Ch. 23 - Microbial Diseases of the Digestive System

Review - Which life stage of an intestinal protozoan is infective? A. The cyst. B. The apicomplexan. C. The flagellate. D. The trophozoite.

A

Review - Which is the most common cause of viral gastroenteritis? A. Norovirus. B. Astrovirus. C. Rotavirus. D. Calicivirus.

A - Norovirus is responsible for 90% of viral gastroenteritis cases.

Microbiome of the Lower small intestine and colon

- 100 trillion bacteria in total - In every gram of feces there is 100 billion bacteria. 40% of weight - Microbiota here are beneficial: microbial antagonism, produce vitamin B7, B9, B12, K - Mucous membrane prevents microbes entering the bloodstream - Most are Bacteroides, G- anaerobe --> Lactobacillus, Escherichia, Enterobacter, Proteus Klebsiella. Bifidobacterium, Clostridium, Shigella, Candida (fungus), Entamoeba (protozoan), Trichomonas (protozoan)

Oral herpes

- AKA "fever blisters", "cold sores" - Painful, itchy, creeping skin lesions on the lips - Fever blisters appear one to two weeks after exposure to an infected individual - Initial infections may be accompanied by flulike symptoms such as malaise, fever, and muscle pain - fluid-filled lesions eventually break, crust over, and fall off (within 7-10 days) to reveal pink healing skin - Subsequent lesions are generally milder - herpetic gingivostomatitis; Severe infections in which the lesions extend into the oral cavity --> often seen in young patients and in patients with lowered immune function due to disease, chemotherapy, or radiation treatment - herpetic pharyngitis; pharynx becomes infected and inflamed - herpes esophagitis; characterized by extremely painful and difficult swallowing, fever, and sometimes chills --> Immunosuppressed individuals may develop this

viral gastroenteritis

- AKA "stomach flu" - inflammation of the mucous membrane of the stomach and intestines, caused by a viral pathogen - general manifestations the same as for bacterial gastroenteritis—abdominal pain and cramping, diarrhea, nausea, and vomiting. - Additional signs and symptoms may include fever, chills, clammy skin, weight loss, or lack of appetite. - Dehydration is the most common complication. - Symptoms generally appear within 24 hours of consuming contaminated food and resolve within 12-60 hours. - Vomiting, bloody stool, life-threatening diarrhea, and dysentery may occur with viral gastroenteritis.

Anisakiasis

- Anisakiasis results from infestation by several parasitic nematodes - Typically asymptomatic - Abdominal pain, nausea, vomiting, and fever may occur - Some individuals develop an allergic rash - Most commonly caused by Anisakis simplex - Complex life cycle with several larval stages - About 20,000 cases occur worldwide - Diagnosis is generally made using endoscopy to visualize worms - Treatment involves removing worms from the intestine by endoscopy or surgery - Prevented by avoiding raw and undercooked marine fish

Dental Caries, Gingivitis, and Periodontal Disease Signs and symptoms

- Caries: appear as holes or pits in the teeth - Gingivitis: non-destructive periodontal disease, gums that are swollen, tender, bright red, or bleeding - Periodontitis: untreated gingivitis, gums pull away from teeth and bone begins to be destroyed.

Pathogen and virulence factors of Peptic Ulcers

- Caused by Helicobacter pylori --> G-, genus has unique structure: helix to curved rod, but not a spirochete Numerous virulence factors - Inhibits acid production by stomach cells - Urease neutralizes stomach acid - Flagella enable burrowing through mucus lining - Adhesins facilitate attachment to gastric cells

Cholera

- Caused by Vibrio cholerae --> G- vibrio - Cholera toxin gene is encoded by bacteriophage --> Toxin triggers secretion of electrolytes by intestinal cells. Water follows electrolytes via osmosis - Pandemics have occurred throughout history - Severe fluid and electrolyte loss due to massive diarrhea --> Dehydration, acidosis, shock, coma, death

Mumps

- Caused by the Mumps virus (-ssRNA) - Humans are the only natural host, infect salivary glands, travels into respiratory system, and becomes systemic. - Acquired by encountering saliva of infected person or contaminated fomites. - Once a very common childhood disease --> Nearly nonexistent in developed countries due to immunization - No specific treatment for mumps, lasts 7-10 days - Infected individuals develop lifelong immunity

Pathogens and Pathogenesis of viral gastroenteritis

- Common viral agents of gastroenteritis are caliciviruses, astroviruses, and rotaviruses. - Caliciviruses and astroviruses are two types of +ssRNA viruses that cause acute gastroenteritis - Both are small, naked, and star shaped and have polyhedral capsids that enter the body through the digestive tract when the person consumes contaminated food or water --> The most studied of the caliciviruses are noroviruses (they cause diarrhea) - rotaviruses are dsRNA - almost spherical and have glycoprotein spikes that act as attachment molecules and trigger endocytosis - naked, though during replication they acquire envelopes but then lose them. - Their transmission is via the fecal-oral route from contaminated food or water - ALL THREE infect cells lining the intestinal tract, where they undergo lytic replication. --> As epithelial cells die, the normal function of the intestinal tract is lost - Infections are generally self-limiting—after the virus has destroyed the epithelial layer, replacement epithelial cells grow, and function is restored.

Diagnosis, treatment, and prevention of Tapeworm Infestations

- Diagnosed by presence of proglottids in fecal sample - Treated with single dose of niclosamide or praziquantel. Remove orally or pass naturally. - Prevention relies on thorough cooking of meats

Diagnosis, treatment, and prevention of Peptic Ulcers

- Diagnosis based on X-ray exam to identify ulcers and presence of H. pylori in clinical specimens - Treat with antimicrobials and drugs that inhibit stomach acid - Prevent by avoidance of fecal-oral transmission

Diagnosis, treatment, and prevention of Cholera

- Diagnosis based on presence of "rice-water stool" --> Watery, colorless, odorless, and flecked with mucus (which looks like rice) - Treat with supportive care and administration of doxycycline --> Reduces duration of diarrhea and volume of stool - Available vaccine provides only short-lived immunity - Proper hygiene is an important preventive measure

Diagnosis, Treatment, and Prevention of bacterial intoxications (toxifications) (food poisoning)

- Diagnosis is generally based on signs, symptoms, and patient history - Tests may be done on samples from vomit, blood, stool, or any leftover food deemed suspicious. - Stool cultures positive for S. aureus are indicative of staphylococcal food poisoning, but other examinations are often inconclusive - Replacement of fluids and electrolytes is the preferred treatment and can be self-administered - Good hygiene and proper food handling reduce incidence.

