Lecture Review
Chapter 24 - Digestive System Infections
1. [24-01] Describe the benefits of having normal flora (microbiota) in the guts – Lecture 11, Slide 4 –
Due to sharing some antigenic properties with pathogens, microbial species of normal flora can train immune system and get it prepared to encounter real pathogens. Normal flora can also suppress growth of harmful microbes by masking binding sites, by using up of available nutrients, or even by direct killing of pathogens. Some bacterial species of normal flora are increasing the effectiveness of food digestion and nutrient extraction. Some bacteria of normal flora, like Escherichia coli, are producing vitamins (biotin and K) that are not produced by hosts but still required for host’s body functioning. It has been shown that some the microbial makeup of digestion system affects the body weight – Gram-negative bacteria can produce hormone-like molecules that direct the host to store more body fat.
Normal flora
Gram-negative: bacteroides, Escherichia
Gram-positive: bifidobacterium, clostridium, lactobacillus, peptococcus, peptostreptococcus, ruminococcus
Fungal: Aspergillus, candida, penicillium, saccharomyces
Due to sharing some antigenic properties with pathogens, microbial species of normal flora can train immune system and get it prepared to encounter real pathogens. Normal flora can also suppress growth of harmful microbes by masking binding sites, by using up of available nutrients, or even by direct killing of pathogens. Some bacterial species of normal flora are increasing the effectiveness of food digestion and nutrient extraction. Some bacteria of normal flora, like Escherichia coli, are producing vitamins (biotin and K) that are not produced by hosts but still required for host’s body functioning. It has been shown that some the microbial makeup of digestion system affects the body weight – Gram-negative bacteria can produce hormone-like molecules that direct the host to store more body fat.
Normal flora
Gram-negative: bacteroides, Escherichia
Gram-positive: bifidobacterium, clostridium, lactobacillus, peptococcus, peptostreptococcus, ruminococcus
Fungal: Aspergillus, candida, penicillium, saccharomyces
2. [24-02] Helicobacter pylori gastritis – Describe signs and symptoms. Describe etiological agent. Describe pathogenesis – Lecture 11, Slides 13, 14 –
Signs & Symptoms: Most cases asymptomatic. 2-4 days incubation. Symptoms develop IF stomach infection is advanced, complicated by (ulcers 20% of cases OR cancer 2% of cases). Advanced infection = Belching, bleeding, vomiting, abdominal pain.
Etiological agent: Helicobacter pylori – Gram-negative, Microaerophile, mobile (lophotrichous) short curved bacillus (epsilon-proteobacteria), alkalophilic
Etiological agent: Helicobacter pylori – Gram-negative, Microaerophile, mobile (lophotrichous) short curved bacillus (epsilon-proteobacteria), alkalophilic
Virulence factors: Urease (produces ammonia), LPS, various exotoxins (phospholipase, cytotoxins, VacA and CagA)
Pathogenesis: Early infection – Once in stomach, H. pylori buries into mucous layer and binds to cells of stomach lining → bacterial urease forms ammonia that neutralizes pH and disturbs tight junctions between epithelial cells → microbacterial phospholipase (Type II exotoxin) causes apical membrane of epithelial cells and mucus cells → cytotoxins VacA and CagA further degrade epithelial cells → Bacterial LPS shows similarities to mucous produced by stomach lining = decrease phagocytosis from immune system WBC → Chronic inflammation and inhibition of mucous production → Stomach lining exposed to acid → killing off epithelial and mucous cells leading to ulcer formation (possibly cancer later).
Pathogenesis: Early infection – Once in stomach, H. pylori buries into mucous layer and binds to cells of stomach lining → bacterial urease forms ammonia that neutralizes pH and disturbs tight junctions between epithelial cells → microbacterial phospholipase (Type II exotoxin) causes apical membrane of epithelial cells and mucus cells → cytotoxins VacA and CagA further degrade epithelial cells → Bacterial LPS shows similarities to mucous produced by stomach lining = decrease phagocytosis from immune system WBC → Chronic inflammation and inhibition of mucous production → Stomach lining exposed to acid → killing off epithelial and mucous cells leading to ulcer formation (possibly cancer later).
