Final exam

Peptic Ulcer

  Erosions of stomach or duodenum lining

*Food is not the causative agent

Peptic Ulcer

Causative agent

Helicobacter pylori

-Gram negative; Vibrio

– Multiple Polar knobbed flagella

Peptic Ulcer

Signs and Symptoms

– Abdominal Pain

-Nausea, vomiting (with or without blood), weight loss, bloody stool

– May lead to internal bleeding and shock (due to perforations of stomach or intestines)

– Signs and symptoms may worsen after you have eaten but again peptic ulcers are not caused by food

 

Helicobacter pylori

Virulence factors

•Adhesions – surface proteins that help in attachment

•Urease enzyme neutralizes stomach acid

•Protein to inhibit acid production

•Enzyme to inhibit digestion by WBCs

 

Inflammatory response and bacterial toxins causes decrease in mucus production

Stomach lining not protected from acidic environment can lead to a Chronic infection

 

Peptic Ulcer

Epidemiology

-Fecal/oral route (ingest something contaminated)

-flies

-20% of humans are asymptomatic carriers

Peptic Ulcers

Diagnose through

-By assessing the damage done to the stomach lining

– by isolating a urease + Gram – vibrio

Peptic Ulcer

Prevention

– change lifestyle to prevent risk factors

-stop drinking and eating spicy foods

– good hygiene to avoid fecal/oral contamination

Peptic Ulcer

Treatment

– combined antibiotic treatment

-Medication to inhibit production of stomach acid

– surgery may be required if ulceration is extensive or perforation is occurs

 

Mumps

Acute viral illness

– Attacks parotid salivary glands; massive swelling of glands (looks like neck is swollen)

– Virus reproduces in the URT and spreads to salivary glands where it destroys epithelium and then releases the virus causing inflammation

 

Mumps

Causative Agent

Enveloped ssRNA Rubulavirus

 

Mumps

Signs and symptoms

– Fever, loss of appetite, headache, parotitis (inflammation of the parotid glands), sore throat

– symptoms are self limiting and usually disappear in about a week

– symptoms are more severe past puberty and may cause orchitis (inflammation of the testes; increases the risk of testicular cancer) or meningitis

-Pregnant women often miscarriage

– Not so worried about the actual virus but the secondary risks

Mumps

Epidemiology

Humans are the only host

– spread through contact transmission, like droplets or fomites

– Peak infection time is from 1-2 days before swelling until swelling subsides

 

Mumps

Prevention

Immunization

-MMR vaccine

-Lifelong immunity

Mumps

Treatment

– alleviating symptoms (not with aspirin because its a viral disease)

– No effective antiviral treatment

Gastroenteritis

Inflammation of stomach or intestines

– Inhibits nutrient absorption and excessive H2O and electrolyte loss

Gastroenteritis

Causative Agents

-Bacterial

-viral

-Parasites

– Poisening by microbial toxins (food borne intoxication)

Gastroenteritis

Signs and symptoms

*** will always be true for any type of gastroenteritis

– diarrhea, loss of appetite, abdominal cramps, nausea, vomiting and possible fever

– typically self-limiting

Dysentery

-severe form of gasteroenteritis

– Profuse diarrhea with mucus and blood (means damage is being done)

Enteric fevers

 

systemic with severe headaches, high fever, abscesses, intestinal rupture, shock and death

– Begins as gasteroenteritis, only turns into this if bacteria is successful at getting into the blood

Dysentery

Epidemiology

Oral/fecal transmission

-occurs worldwide

– water is a common reservoir

-overcrowding and poor sanitation are risk factors

– animals may be a source of infection

dysentery

prevention

-hand washing

– proper food handling and complete cooking

– Pasteurization of milk and juices

– Adequate sanitation

– safe water supplies and water treatment

Dysentery

treatment

-Rapid replacement of fluid and electrolytes (salt, chlorine, potassium, bicarbonate ions: all important for body to properly function)

