1. Chapter 23 Infectious Diseases Affecting the Gastrointestinal Tract

2. Gastrointestinal tract
Mouth
Pharynx
Esophagus
Stomach
Small intestine
Large intestine
Rectum
Anus

3. Figure 23.1 Major structures of the digestive system
Uvula
Tongue
Teeth
Salivary glands
Pharynx
Mouth
Esophagus
Liver
Stomach
Pancreas
Gallbladder
Transverse colon
Duodenum
Ascending colon
Small intestine
Large intestine
Jejunum
Descending colon
Ileum
Sigmoid colon
Rectum
Anus

4. Protection Intestinal surfaces - layer of mucus Secretory IgA
Muscular walls (peristalsis)
Saliva
Stomach acid
Bile
Gut-associated lymphoid tissue (GALT)
Commensal or normal flora

5. Normal flora Numerous species present Oral cavity
Bacteria
Fungi
Protozoa
Oral cavity
more than 550 species of bacteria
Stomach and small intestine
sparsely populated
Large intestine
more than 1011 per gram of contents

6. Diseases Tooth and gum infections Mumps Gastritis and ulcers
Acute Infectious Diarrhea
Acute diarrhea with vomiting
Chronic diarrhea
Hepatitis
Helminthic intestinal infections
Liver and intestinal disease
Muscle and Neurological Symptoms
Liver disease

7. Tooth and gum infections
Dental caries
Periodontal diseases

8. Dental caries Bacterial infection Most common infection
Dissolution of solid tooth surface
Carbohydrates are fermented by bacteria and produce acids

9. Dental Caries/Trench mouth
Streptococcus mutans
The most common communicable disease.
Sucrose fermentation is the culprit.
Prevention = good dental hygiene.
Trench mouth – acute necrotizing ulcerative gingivitis
Treponema vincenti
Necrosis, pain chewing ,
foul odor, fever.

10. The different stages of plaque development, and the degrees of cariogenesis.
Fig stages in plaque development and cariogenesis.

11. Vegetable dye staining tablets enables macroscopic detection of plaque, while microscopic detection by SEM reveals a mixed bacterial aggregate.
Fig The macroscopic and microscopic appearance
of plaque.

12. Features of dental caries.
Checkpoint 22.1 Dental caries

13. Periodontal diseases Periodontitis
Necrotizing ulcerative gingivitis and periodontitis

14. Periodontitis Communities of different bacterial species
Gingivitus – early infection
Periodontitis – late or more serious infection
Plaque
Caculus

15. Necrotizing ulcerative gingivitis and periodontitis
Community of different bacterial species
Severe condition
Synergistic
At risk - poor hygiene, AIDS patients, diabetes, smoking

16. The stages involved in the formation of periodontitis.
Fig Stages in soft-tissue infection, gingivitis, and
Peroidontitis.

17. A radiograph of teeth showing calculus, caries, and bone destruction.
Fig The nature of calculus.

18. Features of periodontal diseases.
Checkpoint 22.2 Periodontal diseases

19. Oral Candidiasis “thrush”
Candida albicans (opportunistic normal flora)
Symptoms: white growths that when scraped off reveal angry red tissue underneath.
Circumstances reduced immunity, antibiotics, pregnancy
Treatment over the counter treatment and prescriptions.

20. Mumps Viral infection Classic gopherlike swelling of the cheeks
Humans are exclusive natural host
Parotitis
Syncytium
Vaccine
Complications

21. Mumps Mumps virus Respiratory droplets
Symptoms- swelling of parotids and other salivary glands, fever, mild pain. Brain and testes can be involved.
MMR vaccination
40 years ago, very common, now usually rare

22. The classic swelling of the cheeks or parotitis.
Fig The external appearance of swollen parotid glands in
Mumps.

23. Paramyxoviruses infect host cells, cause multinucleated cells or syncytia, which enable viruses to pass from an infected cell to noninfected cells.
Fig The effects of paramyxoviruses.