3. [24-03] Helicobacter pylori gastritis – Describe epidemiology. Describe prevention and treatment – Lecture 11, Slide 15 –
Epidemiology: Contagious, non-notifiable disease.
Reservoir: humans.
Transmission – Fecal-oral + oral route (vehicle – contaminated food; vector – houseflies)
Number of cases reported – ≤ 70% of population infected in developing countries, ≤ 40% of pop in US infected. Incidence rate directly related to age.
Mortality rate – About 2-4% of infected die due to complications.
Diagnostics:Fecal antigen assay, Urea breath test, biopsy
Prevention: NO proven preventative measures besides good hygiene?
Treatment: Antibiotics + antacid (antacid stabilizes the antibiotic in the stomach).
Usually easily treated by 2-week course of combined: proton pump inhibitor (antacid), clarithromycin OR amoxicillin/bismuth.
Epidemiology: Contagious, non-notifiable disease.
Reservoir: humans.
Transmission – Fecal-oral + oral route (vehicle – contaminated food; vector – houseflies)
Number of cases reported – ≤ 70% of population infected in developing countries, ≤ 40% of pop in US infected. Incidence rate directly related to age.
Mortality rate – About 2-4% of infected die due to complications.
Diagnostics:Fecal antigen assay, Urea breath test, biopsy
Prevention: NO proven preventative measures besides good hygiene?
Treatment: Antibiotics + antacid (antacid stabilizes the antibiotic in the stomach).
Usually easily treated by 2-week course of combined: proton pump inhibitor (antacid), clarithromycin OR amoxicillin/bismuth.
[24-04] Mumps – Describe signs, symptoms. Describe etiological agent – Lecture 11, Slide 16 –
Signs & Symptoms: Incubation 15-20 days. Starts loss of appetite, headache, fever → Painful swelling of parotid gland w/ earache, pain experienced during talking or chewing (usually last for 1 week for prepubescent) → For puberty/postpubescent = Men suffer from orchitis (swelling of testicles, may lead to sterility), 20% of women suffer from pelvic pain b/c ovary involvement.
*Pregnant women often miscarry.
Signs & Symptoms: Incubation 15-20 days. Starts loss of appetite, headache, fever → Painful swelling of parotid gland w/ earache, pain experienced during talking or chewing (usually last for 1 week for prepubescent) → For puberty/postpubescent = Men suffer from orchitis (swelling of testicles, may lead to sterility), 20% of women suffer from pelvic pain b/c ovary involvement.
*Pregnant women often miscarry.
Possible complications for elderly: meningitis, sudden onset of deafness, death
Etiological agent: Mumps virus – paramyxovirus, enveloped single-stranded (-) RNA genome
Etiological agent: Mumps virus – paramyxovirus, enveloped single-stranded (-) RNA genome
Virulence factors: Double layered envelope.
[24-05] Mumps – Describe pathogenesis. Describe epidemiology – Lecture 11, Slide 17
Pathogenesis: First infects upper respiratory system → replicates in nasopharynx asymptomatically → enters circulatory system and delivered to parotid gland or organs → signs & symptoms resulting from replicating virus that causes strong inflammation reaction → swelling and pain → dying cells are released in large amounts in virus in saliva and urine.
Epidemiology: Communicable, notifiable disease.
Reservoir: humans.
Pathogen does NOT cross placenta.
Transmission – Respiratory droplets (airborne).
Number of cases reported – (2015) 400,000 cases reported worldwide.
Mortality rate – 1 per 100,000 cases
Pathogenesis: First infects upper respiratory system → replicates in nasopharynx asymptomatically → enters circulatory system and delivered to parotid gland or organs → signs & symptoms resulting from replicating virus that causes strong inflammation reaction → swelling and pain → dying cells are released in large amounts in virus in saliva and urine.
Epidemiology: Communicable, notifiable disease.
Reservoir: humans.
Pathogen does NOT cross placenta.
Transmission – Respiratory droplets (airborne).
Number of cases reported – (2015) 400,000 cases reported worldwide.