Diagnosis, treatment, and prevention of Salmonellosis and Typhoid Fever

- Diagnosis made by finding Salmonella in stool - Salmonellosis is usually self-limiting (~7 days) - Typhoid fever can be treated with antimicrobial drugs - Prevented with proper hygiene

Pathogenesis and Epidemiology of Traveler's Diarrhea

- E. coli diarrhea appears 24-72 hours after consumption of the bacterium - Diarrhea is mediated by enterotoxins delivered via a type III secretion system - Shiga-like toxin attaches to the surfaces of neutrophils and is spread by them throughout the body, causing widespread death of host cells and tissues. - Abnormal and massive destruction of red blood cells can clog the filtering system of the kidneys, resulting in life-threatening kidney failure --> called "hemolytic uremic syndrome"; most commonly develops in children after 2-14 days of diarrhea caused by enterohemorrhagic E. coli. - O157:H7 found in almost 50% of beef carcasses in the United States

Epidemiology of amebiasis

- E. histolytica is carried asymptomatically in the digestive tracts of roughly 10% of the world population - Infection arises following consumption of contaminated water or food, ingestion from contaminated hands, or during oral-anal intercourse. - Cockroaches and houseflies can facilitate the spread of cysts under conditions of overcrowding

amebiasis Pathogen, Virulence Factors, and Pathogenesis

- Entamoeba histolytica - motile trophozoite - develops into an infective, resistant, chitin-shelled cyst. Virulent strains of Entamoeba produce adhesion proteins, proteases, proteins that create ion channels in host membranes, and other small proteins that appear to have toxic effects on cells and facilitate invasion. - Avirulent strains of Entamoeba do not produce these four types of proteins and so remain in the lumen of the intestine - Infection begins with ingestion of thick-shelled cysts, which pass successfully through the acid of the stomach and excyst in the small intestine to release trophozoites - These migrate to the large intestine and multiply by binary fission, producing any signs and symptoms in one to four weeks. - Trophozoites use pseudopodia to attach to specific receptors on the intestinal lining, where they feed. - Both trophozoites and cysts are shed into the environment in feces, but trophozoites die - Trophozoites in the lumen of the intestine do little damage and typically produce no symptoms, but when trophozoites invade the peritoneal cavity and bloodstream, amebic dysentery or invasive extraintestinal amebiasis occur. - The difference in severity is due to the production of differing virulence factors by various strains.

Traveler's Diarrhea

- Escherichia coli --> aerobic or facultatively anaerobic, Gram-negative bacilli that ferment lactose to form gas - enterotoxigenic strains (ETEC) cause diarrhea - enterohemorrhagic E. coli (EHEC)—have genes (located on transmissible plasmids) for fimbriae, adhesins, and a variety of toxins that enable EHEC to cause severe foodborne disease - O157:H7; these toxins inhibit protein synthesis, kill cells, and can cause kidney failure, resulting in death --> Shiga-like toxin binds to neutrophils and travels to other areas and causes cell death - E. coli O157:H7 also produces a type III secretion system - One set of secreted proteins disrupts a host cell's metabolism; another set becomes lodged in a cell's cytoplasmic membrane and forms receptors for the attachment of additional E. coli O157:H7 bacteria --> Such attachment apparently enables this strain of E. coli to displace normal harmless strains

Epidemiology of Peptic Ulcers

- Fecal-oral transmission is likely --> Hands, well water, or fomites - Stress may worsen ulcer symptoms

Viral Hepatitis Pathogen and Pathogenesis; Part 2

- HAV: mild, AKA infectious hepatitis --> Clears up in 99% of cases - HBV: occasionally severe (10%), AKA serum hepatitis --> Chronic infection (exocytosis), all body fluids infected - HCV: usually subclinical, AKA chronic hepatitis --> No genetic proofreading, constant mutations and multiple strains within infected person; chronic in 70% - HDV: coinfection causes severe acute disease --> Lacks capsid genes, relies on HBV capsid proteins. Must be within coinfected cell; chronic. - HEV: mild --> Infects many animals, only human-to-human

Epidemiology of Oral Herpes

- HHV-1 accounts for 90% of all cold sores - HHV-2, the normal cause of genital herpes, causes the other 10% of cold sores - HHV-1 is transmitted by close contact with infected individuals who have active lesions - HHV-2 spreads through oral sex with infected partners. - Primary HHV-1 infections typically occur via casual contact during childhood and usually produce no signs or symptoms --> HHV-1 has asymptomatically infected about 80% of children by age two

Dental Caries, Gingivitis, and Periodontal Disease Pathogenesis

- Hard deposits, tartar or dental calculus, form when calcium salts mineralize plaque. - Plaque formation at the base of teeth triggers inflammation, leading to gingivitis. - Inflammation causes oxygen-free pockets to be formed, promoting the growth of Porphyromonas gingivalis. - P. gingivalis secretes proteases that breakdown gingival tissue, degrade bone, and promote tooth loss.