24. Features of mumps.
Checkpoint 22.3 mumps

25. Gastritis and gastric ulcers
Bacterial infection (Caused by Helicobacter pylori)
Pain and lesions (peptic ulcers) in the abdomen
Common for blood type O individuals
Bacteria neutralizes stomach acid environment
Immune response damages epithelium
Possibly zoonotic

26. Stomach Ulcers - gastritis
Inflammation of the gastric lining.
Survives the acidity with urease changes urea into ammonia to neutralize the acid.
Flagella enable burrowing through stomach lining
Adhesins facilitate attachment to gastric cells
Pain, gastric bleeding.
Rx – antibiotics, possibly an acid blocker (Pepcid, Zantac, Tagamet)

27. An endoscope is used to visualize the lesions caused by Helicobacter pylori, causative agent of peptic ulcers.
Fig endoscopy

28. Acute infectious diarrhea
Bacterial infection
Common nonbacterial infection
HKO antigens
Common among population – particular day care centers
Developing countries – serious health effects, fatal
In the U.S., 1/3 due to contaminated food

29. HKO antigens H = flagellar antigen K= capsular antigen
O= cell wall antigen
Ex. E. coli O157:H7

30. Bacterial Salmonella Shigella Shiga-toxin producing Escherichia coli
Non-shiga-toxin E. coli
Campylobacter
Yersinia
Clostridium difficile
Vibrio cholerae

31. Salmonella Contaminated animal products Salmonellosis - mild
Typhoid fever – severe
Normal flora in animals

32. Shigella Primarily a human parasite Infects the large intestine
No perforation of intestine
Dysentery
Exotoxin (shiga-toxin)
Enterotoxin

33. Shigellosis (dysentery)
Shigella species (dysenteriae) Shiga toxins. Goes into intestinal epithelial tissue by phagocytosis, then produces toxins
Fecal to Oral route transmission (only 200 cells needed for infection)
Fever abdominal pain, possible seizures, extreme fluid loss, extreme dehydration resulting in decreased blood pressure and shock.

34. Poor sanitation, cleanliness, lack of clean drinking water are to blame
Antibiotics/re-hydration therapy

35. Shiga-toxin (E. coli) O157:H7 Enterohemorrhagic E. coli (EHEC)
Serious manifestations – hemolytic uremic syndrome, neurologic symptoms
Shiga-toxin gene present on bacteriophage genome
Type III secretion system

36. Non-shiga-toxin (E. coli)
Enterotoxigenic – traveler’s diarrhea
Enteroinvasive – no exotoxin
Enteropathogenic – similar to EHEC
Enteroaggregative – chronic diarrhea

37. Campylobacter Most common bacterial cause of diarrhea
Related to Guillain-Barre syndrome (GBS) – paralysis

38. Campylobacter jejuni has a unique S-shaped and spiral morphology, and is closely related to H. pylori.
Fig Scanning micrograph of Campylobacter jejuni,
Showing comma, S, and spiral forms.

39. Yersinia High degree of abdominal pain Mistaken for appendicitis
Infects the small intestine
Some can affect the lymphatic system (intracellular)

40. Clostridium difficile
Pseudomembranous colitis or antibiotic associated colitis
Capable of superinfecting the large intestine due to drug treatments
Enterotoxins

41. A mild and more severe case of antibiotic-associated colitis.
Fig Antibiotic-associated colitis.

42. Figure 23.9 Pseudomembranous colitis
Lesions

43. Vibrio cholerae Cholera Unique O and H antigens
Cholera toxin (CT) – A-B toxin
Bacteria never enter host cells
Heavy lost of fluid “rice-water stool”
Untreated cases can be fatal

44. Vibrio cholerae has a unique curved shaped and single polar flagellum.
Fig Vibrio cholerae

45. Common nonbacterial
Cryptosporidium
Rotavirus

46. Cryptosporidium Protozoan infection Zoonotic Oocysts Intracellular
AIDS patients are at risk
Associated with fresh water outbreaks