Mortality rate – 1 per 100,000 cases
4. [24-06] Mumps – Describe prevention and treatment – Lecture 11, Slide 18 –
Prevention: Quarantine (for 5 days post-onset of symptoms), MMR vaccine (attenuated mumps vaccine part of combo)
Treatment: No treatment. Disease takes course till immune system mounts a response.
Prevention: Quarantine (for 5 days post-onset of symptoms), MMR vaccine (attenuated mumps vaccine part of combo)
Treatment: No treatment. Disease takes course till immune system mounts a response.
5. [24-07] Describe common characteristics of bacterial infections of lower digestive system – Lecture 11, Slide 19 –
Most common S/S: Short incubation (1-2 days), Diarrhea, loss of appetite, nausea, vomiting
Etiological agents: Mostly enteric bacteria (enterobacteriacea of gamma-proteobacteria) and other non-enteric bacteria (Campylonbacter jejuni, Vibro cholera, Clostridium difficile)
Pathogenesis: Bacteria attach to epithelium using adhesins localized on pili → produce enterotoxins are causing intestinal cells to lose water and electrolytes (diarrhea), some microbes use type III secretion system to manipulate intestinal cells.
Epidemiology: Diseases spread through fecal-oral route through contaminated food/water.
Prevention: Active hand washing, control of water & food supply, few vaccines available (not effective).
Treatment: Oral rehydration therapy, antibiotics are usually not used b/c they suppress normal flora.
Most common S/S: Short incubation (1-2 days), Diarrhea, loss of appetite, nausea, vomiting
Etiological agents: Mostly enteric bacteria (enterobacteriacea of gamma-proteobacteria) and other non-enteric bacteria (Campylonbacter jejuni, Vibro cholera, Clostridium difficile)
Pathogenesis: Bacteria attach to epithelium using adhesins localized on pili → produce enterotoxins are causing intestinal cells to lose water and electrolytes (diarrhea), some microbes use type III secretion system to manipulate intestinal cells.
Epidemiology: Diseases spread through fecal-oral route through contaminated food/water.
Prevention: Active hand washing, control of water & food supply, few vaccines available (not effective).
Treatment: Oral rehydration therapy, antibiotics are usually not used b/c they suppress normal flora.
[24-08] Cholera – Describe signs and symptoms, and etiological agent – Lecture 11, Slide 21 –
Signs & Symptoms: Most cases mild symptoms OR asymptomatic.
5-10% people have severe cholera: Vomiting, rapid heart rate, profuse watery diarrhea (rice-water stool), loss of skin elasticity, dry mucous membranes, low BP, thirst, restlessness
IF untreated severe dehydration and electrolyte imbalance can lead to shock and death.
Etiological agent: Vibrio cholerae – Non-enteric bacteria of gamma-proteobacteria
Signs & Symptoms: Most cases mild symptoms OR asymptomatic.
5-10% people have severe cholera: Vomiting, rapid heart rate, profuse watery diarrhea (rice-water stool), loss of skin elasticity, dry mucous membranes, low BP, thirst, restlessness
IF untreated severe dehydration and electrolyte imbalance can lead to shock and death.
Etiological agent: Vibrio cholerae – Non-enteric bacteria of gamma-proteobacteria
Virulence factors: Type III A-B exotoxin = Cholera toxin (only possible if lysogenic for CTX-phi virus)
6. [24-09] Cholera – Describe pathogenesis – Lecture 11, Slide 22 –
Pathogenesis: Lysogenic V. cholerae (infected with CTX-phi virus) → Enters mouth → since bacteria sensitive to acid (requires large number of cells, ID50 = 100*106 cells) → V. cholerae binds to epithelial cells of small intestine → Produced cholera A-B toxin enters epithelial cell and increases adenylate cyclase (enzyme producing cAMP) → Increased cAMP level causes excessive loss of fluids and electrolytes → epithelial cells secrete large amount of Cl- ions, with water following via osmosis → Infected person may lose 20L of fluid.
7. [24-10] Cholera – Describe epidemiology. Describe prevention and treatment – Lecture 11, Slides 22, 24 –
Epidemiology: Communicable, notifiable.
