My Case Study Solution

Transcription

1 My Case Study Solution By Rosalia Lopez de Alda Andrew had been feeling sick for a few days after going to a Cinco de Mayo barbeque to celebrate with his friends. A couple of days after the BBQ he was having myalgias with a headache. The next day he started having colicky abdominal pain as well as some diarrhea. He found himself going to the restroom multiple times in the day. One day, he began to feel nauseous, was vomiting, and noticed blood in his diarrhea. This prompted him to go to the Emergency Department for further evaluation. On exam, he was febrile. When asked by the doctor what he had eaten at the BBQ, he recalled eating a thick piece of grilled chicken along with some grilled shrimp, steak, corn and potatoes through out the day. To wash down the food he had plenty of beer and water. 1. Give a differential diagnosis of four different diseases Andrew might have and explain why it could be that disease: 1. Campylobacteriosis This is characterized by bloody diarrhea, abdominal pain, headache, fever, and occasional nausea and vomiting. This may cause dehydration. It takes 2-4 days for onset of symptoms and usually goes away on its own after 10 days. Eating contaminated foods, like undercooked chicken or drinking contaminated water or milk commonly transmits this. It may also be transmitted via contact with contaminated animals. This is most likely what Andrew has been infected with as he ate a thick piece of chicken and suffered from all of these symptoms within the given time frame, minus reported fever (1). 2. Salmonellosis This is characterized by diarrhea, fever, and abdominal cramps. In severe cases this may cause dehydration. It takes hours for onset of symptoms and usually goes away on its own after 4-7 days. Eating contaminated foods, like beef, poultry, eggs and milk commonly transmits this. It may also be transmitted via contact with contaminated animal s feces, especially diarrhea. It is a possibility that this is what Andrew has, although Salmonellosis does not develop bloody diarrhea or nausea/vomiting (2). Shigellosis and Ecoli are more likely. 3. Shigellosis - This is characterized by bloody diarrhea, fever, abdominal pain, and tenesmus. It takes 1-2 days for onset of symptoms and lasts 5-7 days. Eating/drinking contaminated foods/liquids, touching contaminated surfaces, or having contact with someone that is infected commonly transmits this. The bacteria may also be found in stool up to a week after symptoms have resolved (3). It is possible Andrew has this as he has had all of these symptoms, minus tenesmus. But it does not mean it should be ruled out until results show otherwise.

2 4. Ecoli This is characterized by watery or bloody diarrhea, abdominal cramps, possible fever, and possible nausea/vomiting. It typically takes 3-4 days for onset of symptoms and may last between 1-10 days. It is transmitted via fecaloral route. Eating contaminated foods/liquids, like raw milk and dairy, or having contact with someone that is infected commonly transmits this (4). It is possible that Andrew has this although he also suffered a headache. These symptoms are extremely similar to the ones he has experienced and are also within the time frame. It is the second most likely differential diagnosis. 2. Andrew was extremely dehydrated. Blood and stool samples were sent for culture and he was started on antibiotics. What gram-negative bacteria would be found in his stool culture that explains this disease s etiology? They would find Campylobacter jejuni in his culture. They would see it is a gram negative, non spore-forming, and curved bacterium. It can live in low levels of oxygen of 5 10% and CO2 of 10% and has motility due to its single flagellum. It also has an outer membrane that consists of lipopolysaccharide (LPS), which makes it hydrophobic. This allows us to subdivide it into Penner serogroups as different serogroups have different antigenic properties. Infection of this bacteria only requires a small dose between organisms. People commonly get infected by eating/drinking contaminated foods, as well as by person-to-person contact, although this is less common. Once a patient ingests the bacteria, they penetrate through mucus layers thanks to their shape and motility and they adhere to the enterocytes in the small and large intestine, typically in the terminal ileum and colon. This is where they colonize. This bacteria rarely causes bacteremia and they tend to stay in the GI tract causing inflammation (5). 3. What are its virulence factors? C. jejuni has many virulence factors: 1. Flagellin for motility, to travel throughout the host, and flagella chemotaxis, to sense the environment and coordinate movement. Its motility is what makes it so virulent. 2. Mucin a positive chemotaxin compatible with the bacteria s colonization of the mucus-filled intestine. 3. Bile and L-fucos also positive chemotaxins. Motility and chemotaxis help lead the bacteria to its colonization site. 4. Adhesion and invasion allows C. jejuni to stay on the host cell long enough to cross into it. Once adhered, the bacterium invades when it is taken up by a cytoplasmic vacuole. 5. Lipopolysaccharides (LPS) in outer membrane plays a role in adherence. The bacteria also evade the immune system by shifting its antigen composition of this outer membrane to make it more difficult for the immune system to recognize them.

