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27 Cards in this Set
- Front
- Back
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Staphylococcal Food Poisoning
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* An intoxication due to staphylococcal enterotoxins present in food. They are heat resistant. Timecourse: 1-48 hours
Symptoms: diarrhea or dysentery,abdominal cramps, nausea, vomiting. Usually not lethal. Treatment: oral rehydration therapy for fluids/electrolytes |
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Shigellosis
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*An infection caused by the gram negative - bacterium Shigella
Timecourse: 12 hour- weeks Transmission: fecal/oral Symptoms: dysentery, tissue damage. Pathogenic mechanisms: Invades M cells by membrane ruffling and multiplies inside the cell. Invades neighboring epithelial cells by capturing the cells actin and propelling itself. Shiga toxin destroys epithelial tissue by halting protein synthesis. Treatment: Antibiotics (ampicillin/quinolones) and fluids |
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Salmonellosis
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* An infection caused by the gram-negative bacterium Salmonella. One of the most prevalent food-borne diseases.
Timecourse: 12 hour- 36 hours Transmission: fecal/oral Symptoms: nausea and diarrhea, complications can include encephalitis/sepsis. Pathogenic mechanisms: Acid tolerance for surviving the stomach, flagella inhibits phagocytosis, able to survive in both macrophages and epithelial cells, blocks phagosome/lysosome fusion, type III secretion system injects several effector proteins (causing membrane ruffling/bacterial internalization and more), contains lots of super oxide dismutases (SOD's), phase variation mechanisms for changing the cell exterior and avoiding immune system, multi-drug resistance |
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Cholera
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*An infection caused by the gram-negative bacterium Vibrio cholerae
Timecourse: 4 hours- weeks Transmission: fecal/oral Symptoms: Mostly mild but when severe can cause severe diarrhea, tissue damage leading to a 50% mortality rate if untreated. Pathogenic mechanisms: Pili and biofilms allow it to survive in water and in stomach, alternate pili expression allows its attachment to the intestine where it releases toxins that cause host cells to secrete water and electrolytes (3-5 gallons/day)! Treatment: Antibiotics and fluids |
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Giardiasis
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*An infection caused by the protozoan Giardia lamblia
Transmission: fecal/oral Symptoms: dysentery, tissue damage. Pathogenic mechanisms: Alternates between and active trophozoite and a cyst which allows it to survive in water. Adheres to the intestinal wall creating mechanical irritation/damage as well as a damaging immune response. Treatment: Metronidazol/quinacrine and fluids |
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Cryptosporidiosis
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*An infection caused by the protozoan Cryptosporidium hominis.
Transmission: fecal/oral Symptoms: self-limiting diarrhea; may be life threatening in immunosuppressed persons. Pathogenic mechanisms: intestinal cell death is due to replication of protozoan inside of cells AND T-cell inflammatory response. Complex lifecycle. Oocyts are excreted in stool and then ingested by new hosts. Treatment: fluids |
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Periodontal Disease
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*An infection primarily caused by gram-negative bacteria of the Porphyromas species.
Transmission: direct contact or fomites Symptoms: bad breath, discoloration of teeth, receding gums, tender/sore gums, bleeding, loose or shifting teeth. Pathogenic mechanisms: Pili/fimbrae facilitate attachment to teeth/gums, biofilm production, hemin allows iron import for bacteria, produces proteolytic enzymes to attack tooth ligaments/tissue (including collagenase), toxins further irritate/inflame gums Treatment: scaling, antibiotics, surgery, personal hygiene (mouth wash, flossing, brushing, etc.) |
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Helicobacter Peptic Ulcer Disease
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*An infection caused by the microaerobic gramnegative bacterium Helicobacter pylori
Transmission: fecal/oral Symptoms: abdominal pain, burping, nausea, vomiting, bloating and weight loss due to damage to stomach lining and ulcer formation Pathogenic mechanisms: Adhesins to bind to membrane lipids and carbohydrates to bind to epithelial lining. Urease neutralizes stomach acid. Epithelial cells are damaged by products of urease plus proteases, cytotoxins and phospholipases. Hcp's stimulate macrophage development. Cytokines released by epithelial cells in response to H. pylori cell wall leads to inflammation of stomach lining. Treatment: Antibiotics (ampicillin/quinolones) and fluids |
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Hepatitis A,B, C, D and E
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An infection caused by several viruses (Picornavirus, Hepadnavirus, Flavivirus, etc.)
Transmission: A- blood and stool B&D- blood and other body fluids C- blood to blood contact D- fecal/oral Symptoms: A& E: fatigue, fever, jaundice, clay-colored feces (may also be asymptomatic) B, C&D: loss of appetite, nausea, vomiting, body aches, fever, dark urine, risk of liver cancer (may also be asymptomatic) Pathogenic mechanisms: replication in hepatocytes Treatment: varies but includes interferons and other antivirals as well as vaccines |
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Staphylococcal Food Poisoning
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* An intoxication due to staphylococcal enterotoxins present in food. They are heat resistant. Timecourse: 1-48 hours
Symptoms: diarrhea or dysentery,abdominal cramps, nausea, vomiting. Usually not lethal. Treatment: oral rehydration therapy for fluids/electrolytes |
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Nematode Helminthic Disease
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*An infection caused by a cylindrical, tapered nematode (over 6,000 parasitic species!)
