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    Helicobacter Pylori-A: Transmission Pathogenesis Incidence Symptoms Other Diseases Vaccine? Stomach Ulcers

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    Sarah Plunkett
    Helicobacter pylori is a bacterium that infects the stomach and causes ulcers. It is adapted to survive in the acidic stomach by producing urease to raise the pH around itself. Around 50% of adults are infected, but illness only occurs when the immune system is compromised. Symptoms include abdominal pain, nausea, and possible internal bleeding. There is no vaccine currently available.

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    Helicobacter Pylori-A: Transmission Pathogenesis Incidence Symptoms Other Diseases Vaccine? Stomach Ulcers

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    Sarah Plunkett
    57 views4 pages
    Helicobacter pylori is a bacterium that infects the stomach and causes ulcers. It is adapted to survive in the acidic stomach by producing urease to raise the pH around itself. Around 50% of adults are infected, but illness only occurs when the immune system is compromised. Symptoms include abdominal pain, nausea, and possible internal bleeding. There is no vaccine currently available.

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    GI Infections

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    Helicobacter pylori is a bacterium that infects the stomach and causes ulcers. It is adapted to survive in the acidic stomach by producing urease to raise the pH around itself. Around 50% of adults are infected, but illness only occurs when the immune system is compromised. Symptoms include abdominal pain, nausea, and possible internal bleeding. There is no vaccine currently available.

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    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    57 views4 pages

    Helicobacter Pylori-A: Transmission Pathogenesis Incidence Symptoms Other Diseases Vaccine? Stomach Ulcers

    Uploaded by

    Sarah Plunkett
    Helicobacter pylori is a bacterium that infects the stomach and causes ulcers. It is adapted to survive in the acidic stomach by producing urease to raise the pH around itself. Around 50% of adults are infected, but illness only occurs when the immune system is compromised. Symptoms include abdominal pain, nausea, and possible internal bleeding. There is no vaccine currently available.

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    Transmission Stomach Ulcersinflamed stomach lining breaks down until it bleeds Helicobacter pylori- a microaerophile and acidophile, this

    spiral bacterium is perfectly adapted for the stomach. Unknown. Mysterious because H. pylori cannot survive outside the body. 50%+ adults are infected.

    Pathogenesis Development- many infected, but illness only starts with immune system compromise and or stress. Mucus declines, and stomach lining is harmed by own acid. Virulence factors catabolize proteins, then uses urease to make ammonia from the amino acids. This raises pH in and around bacterium. Have receptors to stick to stomach cells and block mucus formation Virulence: Secretion systems on pathogenicity islands: P. islands encode multiple proteins that assemble into tiny needles that inject virulence factors into cells. So they live extracellularly, but influence host cells kind of like a virus might. Enterotoxins family of exotoxins released by some of these bugs. Cause salt channels to open on cells, leading to salt effux diarrhea

    Incidence

    Symptoms -abdominal pain -nausea -anorexia -possible internal hemorrhage

    Other

    Diseases

    Vaccine?

    Enterobacteriaceae

    Fecal-oral

    Facultative anaerobes Most are opportunists except shigella and salmonella. All cause disease in other parts of the body Coliforms=normal fecal bacteria, ferment lactose. Non-coliforms = pathogens, do not ferment lactose O, K, H antigens: O is sugar part of LPS; K is capsule sugars, and H are flagellar proteins. Differences in these are used to distinguish serotypes. Most strains= mutualists- make vitamin K, help digest food.

    Enterobacteriaceae Escherichia coli

    Many toxins, including Shiga toxin made by various members of this species. Shiga toxincytotoxin. Blocks eukaryotic cell protein synthesis ETEC: travellers diarrhea EPEC: fimbriae aid attachment to cells and degrade microvilli. Mainly seen in bottle fed infants. EHEC: shiga toxin prod.

    Strain virulence determined by exchangeable genes: genes that increase virulence are on plasmids or pathogenecity islands, so normal E. coli may be transformed or transduced or conjugated into meaner bugs.

    Transmission Enterobacteriaceae Shigellosis

    Pathogenesis 4 shigella species are primary pathogens ID50 is very low 1-10 organisms for worst species Shiga toxin they are E. coli cousins. E. coli may have gotten it from them. Intracellular motility/spread live inside of host cells and run around in cytoplasm until they hit plasma membrane, forming protrusions into neighboring cells. Thus, can spread from cell to cell without exposure to humoral immunity. Virulence: invade the GALT via phagocytic cells lining intestine. Lives in GI macrophages that travel to lymph nodes and, on dying, release bacteria to infect more MFs. LPS released into lymphatic fluid each time.

    Incidence

    Symptoms Range in severity by species from diarrhea dysentery

    Other

    Diseases

    Vaccine?

    Enterobacteriaceae Salmonella enteric Primary pathogen

    Chickens can be transovarially transmitted in chickens so raw eggs can be vehicle

    Fever Gastroenteritis

    Once were multiple species but are now considered one species with multiple serotypes.

    Gastroenteritis: caused by S. enteric serotype Enteridis. Common cause of food poisoning. Complications: 1) Bacteremia seen mainly in immunocompromised: blood and bone infections 2) Enteric fever chronic infection of lymphatic organs and bone Typhoid fever: caused by Salmonella enteric subtype of Typhi

    From travelers from northern world to southern. But requires booster every 2 years

    Clostridium Diff icile Endospores, obligate anaerobe. Infants are a reservoir due to diet and no effect of exotoxins on immature guts. Major hospital problem

    Endospores enter your GI and usually is outcompeted by commensalsunless they are absent due to Abx. Also, survives long time in environment. Produces cytotoxins and enterotoxins.

    Enteritis sulfurous diarrhea Enteric hemorrhage : if cells die, mucosa may ulcerate

    Transmission Cholera Vibrio cholera- C shaped bug Alkaline freshwater acts as reservoir

    Pathogenesis Cholera toxin causes rapid salt and water loss into the bowel lumen

    Incidence Epemicity: South Asia and ssAfrica have regular cases during rainy seasons. Epidemics occur whenever large numbers of people live densely without good sewage treatment

    Symptoms Very intense diarrhea rice water stool Severe abdominal pain

    Other

    Diseases

    Vaccine?

    Campylobacter jejuni

    Reservoir: pets, livestock

    Guillian Barre Syndrome: unknown cause and possibly multiple causes, but C. jejuni highly associated with onset of symptoms Enteritis very common cause, especially from undercooked meat 40-60% gastroenteritis

    Rotavirus

    Kills microvilli cells, resulting in inflammation and decreased nutrient absorption. Fats malabsorbed dsRNA virus is the only one of human clinical importance Often spread to other organs/systems, including nervous, cardiac.

    Major cause of infant death worldwide

    Vaccine standard childhood vaccine

    Enterovirus Large family, including polio, coxackie, more Start in Gi but may more elsewhere Listeriosis A form of food poisoning, high ID50 Listeria monocytogenes

    No treatment known

    Similar to shigella. Live inside of cells and spread intercellularly. May travel in WBCs to other parts of the body.

    Cryptosporidiosis Cryptosporidium parvum Obligate intracellular protest sporozoan, with life cycle kind of like T. gondii, but can use many species as definitive hosts

    Enteritis: in healthy people Meningitis: in immunocompromised people May kill fetus or cause brain damage. Giardia, Toxoplasma, entamoeba review Enteritis: explosive diarrhea, malabsorption for weeks Immunocompromised common people in AIDS patients and may last for life

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