Helminthic Infestations of the Intestinal Tract

- Helminths are macroscopic, multicellular worms - Helminths can infest the GI tract as non-disease-causing parasites - Tapeworm is the common name for a cestode --> Flat, segmented, parasitic helminth --> Tapeworms are intestinal parasites that lack their own digestive system - 4 million Americans are currently infected with a roundworm - Helminths require a high protein diet

Viral Hepatitis Pathogen and Pathogenesis; Part 1

- Hepatovirus Hepatitis A virus (HAV, +ssRNA) - Orthohepadnavirus Hepatitis B virus (HBV, dsDNA) - Hepacivirus Hepatitis C virus (HCV, +ssRNA) - Deltavirus Hepatitis delta virus (HDV, -ssRNA) - Hepevirus Hepatitis E virus (HEV, +ssRNA) Transmission - HAV/HEV: fecal/oral transmission - HBV/HCV/HEV: needles/sex

Tapeworm Infestations Epidemiology

- High incidence --> Regions of inadequate sewage treatment --> Regions where humans live in close contact with livestock

Pathogen and Pathogenesis of Oral Herpes

- Human herpesvirus 1 (HHV-1; previously called herpes simplex virus 1) causes most cases of oral herpes - HHV-2, which usually infests the genitalia, can also infect the oral cavity - After entering the body through cracks or cuts in mucous membranes, herpesviruses reproduce in epithelial cells near the site of infection, triggering inflammation and cell death and resulting in painful, localized lesions on the skin 2-12 days after infection - Herpes virions cause infected cells to fuse with uninfected neighboring cells to form a structure called a syncytium; in this way, herpes viruses spread from cell to cell, avoiding the host's immune system - Lesions usually last two to three weeks - HHV-1 and HHV-2 can eventually establish latent infections in the trigeminal nerve ganglion by entering sensory nerve cells and being carried by cytoplasmic flow to the ganglion - Latent viruses may reactivate later in life when the immune system is suppressed by emotional stress, fever, trauma, sunlight, menstruation, or disease - Reactivated viruses travel down the nerve to produce recurrent lesions as often as every two weeks - Reactivated viruses travel down the nerve to produce recurrent lesions as often as every two weeks. Recurrent lesions are rarely as severe as the initial lesions because of immunological memory - Recurrent lesions are rarely as severe as the initial lesions because of immunological memory.

Epidemiology of Giardiasis

- Infection results from ingesting cysts in contaminated water - Hikers and campers are at particular risk - Diagnosed by microscopic observation of Giardia in stool - Treat with metronidazole or tinidazole - Oral rehydration therapy may be needed - Prevention relies on using good hygiene and filtering water in endemic areas

Viral Hepatitis Diagnosis, treatment, and prevention

- Initial diagnosis made by observation of jaundice, enlarged liver, or fluid in the abdomen - Serological testing can identify viral antigens - HBV diagnosed by viral proteins in body fluids - HCV treatment only needed for chronic infections --> Harvoni, Olysio, Sovaldi, Viekira Pak cure infection - IFN-α and nucleotide analogs help reduce levels of virus - Supportive care for symptoms - Prevent with good hygiene, protected sex or abstinence - Vaccines are available against HAV and HBV --> HAV: 10 years; HBV: lifetime

Viral Hepatitis

- Jaundice, abdominal pain, fatigue, vomiting, appetite loss - Symptoms may occur years after initial infection - Host immune response that kill infected cells cause most of the liver damage

Dental Caries, Gingivitis, and Periodontal Disease Epidemiology

- Most adults have experienced dental caries - Diets high in sucrose increase the risk of decay - Sucrose (table sugar) is the only sugar that can be used to build dextran

Epidemiology of viral gastroenteritis

- Noroviruses cause 90% of nonbacterial gastrointestinal infections, which is about 10% of all cases of gastroenteritis worldwide and have caused outbreaks of gastroenteritis in day care centers, schools, hospitals, nursing homes, restaurants, and, in recent years, numerous epidemics on cruise ships. --> Generally, noroviruses infect school-aged children and adults - Rotaviral gastroenteritis is more common in infants

Giardiasis

- Often asymptomatic protozoan disease - Diarrhea and associated GI symptoms can last up to four weeks. 'Rotten-egg' smell due to H2S --> Severe greasy, frothy, fatty diarrhea - Caused by Giardia intestinalis - Cysts are resistant to chlorine, heat, drying, and stomach acid - Trophozoites in small intestines interfere with breakdown and absorption leading to undigested food which is then broken down by bacteria - Once trophozoite enters colon --> cyst

Pathogenesis and Epidemiology of bacterial intoxications (toxifications) (food poisoning)

- Outbreaks are usually associated with picnics, school cafeterias, or large social functions where food stands unrefrigerated or where food preparation is less than optimal - Staphylococcus does not change the appearance or taste of food - often self-limiting and relatively mild

Pathogenesis of Shigellosis (professor notes)

- Pathogen colonizes cells of the small, then large intestine. Reproduces in cytosol. - Enterotoxins are proteins on Shigella that bind and cause electrolyte and water loss. Similar to cholera toxin. - Shigella can directly invade adjacent cells, thus avoiding immune detection - Shigella is rapidly destroyed in blood, bacteremia does not occur - Shiga toxin, an enterotoxin and cytotoxin, stops protein synthesis, causes cell death and dysentery

Epidemiology of C. diff. (Antimicrobial-Associated) Diarrhea

- Pseudomembranous colitis is a by-product of modern medicine; until the widespread use of antimicrobial drugs, the condition was very rare --> Almost any antimicrobial can trigger the disease, but long-term use of newer, more powerful drugs are more likely to cause problems - elderly, burn patients, immunocompromised individuals, patients who have had a previous case of pseudomembranous colitis, and patients with kidney failure or who are recovering from abdominal surgery are particularly susceptible

Salmonellosis and Typhoid Fever

- Salmonella enterica serotypes (G- bacillus) - Typhi and Paratyphi cause typhoid fever - Enteritidis and Typhimurium cause salmonellosis - Bacteria tolerate acidity of stomach and pass to the intestine and reproduce in vesicles - Type III secretion system introduces toxins that disrupt numerous cellular activities, cause death --> Death of intestinal cells cause fever, cramps, diarrhea - Typhoid fever acquired by contaminated food or water - Salmonellosis often acquired by consuming contaminated eggs

Diagnosis, Treatment, and Prevention of viral gastroenteritis

- Serological tests performed on stool samples can distinguish among surface antigens of caliciviruses, astroviruses, and rotaviruses. - The xTAG Gastrointestinal Pathogen Panel can identify noroviruses and rotavirus strain A. - There is no specific treatment for any of these infections except support and replacement of lost fluid and electrolytes. - Antidiarrheal medications may only prolong symptoms, because diarrhea tends to clear the viruses from the system. - Prevention involves adequate sewage treatment, purification of water supplies, frequent handwashing, good personal hygiene, and disinfection of contaminated surfaces and fomites. - Attenuated oral vaccines against rotaviruses exist and safely protect against up to 98% of severe rotaviral diarrhea cases that would require hospitalization. - Depending on which of two vaccines, pediatricians administer two or three doses beginning at two months of age.