Transmission: ingested eggs from contaminated sheets/clothing/soil or ingested larvae in meat. Larvae also enter skin lesions from contaminated soil Symptoms: gastrointestinal discomfort, listlessness, weightloss, anorexia, vomiting, (may also affect lung and heart) Pathogenic mechanisms: destroy local tissue, release toxic byproducts, stimulate immune response/inflammation |
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Shigellosis
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*An infection caused by the gram negative - bacterium Shigella
Timecourse: 12 hour- weeks Transmission: fecal/oral Symptoms: dysentery, tissue damage. Pathogenic mechanisms: Invades M cells by membrane ruffling and multiplies inside the cell. Invades neighboring epithelial cells by capturing the cells actin and propelling itself. Shiga toxin destroys epithelial tissue by halting protein synthesis. Treatment: Antibiotics (ampicillin/quinolones) and fluids |
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Salmonellosis
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* An infection caused by the gram-negative bacterium Salmonella. One of the most prevalent food-borne diseases.
Timecourse: 12 hour- 36 hours Transmission: fecal/oral Symptoms: nausea and diarrhea, complications can include encephalitis/sepsis. Pathogenic mechanisms: Acid tolerance for surviving the stomach, flagella inhibits phagocytosis, able to survive in both macrophages and epithelial cells, blocks phagosome/lysosome fusion, type III secretion system injects several effector proteins (causing membrane ruffling/bacterial internalization and more), contains lots of super oxide dismutases (SOD's), phase variation mechanisms for changing the cell exterior and avoiding immune system, multi-drug resistance |
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Cholera
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*An infection caused by the gram-negative bacterium Vibrio cholerae
Timecourse: 4 hours- weeks Transmission: fecal/oral Symptoms: Mostly mild but when severe can cause severe diarrhea, tissue damage leading to a 50% mortality rate if untreated. Pathogenic mechanisms: Pili and biofilms allow it to survive in water and in stomach, alternate pili expression allows its attachment to the intestine where it releases toxins that cause host cells to secrete water and electrolytes (3-5 gallons/day)! Treatment: Antibiotics and fluids |
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Giardiasis
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*An infection caused by the protozoan Giardia lamblia
Transmission: fecal/oral Symptoms: dysentery, tissue damage. Pathogenic mechanisms: Alternates between and active trophozoite and a cyst which allows it to survive in water. Adheres to the intestinal wall creating mechanical irritation/damage as well as a damaging immune response. Treatment: Metronidazol/quinacrine and fluids |
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Cryptosporidiosis
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*An infection caused by the protozoan Cryptosporidium hominis.
Transmission: fecal/oral Symptoms: self-limiting diarrhea; may be life threatening in immunosuppressed persons. Pathogenic mechanisms: intestinal cell death is due to replication of protozoan inside of cells AND T-cell inflammatory response. Complex lifecycle. Oocyts are excreted in stool and then ingested by new hosts. Treatment: fluids |
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Periodontal Disease
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*An infection primarily caused by gram-negative bacteria of the Porphyromas species.
Transmission: direct contact or fomites Symptoms: bad breath, discoloration of teeth, receding gums, tender/sore gums, bleeding, loose or shifting teeth. Pathogenic mechanisms: Pili/fimbrae facilitate attachment to teeth/gums, biofilm production, hemin allows iron import for bacteria, produces proteolytic enzymes to attack tooth ligaments/tissue (including collagenase), toxins further irritate/inflame gums Treatment: scaling, antibiotics, surgery, personal hygiene (mouth wash, flossing, brushing, etc.) |
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Helicobacter Peptic Ulcer Disease
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*An infection caused by the microaerobic gramnegative bacterium Helicobacter pylori
Transmission: fecal/oral Symptoms: abdominal pain, burping, nausea, vomiting, bloating and weight loss due to damage to stomach lining and ulcer formation Pathogenic mechanisms: Adhesins to bind to membrane lipids and carbohydrates to bind to epithelial lining. Urease neutralizes stomach acid. Epithelial cells are damaged by products of urease plus proteases, cytotoxins and phospholipases. Hcp's stimulate macrophage development. Cytokines released by epithelial cells in response to H. pylori cell wall leads to inflammation of stomach lining. Treatment: Antibiotics (ampicillin/quinolones) and fluids |
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Hepatitis A,B, C, D and E
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An infection caused by several viruses (Picornavirus, Hepadnavirus, Flavivirus, etc.)