47. Acid-fast staining enables oocysts to be identified, as they stain red or purple.
Fig Acid-fast stain in Cryptosporidium

48. A SEM of Cryptosporidium shows attachment to the intestinal epithelium, prior to intracellular invasion.
Fig Scanning electron micrograph of Cryptosporidium

49. Rotavirus Responsible for most morbidity and mortality from diarrhea
Babies lacking maternal antibodies are at risk
Unique morphological appearance

50. Figure 23.14 Deaths from rotaviral diarrhea are most common in developing countries

51. Viral gastroenteritis, Rotavirus
Characterized by watery diarrhea, fever, vomiting. Fecal to oral route. Best prevention handwashing. Common in school age children.

52. A feces sample containing Rotavirus, which has a unique “spoked-wheel” appearance.
Fig Rotavirus visible in a sample of feces from
A child with gastroenteritis.

53. Features of acute diarrhea.
Checkpoint 22.5 Acute diarrhea

54. Acute diarrhea with vomiting
Food poisoning - toxin
Staphylococcus aureus
Bacillus cereus
Clostridium perfringens

55. Features of acute diarrhea with vomiting.
Checkpoint 22.6 Acute diarrhea with vomiting

56. Chronic diarrhea Enteroaggregative (EAEC) E. coli
Cyclospora cayetanensis
Giardia lamblia
Entamoeba histolytica

57. The protozoan Giardia is typically transmitted by its cysts, which eventually germinates into the trophozoite and damages the jejunum.
Fig The “face” of a Giardia lamblia trophozoite.

58. Giardiasis Giardia lamblia Fecal to oral route,
2 weeks after infection severe cramping, explosive diarrhea, foul smelling gas.
Resistant to chlorine, Day care centers, camping
Metronidazole and quinacrine

59. Features of chronic diarrhea.
Checkpoint 22.7 Chronic diarrhea.

60. Hepatitis Viral infection Inflammation of the liver Jaundice
Hepatitis A
Hepatitis B
Hepatitis C
Inflammation of the liver
Jaundice
Noninfectious conditions can cause hepatitis

61. Hepatitis A virus Low virulence Poor hygiene – fecal-oral
Developed countries – adult
Developing countries- child
Vaccine
Similar to Hepatitis E – pregnant women are at risk

62. Hepatitis B virus High virulence Serum hepatitis Cirrhosis
Dane particle
S antigen
Chronic infection – particularly children
Associated with hepatocellular carcinoma

63. Hepatitis C virus “Silent epidemic” – symptoms not seen for years
Blood contact
Chronic
No vaccine
Liver transplants
Associated with cancer

64. Hepatitis
Hepatitis A – Fecal to oral route. Jaundice, fatigue, loss of appetite, vomiting. Body recovers. 2 vaccines.
Hepatitis B – Blood and sexual contact. Like A but can cause cancer and liver failure, 6% chronic infection. Vaccine is now routine.
Hepatitis C – mostly blood rather than sexual contact % of patients will develop chronic liver disease, symptoms appear about 6 months after infection.

65. Helminthic intestinal infections
Various parasites
Small roundworms to large tapeworms
Eosinophilia
Four major life cycles
Definitive host
Intermediate host
Antihelminthic therapy
Intestinal distress
Intestinal distress with migratory symptoms

66. Examples of four basic helminth life and transmission cycles.
Fig Four basic helminth life and transmission cycles.

67. Pinworms
Enterobius vermicularis – (pin worms) most common worm, 30% of kids and 16 % of adults are infected. Lives in the rectum and exits the anus to deposit eggs.
mebendazole, pyrantel pamoate
Anal itching,
(scotch tape)

68. Figure 23.18 Features of tapeworm morphology-overview

69. An example of the unique morphology of tapeworms, which includes a sucker and hooklets, and the extensive length.
Fig Tapeworm characteristics.