Dental Caries, Gingivitis, and Periodontal Disease Pathogen and virulence factors

- Streptococcus mutans is a frequent cause of caries - G+ coccus - Dextran and pili allow biofilm formation on the tooth --> insoluble, sticky, polysaccharide slime (dextran) - Porphyromonas gingivalis causes periodontal disease - Anaerobic G- bacillus - Proteases break down gingival tissue

Microbiome of the Esophagus, Stomach, Duodenum

- These regions are almost free of microbes - Peristalsis and rapid transport of food helps prevent microbial colonization

Pathogens and Virulence Factors of bacterial intoxications (toxifications) (food poisoning)

- Toxins of Staphylococcus aureus, which is a normal member of the microbiome of the skin and upper respiratory system, cause staphylococcal food poisoning --> common --> processed meats, custard pastries, potato salad, and ice cream - five enterotoxins --> These proteins (designated A through E) stimulate intestinal muscle contractions, trigger nausea, and cause intense vomiting --> heat stable, remaining functional at 100°C for up to 30 minutes, which means they are not usually inactivated by warming or reheating food

Tapeworm Infestations

- Usually asymptomatic, unknown until segments of helminth are passed - Nausea, abdominal pain, weight loss, and diarrhea may occur - Taenia saginata: beef tapeworm - Taenia solium: pork tapeworm - Life cycle divided between a primary and intermediate host --> Humans = primary host --> Cows/pigs= intermediate host

Microbiome of the Tongue and Teeth

- Viridans streptococci are most prevalent - Actinomyces, Lactobacillus, Corynebacterium, Haemophilus, Staphylococcus, Entamoeba (protozoan), Trichomonas (protozoan)

Amebiasis

- a mild to severe dysentery that, if invasive, can cause the formation of lesions in the liver, lungs, brain, and other organs - Entamoeba hisolytica causes - least severe form, luminal amebiasis, occurs in otherwise healthy individuals and is asymptomatic - Invasive amebic dysentery is a more serious form of infection characterized by severe diarrhea, colitis (inflammation of the colon), appendicitis, ulceration of the intestinal mucosa, bloody mucus-containing stools, and pain - most serious disease—invasive extraintestinal amebiasis—potentially fatal lesions of dead and dying intestinal cells form in the liver, lungs, spleen, kidneys, or brain

Dental Caries

- cavities

Diagnosis, Treatment, and Prevention of Shigellosis

- diagnose by shigella in the stool using xTAG Gastrointestinal Pathogen Panel - antimicrobial, such as ceftriaxone, which can shorten the duration of disease and reduce the spread of Shigella to other patients - Resolves in about 7 days - Resistance to antimicrobials among Shigella strains is widespread and increasing worldwide - vaccine in progress

Diagnosis, Treatment, and Prevention of Oral Herpes

- diagnosed by observation of the characteristic recurring lesions - Microscopic examination of infected tissue reveals syncytia. - Positive diagnosis is achieved by immunoassay that demonstrates the presence of viral antigen - Infections with HHV-1 or HHV-2 are among the few viral diseases that can be controlled with chemotherapeutic agents, notably valacyclovir. - Topical application of the drug limits the duration of the lesions and reduces viral shedding, though the drug does not cure the diseases or free nerve cells of latent viral infections. - Patients with active lesions are more likely to spread the disease, but asymptomatic carriers still shed viruses and are contagious - Washing with soap and water may minimize spread of the virus, - most effective prevention depends on avoiding direct contact with infected individuals.

Diagnosis, Treatment, and Prevention of Traveler's Diarrhea

- diagnosed by s/s - xTAG Gastrointestinal Pathogen Panel can identify three pathogenic strains of E. coli - replace lost fluids, electrolytes - Antimicrobials: doxycycline, trimethoprim-sulfamethoxazole, fluoroquinolones, or rifaximin - no vaccine - Antimicrobial drugs prolong the symptoms --> Cause O157:H7 to produce more Shiga-like toxin - Antidiarrheal drugs prolong the symptoms --> Delays expulsion of bacteria from digestive tract

Peptic Ulcers

- erosions of the linings of either the stomach (gastric ulcer) or duodenum of the small intestine (duodenal ulcer) - abdominal pain - shock, in which the cardiovascular system fails to deliver enough blood to vital organs, is usually the major sign of a perforation - nausea, vomiting (with or without blood, which looks like coffee grounds in the vomitus), weight loss, chest pain, or black, tarlike stools

bacterial intoxications (toxifications) (food poisoning)

- food poisonings caused by toxins—the microbe itself is either not present or not the immediate problem

Pathogenesis of C. diff. (Antimicrobial-Associated) Diarrhea

- generally noninvasive; that is, it does not move from the colon into the blood --> stays within the lumen of the colon, producing its two toxins - Toxin A breaks down the junctions holding cells of the colon's mucous membrane together, which triggers inflammation and allows loss of fluid - Toxin B kills the colon's cells outright and induces the formation of lesions that fuse into the characteristic pseudomembrane - Each toxin enhances the action of the other toxin by mechanisms that are not understood

Diagnosis, Treatment, and Prevention of amebiasis

- identification of microscopic, spherical cysts or pleomorphic trophozoites recovered from either fresh stool specimens or intestinal biopsies - Microscopic analysis is necessary to distinguish amebic dysentery from bacterial dysentery - Serological identification of antigens may be used to distinguish E. histolytica from nonpathogenic amoebae. - Treatment involves oral rehydration therapy (vital in severe cases) and antiamebic drugs. - Iodoquinol and paromomycin are effective for asymptomatic infections. - Physicians may prescribe metronidazole followed by iodoquinol for symptomatic amebiasis. - Antibacterial agents may also be prescribed to prevent secondary bacterial infections. - Antidiarrheal medications should be avoided because they may worsen the condition by retaining the organism in the intestinal tract.