Reservoir: Water contaminated with human feces, vegetables fertilized with human feces, contaminated brackish water (shellfish, crab, and plankton from these waters).
ID50 = 100*106 vibrios → IF taking antacids ID50 = 0.01*106 microbes)
Transmission – Fecal-oral route
Number of cases reported – < 10 cases reported every year in US. 100,000 worldwide/yr
Mortality rate – 1.2% fatality rate (Haiti cholera outbreak)
Prevention: Adequate sanitation, safe chlorinated water supplies, oral vaccine (against B-subunit cholera toxin), travelers should practice good hygiene and eat safe food.
Treatment: Oral/intraveinous rehydration with electrolyte replenishment, zinc treatment significantly reduces stool volume and shortens diarrhea.
Epidemiology: Communicable, notifiable.
Reservoir: Water contaminated with human feces, vegetables fertilized with human feces, contaminated brackish water (shellfish, crab, and plankton from these waters).
ID50 = 100*106 vibrios → IF taking antacids ID50 = 0.01*106 microbes)
Transmission – Fecal-oral route
Number of cases reported – < 10 cases reported every year in US. 100,000 worldwide/yr
Mortality rate – 1.2% fatality rate (Haiti cholera outbreak)
Prevention: Adequate sanitation, safe chlorinated water supplies, oral vaccine (against B-subunit cholera toxin), travelers should practice good hygiene and eat safe food.
Treatment: Oral/intraveinous rehydration with electrolyte replenishment, zinc treatment significantly reduces stool volume and shortens diarrhea.
8. [24-addition1] Shigellosis – Describe signs & symptoms, and etiological agent.
Sign & symptoms: Incubation 12hrs – 4days, symptoms last 7 days (severity depends on strain causing disease). Watery, bloody/mucoid diarrhea + fever, stomach cramps, nausea, vomiting → complications: seizures, post-infectious arthritis
Etiological agent: Shigella spp – gamma-proteobacteria, Gram-negative, facultative anaerobe bacillus, usually non-motile outside of cells → can form flagella under certain conditions.
Virulence factors: Heat-stable endotoxin (LPS) & heat-sensitive shiga exotoxins (Stx)
Sign & symptoms: Incubation 12hrs – 4days, symptoms last 7 days (severity depends on strain causing disease). Watery, bloody/mucoid diarrhea + fever, stomach cramps, nausea, vomiting → complications: seizures, post-infectious arthritis
Etiological agent: Shigella spp – gamma-proteobacteria, Gram-negative, facultative anaerobe bacillus, usually non-motile outside of cells → can form flagella under certain conditions.
Virulence factors: Heat-stable endotoxin (LPS) & heat-sensitive shiga exotoxins (Stx)
9. [24-addition2] Shigellosis – Describe pathogenesis.
Pathogenesis: Bacteria taken up by M cells of large intestine in “antigen sampling” → M cells transport Shigella beneath epithelium & present to macrophage → shigella avoids digestion and kills macrophage → Freed Shigella binds to epithelial cell and enters via direct uptake (type III secretion system) → Microbe multiples in host cell & moves via polymerization of “actin tails” → Force from actin tails enough to propel microbe into neighboring cell → produced toxins and inflammation reaction kill infected cells.
Pathogenesis: Bacteria taken up by M cells of large intestine in “antigen sampling” → M cells transport Shigella beneath epithelium & present to macrophage → shigella avoids digestion and kills macrophage → Freed Shigella binds to epithelial cell and enters via direct uptake (type III secretion system) → Microbe multiples in host cell & moves via polymerization of “actin tails” → Force from actin tails enough to propel microbe into neighboring cell → produced toxins and inflammation reaction kill infected cells.
10. [24-addition3] Shigellosis – Describe epidemiology.
Epidemiology: Contagious, notifiable disease
Natural reservoir: Humans and apes
Transmission – Oral-fecal route: direct (hand shake), indirect contacts (fomites), contaminated food and water.
Number of cases reported – USA = 15,000-35,000 cases/yr; Global = 80-165million cases
Mortality –Up to 1,000,000 deaths global annually.
