Reginald Bowen (Gastroenteritis) Case Study

This essay discusses anatomy and physiology, microbiology and pathophysiology issues relating to Reginald Bowen, a 76-year-old male with gastroenteritis. Norovirus is commonly transmitted through fecal-oral route and can be prevented through handwashing, disinfection and application of aseptic techniques in healthcare facilities.

Running head: GASTROENTERITIS 1
REGINALD BOWEN (GASTROENTERITIS) CASE STUDY
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Introduction
The virtual patient for this essay is Reginald Bowen, a 76-year-old male with
gastroenteritis. Reg presented with lethargy, severe abdominal pain, headache, diarrhea,
inability to urinate and vomiting. He has an history of Gastro Esophageal Reflex Disease
(GERD) and Benign Hypertrophic Prostate (BPH). He has a surgical history of Transurethral
Resection of the Prostate and Right Inguinal Repair. His mother died of lung metastasizes
secondary to primary breast cancer. Fecal pathology detected Norovirus Nucleic acid
confirming that he has norovirus. This essay will discuss anatomy and physiology,
microbiology and pathophysiology issues relating to this patient.
Anatomy and Physiology
The gastrointestinal Tract (GIT) which runs from the mouth to the anus. The
alimentary canal of the GIT consists of esophagus, pharynx, mouth, small and large intestines
while the accessory part of the GIT consists of teeth, tongue, salivary glands, gallbladder,
liver and pancreas (Bruggink et al., 2012, pp.1437-1448). The GIT is subject to viral
infections during interaction with the environment. For instance, viral gastroenteritis is
associated with inflammation of the GIT leading to severe abdominal pain, vomiting and
diarrhea. Viral gastroenteritis impairs the normal functioning of organs GIT organs like
intestines and the stomach (Gelberg, 2014, pp.54-66).
The process of digestion involves passage of food along the GIT where it is broken
down into small particles to facilitate nutrient absorption into the blood stream. Chemical
fragmentation of the large molecules of food into clusters of smaller molecules is usually
facilitate by the presence of bacteria and enzymes in the GIT. After nutrient absorption, the
remnants are exposed as excrements via the large intestine (Bruggink et al., 2012, pp.1437-
1448).

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Inflammation of the surface layer of the GIT due to invasion by norovirus disrupts
the rhythmic muscular contraction making the food to be forced back from the digestive
organs leading to nausea and vomiting (Bruggink et al., 2012, pp.1437-1448).The virus
interferes with the normal environment of the bacteria, prevents absorption of sodium and
water and destroys the surface cells of the GIT. This impairs the digestion process leading to
inadequate supply of nutrients to the organisms in the GIT leading to weakness, lethargy and
dehydration (White, Eden and Hansman, 2012, p.70-73).
Microbiology
From the case study, fecal pathology confirmed that patient has viral gastroenteritis
following a detection of norovirus nucleic acid. Noroviruses belong to a diverse category of
single-stranded positive-sense non-enveloped, RNA viruses in Caliciviridae (Lopman et al.,
2012, pp.96-102). The genus Norovirus has Norwalk Virus species. Its strains, serotypes and
isolates are Hawaii, Norwalk, Wilkinson, Desert, Mexico, Snow Mountain and Lordsale
viruses. Norovirus infection is often characterized by nausea, vomiting, diarrhea, abdominal
pain, lethargy and weakness (Lopman et al., 2012, pp.96-102).
Norovirus is directly transmitted from one person to another, fecal-oral route and
indirectly through contaminated food or water. Its replication is often cytoplasmic using the
Positive Stranded RNA transcription method (Thorne and Goodfellow, 2014, pp.278-291).
The translation process involves RNA termination-re-initiation and leaky scanning. It is
commonly diagnosed using Quantitative Polymerase Chain Reaction assays. Norovirus
infection can be prevented through disinfection, handwashing and aseptic techniques in
healthcare facilities (Moore et al., 2013, pp.169-1174).
Pathophysiology

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Norovirus stimulates the destruction of the bowel mucosal lining leading to attempted
tenesmus or defecation as the body tries to remove foreign organisms in the stomach.
Increased motility in the GIT leads to nausea and vomiting and increased frequency of
defecation (White, Eden and Hansman, 2012, p.70-73). Continued bowel destruction leads to
erosion of the mucosal lining due to toxins, action of hydrochloric acid and direction action
of the organism. Erosion of the protective coating of the stomach necessitates destruction of
stomach lining by the acid leading to abdominal pain. The epithelium is usually destroyed as
a result of exudation of blood and serum into the lumen and widespread absorptive
epithelium destruction leading to inefficient absorption of water which consequently results
to diarrhea. (Bruggink et al., 2012, pp.1437-1448).
The body secretes and loses a high amount of bicarbonate and chloride ions in the
bowel following increased peristaltic movements to get rid of the foreign organism (Lopman
et al., 2012, pp.96-102). This inhibits the reabsorption of water and sodium in the bowel
leading to hyponatremia (120mmEq/L) as indicated by the pathology results in the case
study. From the case study, low levels of potassium (0.4mmol/L), chloride ions (65mmEq/L)
and high bicarbonate levels(40mmol/L) are attributed to persistent diarrhea (White, Eden and
Hansman, 2012, p.70-73).
Conclusion
Viral Gastroenteritis is commonly caused by Norovirus. The common signs and
symptoms of viral gastroenteritis are abdominal pain, vomiting, diarrhea and lethargy.
Norovirus is commonly transmitted through fecal-oral route and can be prevented through
handwashing, disinfection and application of aseptic techniques in healthcare facilities.

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References
Bruggink, L.D., Oluwatoyin, O., Sameer, R., Witlox, K.J. and Marshall, J.A., 2012.
Molecular and epidemiological features of gastroenteritis outbreaks involving genogroup I
norovirus in Victoria, Australia, 2002–2010. Journal of medical virology, 84(9), pp.1437-
1448.
Gelberg, H.B., 2014. Comparative anatomy, physiology, and mechanisms of disease
production of the esophagus, stomach, and small intestine. Toxicologic pathology, 42(1),
pp.54-66.
Lopman, B., Gastanaduy, P., Park, G.W., Hall, A.J., Parashar, U.D. and Vinjé, J., 2012.
Environmental transmission of norovirus gastroenteritis. Current opinion in virology, 2(1),
pp.96-102.
Moore, H.C., Manoharan, K.R., Lim, F.J., Shellam, G. and Lehmann, D., 2013. Diverging
trends in gastroenteritis hospitalizations during 2 decades in western Australian Aboriginal
and non-Aboriginal children. The Pediatric infectious disease journal, 32(11), pp.1169-1174.
Thorne, L.G. and Goodfellow, I.G., 2014. Norovirus gene expression and
replication. Journal of General Virology, 95(2), pp.278-291.
White, P., Eden, J.S. and Hansman, G., 2012. Molecular epidemiology of noroviruses and
sapoviruses and their role in Australian outbreaks of acute gastroenteritis. Microbiology
Australia, 33(2), pp.70-73.