– Fluid loss –> drop in blood pressure –> fatalities

– anti-nausea medication to help keep food down

– antimicrobial medications may be used in severe cases

– antidiarrheal medications are bad! Your body is trying to get rid of what is causing the problem

– normal pH is 7.4 – 7.6

Bacterial Gasteroenteritis

 

3 groups of gram negative bacteria account for most bacterial intestinal infections

1. Vibro cholerae (cholera)

2. Enterics (Salmonella, shigella, e.coli) gram negative bacilli

3. campylobacter jejuni: leading cause in the US

Cholera

causative agent

Vibro cholerae, gram –

– most common organism in surface water. Can survive in salt or fresh water but become mobile in fresh water

– High infectious dose

– Bacteria sensitive to stomach acid: most bacteria usually die in the stomach so have to be exposed to a lot

– Adheres to small intestine and multiplies: produces an A toxin

– Bacteris doesn’t enter cells; toxin does

 

          **Are more virulent in human host but normally survive in an alkaline pH

 

Cholera

virulence toxin

AB TOXIN – potent exotoxin

– B toxin binds to cell then A toxin enters cell

– A toxin causes intestinal cells to rapidly pump out electrolytes

– Passive osmotic H2O loss folows: water chases the electrolytes

– Metabolic acidosis

– Shock occurs because of dehydration

 

Metabolic acidosis

when body systems are too acidic because they loss their buffer systems/ bicarbonate ions

Cholera

Signs and symptoms

+ general signs and symptoms of gasteroenteritis

-Heavy loss of fluids

– “rice-water” stools: profuse, colorless, odorless stools flecked with mucus, looks like little peices of rice

– up to 20L of fluid lost per day

– May discharge 1 million bacteria per ml of feces lost

Cholera

treatment

– untreated cases are potential fatal up to 24 hours

– fluid/electrolyte replacement

– tetracycline reduces toxin production

Shigellosis

Causative Agent

aka: bacilliary dysentery

– Shigella sp.: S. dysenteriae (most severe), S. flexneri, S. Boydii, S. sonnei

Low infecting dose: 10 cells

– Bacteria, unlike cholera, is not sensitive to stomach acid

Shigellosis

Signs and symptoms

-fever and dysentery

– Infects cells of large intestine and initiates an intense inflammatory response

– Dead cells slough off and produces areas convered with pus and blood

Shigella sp.

Virulence factors

All species produce enterotoxin

– Affects cells in intestines and type III secretion systems

– have a complex of about 20 proteins that embed themselves in channels of the intestines and facilitates movement of toxin into cell

– S. Dysenteriae produces powerful endotoxin

-Shiga- toxin: if toxin binds to neutrafils (white blood cells) it can enter blood and stop protein synthesis

         – bacteria alone cannot survive in blood

Shigellosis

Treatment

Ciprofloxacin, rifampin or azithromycin may reduce duration and infectivity

– primary treatment is fluid and electrolyte replacement

Travelers diarrhea

Causative agent

Escherichia coli (gram – bacilli, facultative anaerobes)

– have Multiple antigenic strains (O,H,K)

– Virulent strains have fimbriae, adhensions and multiple toxins

Enterotoxigenic E. coli

fecal coliform

– produce enterotoxins

– type III secretion systems

– typically are self limiting

– Test for them using MPN

Enterohemorrhagic E. coli

More severe

 – O157:H7: associated with contaminated food; food poisoning

-Produce potent Shiga-like toxins and type III secretion systems

**Antimicrobials cause an increase in toxin production because it’s gram – which is an endotoxin

Salmonellosis and Typhoid Fever

Causative Agent

Salmonella enterica

-2000 strains (serotypes) or genetic variations

– Typhimurium and Entertidis commonly cause Shigellosis

– Typhi and Paratyphi commonly cause Typhoid Fever, get into mucus membranes and sometimes in blood

