Chapter 18 - Lecture notes 18 PDF

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These are microbiology notes from 2016-2017....

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Structure and function of the Digestive system 1. The digestive system is divided into 2 parts: accessory structures and the GI tract 2. The purpose of the digestive tract is to digest food and to absorb nutrients 3. Undigested foods are expelled from the body in the form of feces

Normal microbiota 1. Normal microbiota refers to microbes that do not cause disease to their host and aid in host bodily functions a. the microbiota is part of the digestive system 2. The stomach and small intestine carry very few microbes because of the low pH environment 3. The large intestine is heavily populated with microbes a. 40% of fecal mass in microbial cell material b. Over 100 billion bacteria can be found in a single gram of feces Oral diseases 1. Teeth are abnormal surfaces, which do not shed cells 2. This allows for the collection of microorganisms and their products 3. We know it as a plaque, although it is complex biofilm Dental caries (tooth decay) 1. Oral bacteria make biofilms which protect them from salivary enzymes and also allow them to adhere to tooth surfaces 2. These bacteria metabolize sucrose and other sugars into lactic acid. Acids dissolve tooth enamel. 3. Streptococcus mutans is the most important cariogenic bacterium a. S. mutans causes more dental caries than any other bacteria of the mouth

S. mutans 1. bacteria of the mouth cannot adhere to a clean surface. However, it only takes a few minutes for them to begin attachment after brushing 2. Saliva carries proteins which coat teeth and allow bacteria to adhere 3. S. mutans attaches and begins to utilize glucose to produce dextran a sticky polysaccharide which aids in attachment 4. the accumulation of bacteria and dextran creates plaque

Plaque 1. Plaque can contain over 400 different bacterial species 2. It is not permeable to saliva, so the lactic acid produced within a plaque biofilm is not washed away or diluted 3. Over time, the accumulation of lactic acid softens and erodes tooth enamel Saliva 1. Saliva contains nutrients that bacteria of the mouth utilize however it also contains many antimicrobial substances a. Lysozyme – helps to protect exposed tooth surfaces b. Crevicular fluid – a tissue exudate, similar to serum, contains phagocytic cells and immunoglobulin which can lower bacterial numbers Enamel 1. Soft enamel may also be caused by lack of fluoride a. Many places add fluorine into the water supply b. Many toothpastes also are supplemented with fluorine c. Fluoride has come under some criticisms lately due to other effects which it has on the body d. Dental and skeletal fluorosis are the major points of contention

Dental caries 1. Dental caries were less of a problem before the 17th century than after it a. This was because refined sucrose was not a major part of the diet 2. Sucrose is a disaccrharide composed of fructose and glucose and is much more cariogenic than just glucose or fructose alone 3. People on high starch (unrefined sugars) diets tend to have fewer caries 4. Sugar alcohols such as mannitol, sorbitol and xylitol are not cariogenic a. Xylitol actually inhibits the metabolism of S. mutans Prevention 1. Lower intake of sucrose 2. Regular brushing, flossing and visits to the dentist 3. Lower the acidity of the mouth Gingivitis 1. Gingivitis is the infection and inflammation of the gums or gingivae a. A characteristic sign of gingivitis is the bleeding of gums while brushing 2. Gingivitis is seen in about half the adult population and occurs when brushing is not regularly performed and plaque is allowed to accumulate 3. An assortment of mouth bacteria cause this disease, it is NOT limited to just one species Periodontitis 1. 2. 3. 4.

When gingivitis progresses to a chronic illness, it is then reffered to as periodontitis About 35% of all adults suffer from this disease The gums become inflamed and pus sometimes forms around the gum sockets It can also lead to a more serious condition known as Vincent’s disease or trench mouth

Bacteria of Large intestine 1. The large intestine is mostly populated by anaerobic bacteria such as Lactobacillus and Bacteroides and facultative anaerobes such as E.coli, Enterobacter, Klebsiellosis and Proteus spp. 2. Most of these bacteria assist in the breakdown of foods and many help produce essential vitamins for the host The GI tract 1. The GI tract is a closed system. It prevents the invasion of pathogens into the rest of the body 2. By strict definition the contents of the GI tract are not “inside” the body a. It is thought of as a hollow tube which passes through the body 3. The GI tract contains several built-in mechanisms to help prevent pathogens from invading a. The acidity of the stomach is such that many pathogens cannot survive

b. The small intestine contains cells which phagocytize bacteria and produce antimicrobial compounds such as defensins and lysozyme Bacterial diseases of GI tract 1. Intoxications a. Staphylococcus b. Clostridium botulinum 2. Infections a. Helicobacter b. Salmonella c. E. coli d. Campylobacter e. Clostridium difficile Bacterial intoxications 1. AS the name implies, bacterial intoxications are the result of consumption of toxins a. The organism does NOT have to be present b. NOT contagious 2. Typically bacteria grow on food that is not properly store or preserved a. They produce toxins 3. People then eat the food without properly heating it to destroy the toxins