Pseudomembranous colitis

- inflammation of the colon, which is covered by a membrane consisting of connective tissue and dead/dying cells - condition is the last state of C. diff-associated diarrhea - life-threatening condition involves inflammation, more than 10 bloody stools per day, and formation of intestinal lesions called pseudomembranes, which are composed of connective tissue, dying leukocytes, and dead colon cells

Gingivitis

- inflammation of the gums - a form of Periodontal disease --> inflammation and infection of the tissues surrounding and supporting the teeth

Bacterial gastroenteritis

- inflammation of the stomach or intestines caused by the presence of bacteria - associated with poorly prepared foods, contaminated washing or drinking water, and communities with poor living conditions General features - Similar manifestations despite different causative agents - Nausea, vomiting, diarrhea, abdominal pain, and cramps - Dysentery produces loose, frequent stool containing mucus and blood - diagnosed by s/s - ID bacterium form stool samples or from suspected food - replace fluids and electrolytes

Signs and Symptoms of bacterial intoxications (toxifications) (food poisoning)

- may range from mild to severe - may differ depending on the toxins present - can be confused with bacterial or viral gastroenteritis - nausea, vomiting, diarrhea, abdominal cramping, discomfort, bloating, loss of appetite, and fever - Some types of intoxications also produce weakness, headache, and difficulty in breathing - Dehydration resulting from fluid loss in diarrhea may become significant, but most cases, exemplified by staphylococcal food poisoning, are self-limiting and last no more than 24 hours

Cryptosporidiosis

- protozoan disease - Severe watery diarrhea (~ 2 weeks) with potentially serious complications - Headache, muscular pain, cramping, nausea, fatigue, and severe fluid and weight loss accompany the diarrhea - Life-threatening malabsorption, hepatitis, and pancreatitis can complicate the disease. - Ampicomplexan Cryptosporidium parvum --> banana-shaped, gliding sporozoite that has an apical complex of organelles specialized for penetrating host cells; thus, it is an apicomplexan --> Sporozoites form thick-shelled oocysts, which are the infective stage, inside cells --> With a complex series of cell divisions and stages, oocysts eventually develop four internal sporozoites, which escape to continue the life cycle - Pathogenicity of C. parvum unclear, but suspected that death of infected cells causes electrolyte and water loss. - Infection results from drinking contaminated water - Treated with fluid and electrolyte replacement - Prevented with proper hygiene - may be fatal in HIV patients

Campylobacter Diarrhea

- responsible for more cases of diarrhea that send people to doctors in the United States than any other bacterium - Campylobacter jejuni --> Gram-negative, slightly curved bacterium with polar flagella --> adhesins, cytotoxins, and endotoxin - study found Campylobacter in 81% of chickens, which are the primary source of human infections - The virulence factors of Campylobacter enable colonization and invasion of the jejunum, ileum, and colon, producing bleeding lesions and triggering inflammation - Campylobacter infections sometimes trigger long-term consequences, such as arthritis or irritable bowel syndrome (IBS) --> 1/1000 cases leads to Guillain-Barre syndrome --> rare autoimmune disorder that damages nerves, resulting in muscle weakness and sometimes paralysis that can last for a few weeks or even for several years - Toxin A mediates inflammation and toxin B kills colon cells producing lesions pseudomembrane formation

Diagnosis, Treatment, and Prevention of Campylobacter Diarrhea

- s/s combined with bacteria in xTAG GPP analysis of stool - severe cases require supportive therapy and the use of antimicrobial drugs such as erythromycin - no vaccine

C. diff. (Antimicrobial-Associated) Diarrhea

- severe form of diarrhea, which is often accompanied by intense inflammation and formation of lesions in the colon, frequently develops in hospitalized patients taking antimicrobial drugs - ranges from 5 to 10 clear, watery, foul-smelling bowel movements per day to a most severe form of intestinal disease called Pseudomembranous colitis - Clostridioides difficile --> Gram-positive, endospore-forming, anaerobic bacillus is part of the normal microbiome of the large intestine - when antimicrobials kill the good bacteria, C. difficile endospores germinate and reproduce out of control, presumably because they have no competition - toxins A & B

Shigellosis

- severe form of dysentery - characterized primarily by fever, abdominal cramps, diarrhea, and sometimes a bloody stool - shigella; 4 types --> Gram-negative, nonmotile bacillus --> S. dysenteriae (produces shiga toxin, causes dysentary), S. flexneri (developing countries), S. boydii, and S. sonnei (in industrialized nations) (most common) - produce type III secretion systems and diarrhea-producing enterotoxins - insert into a host cell's cytoplasmic membrane, forming a channel through which bacterial proteins are introduced into the host cell - bind to surface proteins on epithelial cells lining the intestines, triggering the loss of electrolytes and water - S. dysenteriae secretes Shiga toxin, which is an exotoxin that stops protein synthesis in a host's cells, resulting in a more severe form of shigellosis with a mortality rate as high as 20%

Dysentery

- severe gastroenteritis - characterized by severe diarrhea, often with loose stools containing blood and mucus

Diagnosis, Prevention, and Treatment of C. diff. (Antimicrobial-Associated) Diarrhea

- test stool for Toxins A & B or use xTAG GPP to find C. difficile in the stool - colonoscopy can reveal the yellowish lesions of the pseudomembranes - prevention involves avoid unnecessary use, especially prolonged use, of antimicrobial drugs - endospores of Clostridium are resistant to most disinfectants; therefore, handwashing and wearing gloves are the cornerstones of prevention - Generally, cessation of the causative antimicrobial may be all that is necessary to restore the normal microbiome - Treatment for moderately severe cases entails the use of oral metronidazole or vancomycin - Antidiarrheal drugs should be avoided, because diarrhea is actually beneficial in that it dilutes and eliminates bacterial cells and their toxins - Physicians have successfully treated patients who have had recurrent C. diff. diarrhea with "fecal transplants." --> reestablishes the normal microbiome

The action of cholera toxin in intestinal epithelial cells.

1. Cholera toxin binds to membrane of epithelial cells 2. Portion of toxin (part of A) enters cell 3. A1 activates adenylate cyclase (AC) 4. Cyclic AMP (cAMP) is synthesized 5. Cyclic AMP stimulates cell to secrete Cl-, Na+, and other electrolytes 6. Water follows electrolytes to lumen

The role of Helicobacter pylori in the formation of ulcers

1. Helicobacter pylori neutralizes stomach acid, invades the mucus, and attaches to gastric epithelial cells. 2. Helicobacter, its toxin, and inflammation cause the layer of mucus to become thin. 3. Gastric acid destroys epithelial cells and underlying tissue.