Salmonellosis and Typhoid Fever

Epidemiology

-bacteria is a common intestinal flora of many animals

– contaminated animal products are reservoir

– Reptiles, eggs, and undercooked poultry

– 1/3 of all chicken carriers are contaminated with salmonella

Salmonella

Virulence

– virulent strains tolerate stomach acids and pass to intestines

– toxin induces phagocytosis in intestinal cells

– pathogen reproduces inside phagosome killing host cell

– bacteria (typhi) may pass through intestinal cells into bloodstream

salmonellosis and Typhoid fever

symptoms

typhoid fever is an enteric fever

– Macrophages carry bacteria to liver, spleen, gallbladder and bone marrow

salmonellosis and typhoid fever

treatment

treated with cyprofloxacin or ampicillin

– surgical removal of gallbladder

Campylobacteriosis

Causative agent

 

campylobacter jejuni

Campylobacteriosis

– leading cause of bacterial diarrhea in the United States

– Estimated 1 million cases annually with about 100 deaths

– Associated with poultry

– low infecting dose

 

campylobacteriosis

virulence factors

virulent strains posses adhesions, cytotoxins and endotoxins

– Induce endocytosis in cells of intestines and initiate inflammation and bleeding lesions

– non-motile strains are avirulent (make sure that really means avirulent)

Campylobacteriosis

treatment

– usually mild and self-limiting

– severe cases are treated with ciprofloxacin or azithromycin

Guillain-barre syndrome

complication of campylobacteriosis, 40% of cases get this.

– immune system starts to attack body

Guillain-barre syndrome

signs and symptoms

tingling of the feet leads to progressive paralysis of the legs, arms and rest of the body

– may be associated with autoimmune response

– 80% of people recover completely and 5% die with treatment

Viral Gastroenteritis

Causative agents

– Rotaviruses and Noroviruses

– Both naked RNA viruses

– Both have glycoprotein spikes that help them attack to cells that line intestinal tract

Viral Gasteroenteritis

Epidemiology

        Norovirus epidemics cause 90% of cases, norovirus effects infants especially and can be bad enough that they must be hospitalized

 

        Rotaviruses responsible for 50% infant cases of serious diarrhea

–    600,000 worldwide annual fatalities

Viral gasteroenteritis

treatment

– infect intestinal cells causing cell death

– typically self limiting

– oral vaccine

– Electrolyte replacement

 

Bacterial food intoxication

causative agent

 

Staphylococcus aureus

– halotolerant; grows well in food at room temperature

bacterial food intoxication

epidemiology

associated with cafeterias and social functions

bacterial food intoxification

signs and symptoms

 

        Stimulate muscle contractions, nausea and intense vomiting, diarrhea and cramping

        Acute and self limiting 

–     symptoms begin 4-6 hrs after consumption and end within 24 hrs

bacterial food intoxication

treatment

 

 5 heat stable enterotoxins: not killed by heat

        1000 for up to 30 min will kill bacteria but

toxin will persist

 

          do not treat with antibiotics because you are not treating bacterial infection, you are trying to get rid of a toxin

– self limiting

Botulism

causative agent

-clostridium botulinum

– a very resistant endospore

– obligate anaerobic, gram +, spore forming bacillus

– produce 7 different neurotoxins, one being the most deadly toxins known

Botulism

signs and symptoms

                      12 to 36 hours after interaction with toxin the symptoms will progress and be seen

                                            Dizziness, dry mouth, blurred vision

                                            Abdominal symptoms include pain, nausea, vomiting and diarrhea or constipation

                                            Progressive paralysis

Paralysis of respiratory muscles most common cause of death

3 forms of botulism

Food-born botulism – progressive paralysis of all voluntary muscles due to toxin production

– wound botulism – similar symptoms, begins with colonization and then toxin is dumped into bloodstream

– Infant botulism – bacteria grows in the intestines, producing non-specific symptoms, in the US this is more common, but globally the other two are more common

 

floppy baby syndrome

infant begins to flounder, won’t nurse, may a part of SIDS

Botulism

Epidemiology

food born, wound, infant

Botulism

Prevention

Proper sterilization and sealing of canned food

Prompt wound care

No honey or unpasteurized juices for infants, any child under 1.