Epidemiology: Contagious, notifiable disease
Natural reservoir: Humans and apes
Transmission – Oral-fecal route: direct (hand shake), indirect contacts (fomites), contaminated food and water.
Number of cases reported – USA = 15,000-35,000 cases/yr; Global = 80-165million cases
Mortality –Up to 1,000,000 deaths global annually.
11. [24-addition4] Shigellosis – Describe Prevention and treatment.
Prevention: Over 50 known species of Shigella (no vaccine available). Best prevention is sanitary measures (hand washing, surveillance of food handlers and waters).
IF traveling – avoid street vendors, avoid food consumed raw, peel fruit yourself
Treatment: Usually shigellosis will resolve within 4-7days. Intravenous fluid and electrolyte replacement required.
Antimicrobial treatment IF given early can shorten duration of symptoms and carrier state. However, 20% of shigella strains are reported to be antibiotic-resistant.
Prevention: Over 50 known species of Shigella (no vaccine available). Best prevention is sanitary measures (hand washing, surveillance of food handlers and waters).
IF traveling – avoid street vendors, avoid food consumed raw, peel fruit yourself
Treatment: Usually shigellosis will resolve within 4-7days. Intravenous fluid and electrolyte replacement required.
Antimicrobial treatment IF given early can shorten duration of symptoms and carrier state. However, 20% of shigella strains are reported to be antibiotic-resistant.
Chapter 25 - Blood and Lymphatic Infections
[25-01] Plague – Describe signs and symptoms. Describe etiological agent – Lecture 11, Slides 38, 39 –
Signs & Symptoms: Bubonic plague – Contracted via infected flea bite → 1-6 days enlargement of lymph nodes → high fever, delirium, patchy bleeding under skin.
Pneumonic plague – Contracted via respiratory droplets → within 1-3 days development of cough, high fever, delirium, pneumonia, blood in sputum, rapid shock, death.
Septicemic plague – Develops when microbe enters bloodstream causes shock, disseminated intravascular coagulation, skin bleeding leading to red, black patchy rash.
Etiological agent: Yersinia pestis – Gram-negative, facultative anaerobic bacillus of Enterobacteriacae family
Signs & Symptoms: Bubonic plague – Contracted via infected flea bite → 1-6 days enlargement of lymph nodes → high fever, delirium, patchy bleeding under skin.
Pneumonic plague – Contracted via respiratory droplets → within 1-3 days development of cough, high fever, delirium, pneumonia, blood in sputum, rapid shock, death.
Septicemic plague – Develops when microbe enters bloodstream causes shock, disseminated intravascular coagulation, skin bleeding leading to red, black patchy rash.
Etiological agent: Yersinia pestis – Gram-negative, facultative anaerobic bacillus of Enterobacteriacae family
Virulence factors: Capsule, biofilm, chromosome PsaA protein (adhesin), for pathogenic variant needs to carry all three plasmids that contain genes for F1 (part of capsule), Pla (plasminogen that destroys C3b, C5a, clots), V antigen (control type III secretion system), YOP proteins (interferes with phagocytosis and immune response).
12. [25-02] Plague – Describe pathogenesis – Lecture 11, Slide 39 –
Pathogenesis: Yersinia pestis forms biofilm and blocks digestive tract of infected flea → starves flea and forces it to bite more frequently → pathogen enters humans via flea bite from infected flea → Pla prevents formation of clots and inactivates C3b and C5a, preventing opsonization, MAC formation and inflammation reaction → microbe enters local lymph nodes where they are taken up by macrophages → bacteria replicate inside macrophages → acute inflammation reaction develops in lymph nodes forming “buboes” characteristic of plague → infected macrophages die and release bacteria → infected lymph nodes may become neurotic and release large number of bacterial cells into blood stream → turns bubonic plague, septicemic w/ symptoms of skin hemorrhage, shock, disseminated, intravascular, coagulation, and death. (In 20% of cases infection spreads to lungs turning non-contagious bubonic plague into highly contagious pneumonic plague).