Staphylococcus Enterotoxicosis 1. The causative bacteria is Staphylococcus aureus a. The bacterium is heat tolerant, resistant to desiccation and osmotic stress and produces enterotoxins b. Enterotoxins cause GI upset by binding to host cell receptors  Kills enterocytes, cells that cover the intestines c. Because this is an intoxication, antibiotics are NO value S. aureus Transmission

1. A good percentage of the population carries S. aureus in their nares which can then contaminate foods 2. It is a big problem at picnics and potlucks because of the lack of refrigeration 3. The bacteria is usually found in creamy foods, such as potato salads and custards as well as in cured food such as ham a. The osmotic pressure of these foods prevent other microbes form growing, so S. aureus has very little competition 4. There may be NO outward appearances of the food being spoiled

S. aureus signs and symptoms

1. 2. 3. 4. 5.

The toxin produced is heat stable so can be present even in foods that have been reheated The onset of disease is rapid, usually less the 12 hours Once ingested, the toxin triggers the brain’s emetic, or vomiting response. This is usually followed by diarrhea and severe abdominal cramping The disease is self-limiting (symptoms resolve all on their own) after about 24 hours, meaning that treatment by physician is generally NOT necessary

Prevention of Staphylococcal Enterotoxicosis 1. The best way to prevent Staphylococcal Enterotoxicosis is to prevent the production of the toxin a. Maintain foods at the proper temp  Keep cold foods cold to slow toxin production  Keep hot foods hot to prevent bacterial colonization  Discard leftovers that were not promptly refrigerated b. Prevent contamination of foods with Staphylococcus aureus  Proper hygiene  Clean food prep surfaces  Clean kitchen linens regularly

Botulism 1. Caused by the agent Clostridium botulinum 2. Observed effects are a direct effect of the toxins produced by the organism 3. Outbreaks are rare and are normally confined to food consumption a. Wound botulism is possible and is similar to tetanus infection 4. Most outbreaks are a result of home canning operations where the products are NOT heated prior to consumption Traditional disease 1. Once consumed, the toxin will the bind to nerve endings, blocking the release of neurotransmitter acetylcholine a. This prevents nerve firing and results in a flaccid paralysis 2. The flaccid paralysis typically lasts 1-10 days a. Death occurs from cardiac and pulmonary failure b. Death rates depend on the type of toxin, produced but can be as high as 70% untreated cases

Disease outcome

1. Infection does NOT equal immunity a. The toxic dose is so low that it is usually not sufficient to generate lasting immunity 2. Infant botulism does occur about 250 cases per year in the U.S. associated with the consumption of honey a. Infants do not have developed normal flora, and the bacteria can colonize the intestines Treatment 1. Treatment of botulism is usually supportive 2. Toxin binds irreversibly, and thus, nerve endings must be given time to regenerate a. This is an extremely slow process, that can take months to occur b. It is not uncommon for life support to be provided in many cases 3. Antibiotics are usually worthless (the toxin is performed) 4. Antitoxin serum is usually administered, although it will not work on bound toxin Prevention 1. Most cases of botulism in the US is tied to home canning practices a. Proper canning techniques must be used to prevent botulism a. Cooking foods in a pressure cooker for minimum of 15min at 121 C b. Maintaining aseptic conditions while actually canning c. Heating canned items fully prior to consumption d. Never eating foods from containers that are damaged or bulging 2. Infant botulism is prevented by NOT feeding honey to infants (less than 1 year old)

Helicobacter 1. Most bacteria are not capable of colonizing of the stomach a. This is due to the low pH and proteolytic enzymes which reside there 2. Helicobacter pylori is an exception to this rule a. It produces large amounts of urease, which converts urea into ammonium b. Creates microenvironment, base.. acts as buffer our acid c. This results in a localized area with higher pH 3. This allows the bacteria to colonize the mucosal surface, and cause peptic ulcers