Botulism

Treatment

Antitoxins: only going to neutralize circulating toxins

– Gastric washing and surgical removal or tissues which will dislodge bacteria

– Artificial respiration may be required

– anti-microbials given to kill bacteria in infant and wound botulism

– A mouse bioassay

Mouse bioassay

take what they think is contaminated and inject a mouse to see if it dies, second mouse they inject a contaminated substance and botulism antitoxin to see if mouse doesn’t die

Hepatitis

Autoimmune disease

– alcohol/drug abuse, genetic disorders, viral infection

– 5 different types

– Hep A (HAV); HBV; HCV; HDV; HEV

HAV

infectious type of herpes

HBV

– serum hepatitis, associated with pancreatic cancer

HCV

chronic hepatitis, major source of damage to the liver so badly that people need a liver transplant, spread through contaminated needles and spread of body fluids

HDV

Requires co-infection with HBV, does not have genetic material to make protective protein covering so on its own it cannot cause disease so it steals protein coverings from hepatitis B virus. Only problem when accompanied with hepatitis B is that people that have both are at a much greater risk for liver cancer

HEV

Enteric hepatitis

signs and symptoms

– Jaudice; yellowing of the skin and the whites of eye due to the buildup of beliruvin

-nausea

-vomiting

-fatigue

-fever

-weight loss

Complications can occur from chronic infection like hep b or c

-Cirrhosis: liver replaced with fibrous nonfunctional tissue, liver failure, liver cancer (linked to hep B), and death

– most damages is caused by host defenses – from your own immune response trying to kill infected cells

Enteric Hepatitis

Transmission

contaminated food and water, fomites and sexual contact

Enteric hepatitis

Treatment

-supportive care for symptoms

-anti-virals or interferon may help against HBV or HCV

– Passive immunotherapy

Enteric Hepatitis

Prevention

        Avoiding exposure by practicing good hygiene and protected sex or abstinence

        Vaccines are available against HAV and HBV

        Avoid fecal contamination

        Go over chart, know how its transmitted, if it will develop, what they are associated with

Protozoal Diseases of the GI Tract

 

         Most significant human pathogens worldwide

         Few are intestinal pathogens

         Transmitted by fecal to oral route

        Fecal contaminated water

        May be zoonotic

Giardiasis

Causative agent

 

              – Giardia intestinalis

Flagellated, pear shaped

      –Two nuclei

    – Exists in two forms

A.   Feeding trophozoite

B.   Dormant cyst (Tough chitin shell)

Giardiasis

Cyst and Trophozoitis

 

        Cyst infective stage: giant suction cup that allows it to attach to the digestive tract 

         Resists stomach acid

         Two trophozoits per cyst

        Trophozoits attach to epithelium of small intestine with adhesive disk

        In severe cases, may cover entire intestinal surface

Giardiasis

epidemiology

        Transmission usually fecal-oral route

        May be zoonotic

         Beavers, raccoons, muskrats, dogs, cats

         Sometimes called “Beaver Fever” because beavers are such a prominent reservoir

        Single stool can carry 300 million cysts

         Cysts can survive in cold water up to 2 months

         Chlorination often ineffective against cysts, normally the primary means of cleaning water but these are resistant, only way to remove them  is filtration

 

Gardiasis

Prevention

        Filtration or boiling of water, boiling water for 10 minutes

        Good hygiene practices

        Sanitary disposal of feces: humans and animals

        Safe sex

Gardiasis

Treatment

Diagnosed by cysts of trophozoites in stool

 

        Fluid and electrolyte replacement

        Metronidazole or quinocrine , both are eukaryotic pathogens and antiprotozoal drugs

Cryptosporidosis

Causative agent

        Cryptosporidium parvum

         Multiplies cells of small intestine

         Apicomplexan : nonmotile but do have an apical complex that helps this cell penetrating into host cells