70. Helminthic Infestations of the Intestinal Tract
Tapeworm Infestations
Signs and symptoms
Usually asymptomatic
Nausea, abdominal pain, weight loss, and diarrhea may occur
Pathogens
Taenia saginata – beef tapeworm
Taenia solium – pork tapeworm
Life cycle divided between a primary and intermediate host
© 2012 Pearson Education Inc.

71. Ascariasis Fecal oral route
Asymptomatic, coughing, bile duct or intestinal obstruction
Good hygiene, mebendazole pyrantel pamoate
Wash fruits and vegetables well!! Contaminated soil
Weird life cycle

72. Migration of some helminths is due to their hook or oral cutting plates which anchors it to the host intestinal villi.
Fig Cutting teeth on the mouths

73. Hookworm Necator (hookworm)
Very small worms, continually take blood meals, causing chronic bleeding, anemia, bloody stool,
nausea, vomiting, weakness, fatigue
Hookworms are acquired
through the feet (skin).
Animals carry hookworm, can
transmit, but with good sanitation
usually do not.

74. An example of the migratory nature of Strongyloides.
Fig A patient with disseminated
Strongyloides infection.

75. Examples of some antihelminthic therapeutic agents and their effects.
Table 22.1 Antihelminthic therapeutic agents and their effects.

76. Features of intestinal distress.
Checkpoint 22.9 Intestinal distress.

77. Features of intestinal distress plus migratory symptoms.
Checkpoint Intestinal distress plus migratory symptoms.

78. Liver and intestinal disease
Helminth infection
Begins in the intestine and migrates to the liver
Liver flukes
Definitive and intermediate host

79. An example of the sheep live fluke Fasciola hepatica.
Fig Fasciola heepatica, the sheep liver fluke

80. Features of liver and intestinal diseases.
Checkpoint Liver and intestinal disease.

81. Muscle and neurological disease
Protozoan infection
Trichinosis
Life spent entirely in mammal host
Common to the U.S. and Europe
Pork, bear meat

82. Trichinosis
Trichenella – (trichina worm) found in pigs, rats, and bears. Acquired through undercooked meat.
The larvae travel through the bloodstream and deposit into any muscle tissue.
Fever, muscle pain, malaise
Autopsies reveal 15% of people have some amount of trichinosis.
Can be severe if many
larvae are ingested

83. Features of muscle and neurological symptoms.
Checkpoint Muscle and neurological symptoms

84. Liver disease Helminth infection Schistosomiasis Blood flukes
Evades host immune system by coating itself with proteins from the host bloodstream
Endemic

85. The life of Schistosoma is complex.
Fig Stages in the life cycle of Schistosoma.

86. Features of liver disease caused by blood flukes.
Checkpoint Liver disease

87. Summary of the diseases in the gastrointestinal tract.
Taxomonic organization of microorganisms causing
Disease in the GI tract.

88. Infectious Diseases Affecting the Gastrointestinal Tract.
Fig. 22.p730

90. A cross section of a tooth showing all the major structures associated with the crown and root.
Fig The anatomy of a tooth.

91. Cases of typhoid fever and salmonelloses.
Fig Data on the prevalence of typhoid fever and
other salmonelloses

92. Infection of the large intestine by Shigella dysenteriae.
Fig The appearance of the large intestional mucosa
In Shigella dysentery.

93. EAEC E. coli can be identified by its ability to adhere to human cells in aggregates.
Fig Enteroaggregative E. coli adhering to epithelial cells.

94. The protozoan Cyclospora can be identified by the acid-fast stain, in which large cysts stain pink to red and have a wrinkled outer wall.
Fig An acid-fast stain of Cyclospora in a human
Fecal sample.

95. Entamoeba histolytica have different cellular forms, which includes a trophozoite that contains a karyosome and hosts cells (rbc) and bacteria, and a mature cyst which undergoes excystment.
Fig Cellular forms of Entamoeba hystolytic