Incidence 1. About 30-50% of the population in developed countries colonize with Helicobacter pylori a. The exact mechanism of transmission is not known, may involve direct transmission through saliva or ingestion of organism through contaminated water and food 2. Of these, about 15% will develop peptic ulcers a. This seems to be dependent on host factors b. For example, people with blood type O are at greater risk 3. About 3% of colonized individuals will develop gastric cancer as a result of infection Symptoms 1. Not everyone colonized with H. pylori will develop peptic ulcers and the symptoms of that ulcer will vary, and include a. An ache or burning in your abdomen b. Abdominal pain that is worse when your stomach is empty c. Nausea d. Loss of appetite e. Frequent burping f. Bloating g. Unintentional weight loss Treatment and prevention 1. Diagnosis of H. pylori is done through multiple tests a. Blood tests can look for the presence of antibodies against the organism b. Breath test tests for the presence of urea in the stomach c. Stool testing can be done to look for the presence of H. pylori antigens in the feces d. Endoscopy can be performed and a biopsy taken with subsequent culturing of the organism 2. Treatment is usually antimicrobial theraoy, typically coupled with acid blockers

a. The acid blockers aid in the healing of the ulcer b. This is effective even with gastric cancer 3. There is no truly effective way to prevent colonization with the organism

Salmonellosis 1. Salmonella spp. Are G- facultative anaerobic, non-endospore forming rods 2. The nomenclature of Salmonella is different a. All Salmonella are grouped into the genus Salmonella b. Most of the relevant pathogenic strains will belong to the species enterica c. The Salmonella enterica is broken down into 2 serotypes, many with their own name  There is literally thousands of known serotypes Salmonella identified so far. d. The 3 primary pathogenic groups we see causing disease in the US are  Salmonella enetica serovar Enteriditis (often just called S. enterica)  Salmonella enetica serovar Typhimurium (often called S. typhimurium)  Salmonella enetica serovar Typhi (often called S. typhi) Salmonella gastroenteritis 1. Salmonellosis (aka Salmonella gastroenteritis) is primarily caused by S. enterica serovars Enteriditis and Typhiumurium a. One of the most common causes of diarrhea in the US  Causes estimated 1.4 million cases annually b. Most people infected by ingestion of contaminated food and water  Poultry, including eggs are common sources  All meats can be contaminated  Cross contamination is a major problem  It can grow on vegetables and fruits  Pets, including cats and reptiles, can also shed the bacteria Pathogenesis 1. After ingestion, the Salmonella passes through the stomach to the intestines a. They bind to Microfold or M cells and enter these cells  They will replicate in these cells which causes inflammmetion and subsequent diarrhea  This typically occurs after 12-36 hours incubation period  Occasionally they escape the M cell, and enter the blood stream 2. Once in the blood stream they will colonize the liver and spleen where they will replicate some more 3. Eventually, they make their way back to the intestines

Signs and symptoms

1. Primary signs and symptoms of salmonellosis include a. Diarrhea b. Fever c. Nausea d. Abdominal cramping 2. Treatment of Salmonellosis is typically supportive a. Oral rehydration is most common b. IV rehydration in severe cases c. Antibiotics are typically NOT needed Prevention 1. Prevention of salmonellosis is achieved several ways a. Fully cook meats and eggs b. Prevent cross contamination c. Do not prepare food or drinks for others while recovering from salmonellosis d. Wash or peel vegetables prior to consumption e. Wash hands often Typhoid fever 1. S. enterica serovar Typhi causes much more severe disease, called typhoid fever 2. S. Typhi does NOT natural colonize animals a. They only reservoir of infection is human 3. After ingestion, an incubation period of 1-2 weeks is followed with the appearance of symptoms a. Poor appetite b. Headaches c. Generalized aches and pains d. High fever e. Lethargy f. Diarrhea 4. Symptoms can last 3-4 weeks Disease transmission 1. Typhoid fever is spread through the ingestion of contaminated water and food a. Infected individuals shed the bacteria which then contaminates the items through fecal-oral contamination b. Additionally, some people develop a carrier state after the infection  3-5% never show symptoms, becoming asymptomatic carriers  An additional 1-3% become chronic carriers, shedding the organism for life

Treatment and prevention

1. Both the carrier state and the diseased states can be treated with the administration of cephalosporin for several weeks 2. There are 2 vaccines but they are only given to high risk professionals and persons traveling to endemic regions a. There has been an increased interest in these vaccines recently, as the prevalence of antimicrobial resistant strains has been rising 3. Beyond vaccination, prevention can be accomplished a. Good hygiene b. Getting tested and treated c. Avoiding sick individuals until they are treated