Life cycle of Anisakis.

1. Marine mammals excrete eggs 2. Two larval stages develop inside eggs 3. eggs hatch and larvae swim freely 4. krill eat larvae 5. fish eat krill 6. fish eat fish 7a. Marine mammals eat infected fish. Larvae mature, mate, and lay eggs in intestine. 7b. Humans eat infected, raw, or undercooked fish and become accidental hosts

Life cycle of Taenia solium.

1. eggs and egg-filled proglottids are passed into environment in feces 2. Intermediate hosts ingest eggs on contaminated food 3. eggs hatch into larvae that penetrate the intestinal wall and migrate to other tissues 4. larva develops into a cysticercus in muscle 5. human ingests cysticercus in raw or undercooked contaminated meat 6. cysticercus excysts and attaches to mucosa of small intestine as a scolex, which matures 7. adult worm forms new proglottids 1. cycle repeats

Pathogenesis of Shigellosis

1. pathogen attaches to epithelial cells in the large intestine 2. shigella triggers endocytosis 3. shigella multiplies in cytosol 4. shigella invades neighboring epithelial cells, thus avoiding immune defenses --> polymerizes the host's actin fibers, propelling itself out of the host cell and into adjacent cells 5. an abscess forms as epithelial cells are killed by the infection 6. shigella that enters the blood is quickly phagocytized and destroyed. No bacteremia.

The events in salmonellosis.

1. salmonella attaches to epithelial cells lining the small intestine 2. salmonella triggers endocytosis 3. salmonella multiplies within food vesicle 4. Salmonella kills host cell, inducing fever, cramps, and diarrhea 5. Bacteremia: Salmonella Typhi and Paratyphi move into bloodstream and can become systemic (Typhoid Fever)

Review - Which pathogen causes extreme watery, colorless, odorless diarrhea, which can lead to dehydration and death within a day? A. Staphylococcus aureus. B. Salmonella enterica. C. Clostridium difficile. D. Vibrio cholerae.

D - The rapid loss of fluids can lead to shock and death within hours after onset of cholera.

Review - What is the difference between replication of Shigella and Salmonella in intestinal epithelial cells? A. Salmonella replicates in phagosomes (food vesicles), whereas Shigella replicates in the cytosol. B. Shigella can cause bacteremia, whereas Salmonella is usually phagocytized if it enters the bloodstream. C. Salmonella infects neighboring cells, whereas Shigella does not. D. Shigella triggers endocytosis upon attachment to intestinal epithelial cells, whereas Salmonella enters the cell directly.

A

Review - Which is the most common bacterium found in the oral cavity? A. Porphyromonas gingivalis. B. Clostridium difficile. C. Helicobacter pylori. D. Viridans streptococcus.

D - Viridans streptococci are alpha-hemolytic members of the genus Streptococcus and are the most common bacterium of the mouth

Oral Herpes - Which is the more likely cause of these lesions, HHV-1 or HHV-2?

Approximately 90% of oral herpes lesions are caused by human herpesvirus 1.

Review - What is dysentery? A. Severe diarrhea with vomiting. B. A severe diarrhea with blood and mucus. C. Severe diarrhea with rash. D. Severe diarrhea with fever.

B

Review - What is the "danger zone" in food preparation? A. A range of fecal matter concentrations in food that is likely to result in disease. B. A range of temperatures that are optimal for pathogen replication. C. A range of temperatures that is dangerous to pathogens, because it makes them easier to kill. D. A range of bacterial concentrations that is most likely to cause disease.

B - In the danger zone temperatures, pathogens divide rapidly.

Review - Why is the liver considered part of the digestive system? A. It produces hydrochloric acid, which limits microbial growth in the stomach. B. It produces bile, which helps digest fats. C. Food passes through the liver, which helps grind up the food. D. It produces gastric juices, which help digest food in the stomach.

B - The liver produces bile, which is excreted into the duodenum, where it breaks up fats

Review - How does Shiga toxin damage cells? A. It helps Shigella bacteria attach to host intestinal cells. B. It causes leakage of cell membranes so that cells die. C. It stops protein synthesis in cells, killing them. D. It damages mitochondria so that cells do not produce enough energy and subsequently die.

C

Review - Which disease does the acidophile Helicobacter pylori cause? A. Acute necrotizing ulcerative gingivitis. B. Periodontal disease. C. Peptic ulcers D. Osteomyelitis.

C

Review - Which organism causes the form of gastroenteritis known as traveler's diarrhea? A. Salmonella enterica. B. Shigella dysenteriae. C. Escherichia coli. D. Clostridium difficile.

C

Review - Which tissue does mumps virus infect? A. Liver. B. Intestinal cells. C. The salivary gland tissue. D. Epithelial cells near the lips.

C

Review - Which of these hepatitis viruses is transmitted more commonly through the fecal-oral route? A. Hepatitis C virus. B. Hepatitis D virus. C. Hepatitis A virus. D. Hepatitis B virus.

C - Hepatitis A virus is transmitted more commonly through consumption of food contaminated with fecal material containing hepatitis A virus.

Review - Which hepatitis virus causes most hepatitis deaths in the United States? A. Hepatitis A virus. B. Hepatitis B virus. C. Hepatitis C virus. D. Hepatitis E virus.

C - Hepatitis C virus kills 10,000 to 20,000 Americans each year.

Review - The environment inside the human intestinal tract lacks oxygen. Name all of the following groups of microbes can grow in the intestines. A. Obligate anaerobes and aerotolerant anaerobes. B. Obligate anaerobes and facultative anaerobes. C. Obligate anaerobes, facultative anaerobes, and aerotolerant anaerobes. D. Microaerophiles, obligate anaerobes, and facultative anaerobes.

C - Obligate anaerobes, facultative anaerobes, and aerotolerant anaerobes can all grow in the absence of oxygen. Obligate aerobes and microaerophiles require the presence of oxygen, whereas obligate anaerobes, facultative anaerobes, and aerotolerant anaerobes can all grow in the absence of oxygen.