3 6. Sialic acid contained in its core oligosaccharide, it resembles gangliosides and plays an important role in the contraction of Guillians Barre syndrome, a neurological disease. 7. Cytolethal distending toxin stops the cell s growth cycle in G2, which causes the cell to eventually die (accounts for bloody diarrhea). It contains portions CdtA, CdtB (can disrupt DNA in the cell), and CdtC. Little is known about how its structure contributes to its function, but it is believed to cause immunosuppression. 8. Siderophores heme compound that allows it to acquire iron for nutrient sustenance through electron transport, anaerobic respiration, and energy metabolism. 9. Superoxide dismutase gets rid of the reactive oxygen species superoxide which could harm the cell's DNA or membrane factors. 10. Antibiotic resistance to tetracycline, erythromycin, ciprofloxacin, kanamycin, nalidixic acid, and chloramphenicol (6). 4. How is it diagnosed? What is the treatment and what are some ways of prevention? Diagnosis is traditionally done by culture of a stool sample on selective media incubated at 42 C (107.6 F) for 72 hours in reduced O2 tension. Dark-field microscopy can give an initial idea as to the type of bacteria is in the culture when motile and curved, spiral, or S-shaped rods are visualized. Rapid culture-independent tests have become move available for Campylobacter enteritis. Stool antigen testes are also available although not very reliable. Nucleic acid based tests have recently been approved and appear to have higher sensitivity and specificity than the stool antigen tests. The disease generally tends to resolve itself after about 1 week. Although rates of antibiotic resistance have greatly increased in the past 20 years, empiric antibiotic therapy can be administered help decrease symptoms while awaiting a diagnosis. Otherwise, will simply treat symptoms and make sure the patient stays hydrated. No vaccine is available. (1). 5. What is its taxonomy? Bacteria > Proteobacteria > Epsilon Proteobacteria > Campylobacteria > Campylobacterales > Campylobacteraceae > Campylobacter > C. jejuni (7). 6. A couple of days after Andrew was discharged from the hospital, he returned again for severe Right Lower Quadrant abdominal pain. On exam he had a positive McBurney s sign. His CT scan showed acute appendicitis. What are possible complications of this disease? Possible complications include:

4 1. Guillan-Barre Syndrome (GBS) occurs when the Campylobacter antibodies attack the patient s nerve cells. This develops a few weeks after primary diarrheal illness. It is the most common cause of acute generalized paralysis in the western world. 2. Reactive Arthritis inflammation in the joints, eyes, or reproductive/urinary organs. Symptoms tend to develops almost 3 weeks after primary illness. Campylobacter may also cause appendicitis, as it has for Andrew, or invade the abdominal cavity, the heart, gall bladder, urinary tract, blood stream or central nervous system. (8). 7. Compare the epidemiology of this disease in the US vs. Europe In the past 10 years, there has been a rise in the global incidence of campylobacteriosis. The numbers of cases have increased in North America, Europe, and Australia. Based on 10 years of outbreak data from1998 to 2008, there are approximately 845,024 campylobacteriosis cases with 8,463 hospitalizations and 76 deaths in the United States. Mostly children are infected. The U.S. Food-Borne Diseases Active Surveillance Network (1996 to 2012) reported an annual incidence of 14.3 per 100,000 population for Campylobacter infection with a 14% increase in the incidence in 2012 compared to the period (9). In Europe, 240, 379 cases of campylobacteriosis were reported and confirmed by 26 EU and two EEA countries with most patients being children. There is an overall rate of 59.8 cases per population in the EU/EEA. According to the European Centre for Disease Prevention and Control, the cases from Germany (70 530), the United Kingdom (66 790), the Czech Republic (20 750) and Spain (11 481) represented 71% of all reported confirmed cases. Over the past five years, Germany, the United Kingdom and the Czech Republic have had the highest yearly number of cases. Compared to the previous year, cases increased in 25 countries in 2014; a decrease was reported in only three countries (Belgium, Estonia, and Cyprus). Children under five years of age are typically the most affected group of people in the majority of countries, claiming about 187 cases per population in 2014 (range by countries from 5.0 to cases per population per year). It has also been observed that campylobacteriosis shows a seasonality with the number of cases peaking in July (10). Works Cited 1. "Travelers' Health." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 10 July Web. 04 May <

5 2. "Salmonellosis - Topic Overview." WebMD. WebMD, LLC., Web. 20 Apr < 3. "General Information." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 03 Aug Web. 20 Apr < 4. "E. Coli Symptoms." Mayo Clinic. Mayo Foundation for Medical Education and Research, 01 Aug Web. 04 May < 5. Lydyard, Peter, Michael Cole, John Holton, Will Irving, Nino Porakishvili, Pradhib Venkatesan, and Kate Ward. "Campylobacter Jejuni." Case Studies in Infectious Disease (2009): Garlandscience.com. Taylor & Francis Group. Web. 5 May < 6. "Campylobacteriosis." Microbewiki. MediaWiki, 11 Feb Web. 5 May < 7. "Campylobacter Jejuni." Microbewiki. MediaWiki, 16 July Web. 5 May < 8. Clark, Marler. "Campylobacter." Foodboorne Illness. Outbreak, Inc., Web. 06 May < 9. Kaakoush, Nadeem, Natalia Castaño-Rodríguez, Hazel M. Mitchell, and Si Ming Man. "Global Epidemiology of Campylobacter Infection." Journals.ASM.org. American Society for Microbiology, 1 July Web. 6 May < 10. "Annual Epidemiological Report 2016 Campylobacteriosis." ECDC. European Centre for Disease Prevention and Control, Web. 06 May <