Cholera 1. Cholera is one of the most severe GI diseases of humans a. Caused by Vibrio cholera a curved G- rod that produces a single polar flagellum 2. Transmission of cholera typically occurs through water supplies that have been contaminated with fecal mater a. IT is tolerant to brackish (salty) water, and is a common inhabitant of estuaries  Raw oysters b. Are good biofilm formers, and can readily contaminate fresh water c. Can enter a viable but non-cultivable state, making detection difficult Pathogenesis 1. Once ingested, they traverse the stomach and reach the SI a. They are not tolerant to stomach acid, making people on antacid treatment more susceptible 2. Most people will develop symptoms within a few hours, but incubation periods up to 5 days have been reported 3. In the SI they secrete cholera toxin which binds to host and enters host cells a. Inside the host cell, the toxin results in the pumping of chloride ions out of the cell b. This results in a flowing of electrolytes and water into the intestines Symptoms 1. The massive influx of water into the intestines produced by cholera toxin can result in 3-5 gallons of diarrhea per day a. It occurs so rapidly that the mucosal lining of the intestines can be lost resulting in “rice water stools” b. The sudden loss of so much water can lead to dehydration  Dry mucus membranes  Low blood pressure  Muscle cramping  Shock and death if not treated, are possible c. In addition to diarrhea, severe violent vomiting is also common

Treatment and prevention 1. Treatment of cholera is replacement of fluids a. In severe cases, antibiotics CAN be given, but their necessity is questionable  Can shorten duration, but resistance is possible 2. A vaccine exists to prevent cholera but it is not very good a. Immunity is only achieved 50% of vaccinates, and it only lasts a few months b. When contamination of water is possible, water for all purposes must be disinfected prior to consumption  Boiling, chemically disinfected or bottled  Additionally, cook all foods potentially infected with the organism

Escherichia coli 1. Escherichia coli is one of the most abundant microbes in the human digestive tract a. Most strains are harmless, but a few can cause diseases 2. There are 3 common strains of pathogenic E. coli in the US a. Enterotoxigenic (ETEC) b. Enteropathogenic (EPEC) c. Enterohemorrhagic (EHEC)  These are also called STEC 3. All of these transmitted by the fecal-oral route, resulting in diarrhea 4. However, the way they produce disease differs based on serotype E. coli

1. Enterotoxigenic E. coli binds to, but does NOT invade intestinal cells a. It produces 2 toxins , a heat stable and heat labile toxins b. These toxins can then act on epithelial cells, causing disease 2. Symptoms include diarrhea, vomiting, and low grade fever a. Common cause of travelers diarrhea 3. Symptoms will generally resolve on their own in 3-7 days a. Supportive therapy is usually the only treatment EPEC 1. Enteropathogenic E. coli bind tightly to the host intestinal cells a. This binding results in disruption of the tight junctions and fluid influx into the intestinal lumen, and profuse watery diarrhea b. Is a cause of travelers diarrhea in adults, can be fatal in infants 2. Supportive therapy (i.e. fluid replacement) is the primary treatment

EHEC

1. Enterohemorrhagic E. coli has made the news quite a bit in past years a. The most common serotype is O157:H7 2. EHEC is very closely related to Shigella and it is speculated that E. coli recently acquired the genes for its Shigella-like toxin from Shigella 3. EHEC produces Shiga-like toxin as it binds to the intestinal mucosa. The toxin causes the intestinal lining to slough, causing bloody diarrhea 4. The infectious dose is less than 100 organisms Sources of E. coli 1. It is estimated that 50% of feedlot cattle are infected with EHEC a. 90% of all ground meats are contaminated with EHEC but in very low numbers 2. Most cases of EHEC are not from meats but from green leafy vegetables and sprouts a. The contamination can occur in the field from agricultural runoff or on the table from cross contamination 3. Other cases are from children visiting farms and petting zoos HUS 1. What makes EHEC infections so problematic is a condition called hemolytic uremic syndrome a. The Shiga-like toxin produced is absorbed into the bloodstream and goes to the kidneys b. There it binds to the Glomerulus where it causes blood clot formation and RBC lysis c. This in turn clogs, damages and ultimately destroys the Glomerulus d. Renal failure and death can occur 2. Children are far more sensitive than adults to these effects Treatment and prevention 1. Treatment of E. coli infections is typically supportive replacement of fluids a. Antibiotics can be administered for severe cases b. HUS requires additional treatment  Blood and plasma transfusions  Dialysis  Low protein diets  Administration of blood pressure lowering drugs to prevent further kidney damage 2. Prevention of E. coli is accomplished by a. Cooking raw meat, esp. ground meats b. Preventing cross contamination...