Review - Which is the active, feeding stage of a protozoan? A. An apicomplexan. B. A cyst. C. A trophozoite. D. A mitosome.

C - The feeding stage of a protozoan is a trophozoite. The trophozoite is the active, feeding stage of protozoa that can cause disease.

Diagnosis, treatment, and prevention of Dental Caries, Gingivitis, and Periodontal Disease

Caries - Diagnosed by visual inspection - Treat by filling cavities if caught early Gingivitis - Diagnosed by inspection of gums - Treat by scaling and use of antibacterial rinses - Prevention involves good oral hygiene

Disease at a Glance - Caries (cavities)

Cause -- Bacteria, particularly Streptococcus mutans (Gram-positive coccus). Virulence factors -- Fimbriae and other adhesins; formation of biofilm called plaque and tartar; metabolizes sucrose into dextran; produces acid from sugars. Portal of entry -- Ingestion. Signs and symptoms -- Demineralization of tooth, resulting in pits and holes; tooth pain. Incubation period -- Acid production begins immediately. Susceptibility -- Everyone, especially people with a high-sucrose diet. Treatment -- Physical removal of plaque and tartar; filling of pits and holes. Prevention -- Avoidance of foods containing sucrose; regular tooth-brushing and flossing; fluoridation.

Disease at a Glance - Peptic Ulcer Disease

Cause -- Helicobacter pylori (Gram-negative, slightly helical motile bacterium). Virulence factors -- Flagella, adhesins, enzymes that inhibit phagocytosis, protein that blocks stomach acid production, urease. Portal of entry -- Probably through the mouth from fecal contamination of food or drink. Signs and symptoms -- Abdominal pain 30 minutes to several hours after eating or skipping a meal, pain that is relieved with antacids or milk, heartburn, indigestion, nausea, vomiting of blood, weight loss, fatigue, and dark or bloody stools. Incubation period -- Variable. Susceptibility -- Anyone who becomes colonized with H. pylori, particularly people with a family history of ulcers, who use tobacco, aspirin, ibuprofen, or other nonsteroidal anti-inflammatory medications, or who consume excessive alcohol. Treatment -- Amoxicillin and clarithromycin given in conjunction with acid-blocking drugs for one to two weeks. Prevention -- Good personal hygiene, adequate sanitation and proper food handling to decrease fecal-oral transmission, and lifestyle changes to reduce risk, including dietary changes to reduce stomach acid imbalances and reducing consumption of alcohol, tobacco, and aspirin-like pain medication.

Disease at a Glance - Viral Hepatitis

Cause -- Hepatitis A virus (naked, positive, single-stranded RNA virus); hepatitis B virus (enveloped, partly double-stranded DNA virus); hepatitis C virus (enveloped, positive, single-stranded RNA virus); hepatitis delta virus (delta agent) (incomplete negative, single-stranded RNA virus); hepatitis E virus (naked, positive, single-stranded RNA virus). Virulence factors -- Intracellular replication cycle, adhesins. Portal of entry -- A and E—ingestion via fecal-oral route; B, C, delta—parenteral (blood- and fluid-borne) transmission. Signs and symptoms -- Jaundice, fatigue, abdominal pain, loss of appetite, nausea, and diarrhea. Additional symptoms: A—fever; B—vomiting and joint pain; C—dark urine; delta—vomiting and dark urine, E—vomiting and dark urine. Incubation period -- A—15 to 45 days; B—70 to 100 days; C—42 to 49 days; delta—7 to 24 days; E—15 to 60 days. Susceptibility -- Adults generally display more symptoms than children do and are at greater risk because of behavioral activities, though children are more at risk for chronic infections and complications thereof. Treatment -- For all—supportive therapy and rest; also: A—anti-HAV immunoglobulin; B—alpha interferon, adefovir dipivoxil, and lamivudine; C—sofosbuvir, ribavirin, and ledipasvir; delta— control of HBV coinfection. Prevention -- Practice good hygiene and drink sterilized water, especially when traveling in areas endemic for hepatitis A and E. Limit activities where body fluids may be acquired (such as sexual intercourse, sharing needles) to help prevent transmission of hepatitis B, C, and delta. Vaccines against hepatitis A virus and hepatitis B virus are available.

Disease at a Glance - Mumps

Cause -- Mumps virus (enveloped, helical, unsegmented, negative, single-stranded RNA virus of genus Rubulavirus). Virulence factors -- Adhesins, intracellular replication cycle. Portal of entry -- Mucous membranes of the upper respiratory tract. Signs and symptoms -- Parotitis (swelling of the parotid salivary glands), face pain, fever, headache, and sore throat are the most common symptoms. Some infections may be asymptomatic. Incubation period -- 12-24 days. Susceptibility -- Unimmunized individuals are at risk. Treatment -- Comfort care only, including hot or cold packs, soft foods, fluids, and warm-water gargles. Prevention -- MMR vaccine.

Disease at a Glance - Salmonellosis and Typhoid Fever

Cause -- Serotypes Typhi or Paratyphi of Salmonella enterica (Gram-negative, peritrichous bacillus) cause typhoid fever; serotypes Enteritidis and Typhimurium commonly cause salmonellosis. Virulence factors -- More than 2000 serotypes; ability to tolerate low pH; adhesins; type III secretion system; toxins that disrupt mitochondria, inhibit phagocytosis, rearrange cytoskeletons of eukaryotic cells, or induce apoptosis. Portal of entry -- Mouth and mucous membranes of the intestine by fecal-oral transmission; this involves ingestion of food or water contaminated with sewage from a carrier or ingestion of food directly handled by an asymptomatic carrier. Signs and symptoms -- Gradually increasing fever, headache, muscle pains, malaise, and loss of appetite that may persist for a week or more; "rose spot" rash may appear on lower chest and abdomen. Gastrointestinal symptoms common to other forms of bacterial gastroenteritis may occur. With typhoid fever, life-threatening complications are possible, including intestinal hemorrhage, perforation, kidney failure, or peritonitis (inflammation of the peritoneum). Incubation period -- 8-48 hours. Susceptibility --Travel to countries lacking adequate sanitation; contact with asymptomatic carriers. Treatment -- Fluid and electrolyte replacement are indicated for salmonellosis; antimicrobials (a combination of ceftriaxone and ciprofloxacin is recommended) are used against typhoid fever. Carriers may require removal of the gallbladder to end carrier status. Prevention -- Proper and adequate sanitation and food handling, immunization for travelers to endemic areas, and preventing carriers from working as food handlers.​

