation in host cells via direct adherence to epithelial cells. Motility also affects V. Cholerae as the flagella allows bacteria to swim through the lumen of the small intestine to epithelial cells in the crypts (intestinal gland). Cholera toxin A-B is secreted by the bacterium which causes the host to lose large amounts of water and ions. This toxin stimulates a cascade of events using cAMP and adenylate cyclase system effecting the osmotic balance of ions in the cell. Without these one or more of these virulence factors, V. Cholera would be ineffective in causing infection to the host (14). Virulence factors of Salmonella include adhesion, invasion and toxic genes clustered in ‘salmonella pathogenicity islands’ (SPI) within the chromosome. Diagnosis of infections involves taking a biopsy during endoscopy, rectal swabs or diarrhoeal stools. Bacterial culture or real-time PCR (polymerase chain reaction) can rapidly detect the presence of bacteria and any mutations to predict antibiotic resistance (13).
Central nervous system (CNS) infections are very complex and specialised due to anatomy of the brain and meninges. Aetiological agents of Meningitis include bacteria such as Haemophilus influenzas, Neisseria meningitidis or Streptococcus pneumoniae which grow rapidly in cerebrospinal fluid. Viruses such as enteroviruses and mumps virus can also act as aetiological agents by infecting meningeal and ependymal cells. Abscesses of the brain are mainly caused by purulent infections and inflammation caused by the presence of pyrogenic bacteria, most commonly Streptococcus. CSF examination occurs and an abscess is identified by a hypodense area with pus. Bacteriologic diagnosis can only be obtained by culturing an aspirate of the abscess cavity (15). N. meningitidis’ pathogenicity is based on many virulence factors. For example the production of IgA 1 protease which reduces the hosts immune defence of using IgA antibodies to breakdown the pathogen. Production of lipopolysaccharides stimulate the release of tumour-necrosis-factor alpha (TNF-α) which destroys host cells. N. meningitidis also produces proteins such as PorA/B to insert into host cell membranes which causes apoptosis of these cells and aids invasion. Virulence of enteroviruses relate to many factors such as cell tropism and viral infection-induced cell death (16). Diagnosis involves microbiologic examination of the CSF; bacterial infections increase the polymorphonuclear cell response and reductions in sugar content. Bacteria can be seen on smears if cultured. Viruses can be grown from the CSF, but this requires specialise viral cultures. Rapid diagnosis may be achieved through demonstrating antigens of bacterial/viral presence (17).
- Olsson, A. R., et al. (2004). "Aetiological factors of importance for the development of rheumatoid arthritis." Scand J Rheumatol 33(5): 300-306.
- American Osteopathic Association. 142 E. Ontario St. Chicago. https://osteopathic.org/what-is-osteopathic-medicine/sore-throat/
- Renner, B., Mueller, C.A. & Shephard, A. Inflamm. Res. (2012) 61: 1041. https://doi.org/10.1007/s00011-012-0540-9
- Esneau, C., et al. (2019). Chapter 2 - Rhinovirus diversity and virulence factors. Rhinovirus Infections. N. Bartlett, P. Wark and D. Knight, Academic Press: 25-59.
- Patterson MJ. Streptococcus. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 13. Available from: https://www.ncbi.nlm.nih.gov/books/NBK7611/
- Ronald AR, Alfa MJ. Microbiology of the Genitourinary System. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 97. Available from: https://www.ncbi.nlm.nih.gov/books/NBK8136/
- Bio SB. (2020). Treponema Pallidum - Polyclonal - Bio SB. [online] Available at: https://www.biosb.com/biosb-products/treponema-pallidum-polyclonal/
- Web.biosci.utexas.edu. (2020). Herpes. [online] Available at: http://web.biosci.utexas.edu/field/mic361a/herpes.htm
- Ratnam S. (2005). The laboratory diagnosis of syphilis. The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale, 16(1), 45–51. doi:10.1155/2005/597580.
- Singh, A., Preiksaitis, J., Ferenczy, A., & Romanowski, B. (2005). The laboratory diagnosis of herpes simplex virus infections. The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale, 16(2), 92–98. doi:10.1155/2005/318294
- WHO, 1999; National Intelligence Council, 2000.
- Sell, J. and B. Dolan (2018). "Common Gastrointestinal Infections." Prim Care 45(3): 519-532.
- Healthcare-in-europe.com. (2019). Diagnosing gastrointestinal infections. [online] Available at: https://healthcare-in-europe.com/en/news/diagnosing-gastrointestinal-infections.html# [Accessed 9 Dec. 2019].
- KE, C. (2019). Regulation of virulence in Vibrio cholerae: the ToxR regulon. - PubMed - NCBI. [online] Ncbi.nlm.nih.gov. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17661707 [Accessed 16 Oct. 2019].
- Johnson RT. Microbiology of the Nervous System. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX):
- Pham, N. (2019). CNS infections in the infant/child, CNS infection, meningitis, encephalitis, encephalopathy, myelitis, abscess - Cancer Therapy Advisor
- University of Texas Medical Branch at Galveston; 1996. Chapter 96.
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