13. [25-03] Plague – Describe epidemiology. Describe prevention and treatment – Lecture 11, Slide 39 –
Epidemiology: Communicable, notifiable zoonosis.
Reservoir: Rodents, prairie dogs (US)..
Transmission – Infected flea bite (bubonic plague) or Respiratory droplets (pneumonic plague)
Number of cases reported – 7 cases annually US, Internationally occurs mostly in Africa and Madagascar.
Mortality rate – 66% w/o antibiotics, 8-10% w/ antibiotics
Prevention: NO vaccine available. Rodent control to prevent infected flea spread. Tetracycline prescribed as prophylaxis to those exposed to infection.
Treatment: Disease easily treated by antibiotics (tetracycline, ciprofloxacin, gentamycin) IF given within 24 hours of onset of signs and symptoms.
Epidemiology: Communicable, notifiable zoonosis.
Reservoir: Rodents, prairie dogs (US)..
Transmission – Infected flea bite (bubonic plague) or Respiratory droplets (pneumonic plague)
Number of cases reported – 7 cases annually US, Internationally occurs mostly in Africa and Madagascar.
Mortality rate – 66% w/o antibiotics, 8-10% w/ antibiotics
Prevention: NO vaccine available. Rodent control to prevent infected flea spread. Tetracycline prescribed as prophylaxis to those exposed to infection.
Treatment: Disease easily treated by antibiotics (tetracycline, ciprofloxacin, gentamycin) IF given within 24 hours of onset of signs and symptoms.
14. [25-Addition1] Infectious mononucleosis – Describe signs & symptoms.
Signs & Symptoms: Long Incubation of 30-60 days. Fever, sore throat covered in pus, fatigue, enlarged lymph nodes and spleen → fever and sore throat disappear within 2 weeks → lymph node enlargement disappears within 3 weeks → in general complete recovery 4 weeks, severe exhaustion and difficulty concentrating may last for months.
Etiological agent: Epstein-barr virus – double stranded, enveloped virus.
Virulence factors: (generic)Has antigens that allow the microbe to bind to the host organism.
Signs & Symptoms: Long Incubation of 30-60 days. Fever, sore throat covered in pus, fatigue, enlarged lymph nodes and spleen → fever and sore throat disappear within 2 weeks → lymph node enlargement disappears within 3 weeks → in general complete recovery 4 weeks, severe exhaustion and difficulty concentrating may last for months.
Etiological agent: Epstein-barr virus – double stranded, enveloped virus.
Virulence factors: (generic)Has antigens that allow the microbe to bind to the host organism.
15. [25-04] Infectious mononucleosis – Describe pathogenesis – Lecture 11, Slides 40, 41 –
Pathogenesis: Virus infects and kills epithelial cells of mucous membrane in throat and mouth (causes pharyngitis) → replicating virus enters lymphatic system → retained in lymph nodes → some virions escape and enter bloodstream → infects B cells randomly → two opportunities (productive infection/non-productive infection) → Productive infection: infected cell is quickly killed by cytotoxic T cells OR Non-productive infection: virus turns into provirus and immortalizes the B cell → actively replicates forming multiple cells that undergo differentiation to produce antibodies → forms large variety of antibodies randomly (called heterophiles) not needed by body → production of large quantities of antibodies that recognize different antigens, even self-antigens → increased risk of autoimmune diseases (lupus, MS, rheumatoid arthritis, IBD, celiac disease, DM1).
[25-05] Infectious mononucleosis – Describe epidemiology. Describe prevention and treatment – Lecture 11, Slide 42 –Epidemiology: Contagious, notifiable disease.
Reservoir: humans ONLY.
Transmission – Oral route with infected saliva, mouth-to-mouth kissing, can persist up to 18months in saliva.
Number of cases reported – Distributed world wide, particularly in crowded disadvantaged areas, occurs almost exclusively in those who lack immunity.
Mortality rate – 1% disease rarely causes death. Deaths mostly due to complications.
Prevention: NO vaccine. Avoid exposure with saliva of another person.
Treatment: Acyclovir inhibits productive infection. NO activity on latent virus.
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