Disease at a Glance - Staphylococcal Intoxication (Food Poisoning)

Cause -- Staphylococcus aureus (facultatively anaerobic, Gram-positive cells arranged in clusters). Virulence factors -- Heat-stable enterotoxins, salt tolerance Portal of entry -- Toxin crosses mucous membranes of the intestinal tract following consumption of contaminated food; Staphylococcus is not directly involved in the disease. Signs and symptoms Nausea, vomiting, diarrhea, cramping, discomfort, bloating, loss of appetite, and fever; all lasting 24 hours or less. Incubation Period -- Four to six hours. Susceptibility -- Everyone is susceptible because the organism is a normal member of the microbiome, but intoxication results only when inoculated food is improperly refrigerated or undercooked prior to consumption. Treatment -- Self-administered replacement of fluids and electrolytes. Prevention -- Thorough handwashing before and after handling foods, cleaning utensils between use on different foods, and prompt refrigeration of leftovers all decrease risk of staphylococcal food poisoning.

Disease at a Glance - Cholera

Cause -- Vibrio cholerae (comma-shaped Gram-negative bacillus). Virulence factors -- Type III secretion system, enterotoxins; cholera toxin. Portal of entry -- Ingestion of contaminated water or raw/undercooked seafood. Signs and symptoms -- Sudden onset of "ricewater" diarrhea, dehydration (dry skin, excessive thirst, rapid yet diminished pulse, lethargy, sunken eyes), abdominal cramps, nausea, and vomiting. Death can occur within hours; the mortality rate is 25-50% in untreated patients, reduced to 1% with treatment. Incubation period -- Generally two to three days, although an infected person may show symptoms in a few hours in some cases. Susceptibility -- Humans living in endemic areas, especially in poverty-stricken areas; children tend to be affected more than adults are. Treatment -- Fluid and electrolyte replacement and administration of doxycycline. Prevention -- When in endemic areas, boil water, eat only cooked food (especially seafood), avoid raw vegetables and fruit, and wash hands frequently. A vaccine against Vibrio cholerae is available.

Disease at a Glance - Bacterial Diarrhea

Causes -- Primarily Escherichia coli, Shigella spp., Campylobacter jejuni (Gram-negative bacilli), and Clostridioides difficile (Gram-positive, anaerobic, endospore-forming bacillus). Virulence factors -- Adhesins, enterotoxins, Shiga toxin, ability to evade phagocytosis, ability to move between adjoining cells (Shigella), Shiga-like toxin (Escherichia), endotoxin (Gram-negative bacteria), endospore (Clostridioides). Portal of entry -- Ingestion via fecal-oral route; C. difficile normally lives in 5% of Americans. Signs and symptoms -- Abdominal cramps, bloody stools, nausea, vomiting, and diarrhea; C. difficile can additionally cause pseudomembrane formation. Incubation period -- A few hours to days or weeks. Susceptibility -- All humans are susceptible, but Gram-negative infection is generally worse in children and immunocompromised individuals; C. diff. is more prevalent in patients undergoing antimicrobial treatment. Treatment -- Rehydration via fluid and electrolyte replacement; antimicrobials may shorten the duration. Prevention -- Eat only thoroughly cooked meat products and pasteurized milk and juices; serve food piping hot; and practice good hygiene.

Review - Which form of gastroenteritis is the most common reason people seek medical attention? A. Shigellosis. B. Pseudomembranous colitis. C. Typhoid fever. D. Campylobacter diarrhea.

D

Review - Which viral gastroenteritis can be prevented by immunization? A. That of astrovirus. B. That of sapovirus. C. That of norovirus. D. That of rotavirus.

D - A live attenuated vaccine protects against severe rotavirus cases.

Review - How can the bacteria that cause dental caries invade teeth? A. They have specialized structures that can invade the hardened teeth enamel. B. Teeth have tiny pores through which bacteria can gain access to the dentin underneath the tooth enamel and the pulp on the inside. C. They produce degradative enzymes that break down tooth enamel. D. They produce acid, which dissolves tooth enamel, giving bacteria access to dentin and the pulp inside it.

D - Bacteria that cause dental caries ferment sugars to produce acid, which damages teeth, allowing the bacteria to invade.

Review - What is the term used for viruses of eukaryotes that can remain in a cell for years without replicating until they are reactivated? A. Stasis. B. Persistence. C. Lysogeny. D. Latency.

D - Latent viruses can remain in the chromosomes of cells for an extended period of time. Latent viruses can remain inside the cell for an extended period of time without replicating until they are reactivated at a later date.

Pinworm Infestations

Pinworms are nematodes - Long, thin, unsegmented, cylindrical helminth - Perianal itching, irritability, decreased appetite - One-third of cases are asymptomatic - Caused by Enterobius vermicularis - Females deposit eggs in the perianal region at night - Eggs can be dislodged and spread the disease - Infections commonly occur in children - Enterobius is the most common parasitic worm in the U.S. - Diagnosis based on identification of eggs or adult pinworms - Treatment with pyrantel pamoate or mebendazole - Prevention requires strict personal hygiene

Salmonellosis and Typhoid Fever - points from book

❶ Salmonella is ingested in contaminated water or food, particularly chicken eggs. ❷ Bacterium passes through the stomach, attaches to cells lining the small intestine, and induces endocytosis. ❸ The pathogen eventually kills host cells. ❹ This triggers fever, abdominal cramps, and diarrhea. ❺ Cells of serotype Typhi can subsequently enter the blood, where they are phagocytized but not digested. ❻ Phagocytes carry Salmonella serotype Typhi to the liver, spleen, bone marrow, and gallbladder. ❼ Salmonella serotype Typhi can establish semipermanent infection in the gallbladder. Carriers can remain infected for years even with treatment. ❽ Salmonella is shed in feces.​