Transmission: A- blood and stool B&D- blood and other body fluids C- blood to blood contact D- fecal/oral Symptoms: A& E: fatigue, fever, jaundice, clay-colored feces (may also be asymptomatic) B, C&D: loss of appetite, nausea, vomiting, body aches, fever, dark urine, risk of liver cancer (may also be asymptomatic) Pathogenic mechanisms: replication in hepatocytes Treatment: varies but includes interferons and other antivirals as well as vaccines |
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Nematode Helminthic Disease
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*An infection caused by a cylindrical, tapered nematode (over 6,000 parasitic species!)
Transmission: ingested eggs from contaminated sheets/clothing/soil or ingested larvae in meat. Larvae also enter skin lesions from contaminated soil Symptoms: gastrointestinal discomfort, listlessness, weightloss, anorexia, vomiting, (may also affect lung and heart) Pathogenic mechanisms: destroy local tissue, release toxic byproducts, stimulate immune response/inflammation |
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Gonorrhea
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*Infection caused by Neisseria gonorrhoeae, a gram-negative diplococci.
Transmission: STD Symptoms: burning and pain while urinating, increased urination, sore throat. Pain in testicles, red/swollen opening of penis (Men). Vaginal discharge and/or pain in lower abdomen (Women). Pathogenic mechanisms:Pili and Opa proteins help attach to epithelial cells or phagocytes and stimulates endocytosis into the cell, also inactivate immune response. Antigenic variation of surface proteins. Bacterial cell lysis leads to lipooligosaccharide (LOS) release which stimulates inflammatory response, antibiotic resistance Treatment: many types of antibiotics |
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Syphilis
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*Infection caused by the gram negative spirochete Treponema pallidum.
Transmission: STD and also kissing Symptoms:small sores called chancre appear first, next a red/brown skin rash on hands and feet with mucous membrane lesions, fever, swollen lymph glands, soar throat, etc. Only 15% of people develop late stage: damage to internal organs, nerves, bones causing paralysis, numbness, gradual blindness, dementia, difficulty coordinating muscles,possible death. Pathogenic mechanisms: Corkscrew motility allows swimming in gel-like fluids and penetration of mucous membranes and hook end attaches to cell. Produces several lipoproteins that induce inflammatory response. Treatment: injection of penicillin |
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Vaginitis- Candida albicans
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*Infection of the vagina caused by Candida albicans, a yeast
Symptoms: yeasty discharge from vagina, irritation/pain, pH<4; causes significant morbidity/mortality in immuno compromised persons. Pathogenic mechanisms: adhesins for adhesion to host cells, antigenic variation, morphogenesis (switches growth forms) Treatment: antifungal |
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Vaginitis- Trichomonas vaginalis
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*Infection of the vagina caused by Trichomonas vaginalis, a protozoan (5-8 million infections/year in US)
Symptoms: foul smelling greenish/yellow vaginal discharge and irritation, benign unless pregnant, then linked to low birth weight/preterm delivery. Pathogenic mechanisms: adhesins, etc. for adhesion to host cells, also proteinases that may degrade extracellular matrix proteins like collagen Treatment: Metronidazole (deactivates enzymes in anaerobic organisms) |
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Genital Herpes
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*Infection caused by Herpes Simplex Virus (HSV). Over 1/4 of persons over the age of 25 are infected!
Transmission:STD, can cause spontaneous abortion/birth defects Symptoms: painful vesicles on genitals, recurrances from viral latency in nerves Pathogenic mechanisms: After infection it travels up nerve endings to sensory nerve cells where it remains latent for a lifetime. Intial outbreak and reoccurances are due to viral production/replication in nerve cells. These offspring travel down the nerve axon to the terminals on the skin and are released (causing blisters). Treatment: acyclovir for suppression of symptoms (no cure) |
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Genital Warts
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Infection caused by the Human Papillomavirus (HPV), > 1 million cases/year in the US
Transmission: STD Symptoms: mostly asymptomatic, less than 1% develop genital warts, also causes 99% of cervical cancers and some cancers of the penis. 90% of cases clear on their own. Pathogenic mechanisms: infects keratinocytes of the skin or mucous membrane. Viral replication can lead to warts. Viral E7 protein inhibits apoptosis and can lead to cancer Treatment: Imiquimod, removal of warts Prevention: Gardisil vaccination and safe sex ractices |
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Urinary Tract Infections (UTI)
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*An infections usually caused by Uropathogenic E. coli (UPEC). Can lead to pyelonephritis
Transmission: fecal to urinary tract Diagnosis: >100 CFU/ml urine Pathogenic Mechanisms: pili for invasionand adherence to bladder lining, hemolysin toxin (exfoliates bladder lining and kills macrophages), intracellular growth, type III secretion system, can remain dormant for weeks allowing it to evade the antibiotics/immune system, antibiotic resistance Treatment: antibiotics (trimethoprimsulfamethexazole (sulpha drugs) |