         Exists in two forms

         Acid fast oocyst: tough protective stage

         Sporozoite: active feeding stage

Criptospoidosis

Virulence factors

  Oocyst releases 4 bannana shaped sporozoites into small intestine

  Sporozoites invade epithelium

   Cause deformity in cells and villi (fingerlike projections that increase surface area for nutrient absorption)

   Initiates inflammatory response

  Water secretion increases & nutrient absorption decreases

Cryptosporidosis

Signs and symptoms

  Fever, headache, loss of appetite, nausea, abdominal cramps and profuse watery diarrhea

  Can last for months

  Usually self limiting and only life threatening in immunosuppressed people

  May be life threatening in immunocompromised individuals

   Hepatatis, pancreatitis

criptosporidosis

epidemiology

   Individuals can expel organisms for up to 2 weeks after diarrhea ceases

  Person-to-person spread occurs

  Cysts can survive long periods in food and water

   Resistant to chlorination but too small for most filters 

  Zoonotic with a wide host range

  Diagnosed by oocysts in stool

Cryptosporidiosis

Prevention

  Careful monitoring of municipal water supplies

  Pasteurization of drinks

  Sanitary disposal of feces

  Immunodeficient should avoid contact with animals and recreational water activities

cryptidosporidiosis

Treatment

– replacement of water and electrolytes

amebiasis

causative agent

   Entamoeba histolytica

  Exists in two forms

   Feeding trophozoite

   Dormant cyst

3 forms of amebiasis

  Luminal –asymptomatic: what happens when you’re exposed to an averialent form, cannot attach because they do not have attachment  

  Amebic dysentery – more severe; dysentery, colitis and ulceration of mucosal lining

  Invasive extra-intestinal –necrotic lesions form in liver, lungs, spleen, kidneys and brain, when pathogens get in blood stream causing infection to become systemic

amebiasis

epidemiology

 

  Transmission usually fecal-oral route

   Cysts survive 1-2 weeks in environment

  No animal reservoir, humans are the only carriers

   10% of global population are carriers

  3rd leading cause of parasitic death 

   50 million cases and 100,00 deaths annually

amebiasis

Prevention

  Disinfection, filtration and boiling of water

  Sanitary disposal of feces, only human feces

  Good hygiene practices

  Safe sex

amebiasis

treatment

  Oral rehydration

  Metronidazole or iodoquinol 

  Diagnosed by cysts or trophozoites in stool

Helminthic Infestations

-Macroscopic, multi-cellular parasitic worms

-cestods and nematodes

cestodes

  Flat, segmented, monoecious: have both male and female reproductive parts, they can impregnate themselves

  Intestinal parasites that lack complete digestive system

nematodes

  Round, un-segmented, diecious, sexually dimorphic

  Complete digestive system and protective cuticle

Tapeworm infestations

  Cestodes: flat segmented worm

   Taenia saginata – beef tapeworm

   Taenia solium – pork tapeworm, its intermediate host of the pig

Tapeworm

signs and symptoms

   Usually asymptomatic

   nausea, abdominal pain, weight loss, and diarrhea may occur

   Worm may cause intestinal blockage

   Individuals are sexually dimorphic

tapeworm

epidemiology

   Highest incidence poor rural areaes

   Inadequate sewage treatment

   Humans live in close contact with livestock

  Diagnosed by presence of proglottids in feces

Tapeworm

prevention

relies on thorough cooking of meats and sewage treatments

Tapeworm

treatment

  Niclosamide or praziquantel: antihelminth drugs

  May require surgical removal of worm of they get long enough, some can get meters long

Pinworm infestation

causative agent

   diascious

  Nematode

   Enterobius vermicularis

   Sexually dimorphic

Pinworm Infestation

signs and symptoms

   perianal itching

– irritability

-decreased appetite all due to male and females worms in intestines where they steal nutrients

-they mate in intestines

-at night female will travel out of the body lay eggs around the anus and go back in causing the irritation

Pinworm infestation

epidemiology

– Infections commonly occur in children

– most common parasitic worm in the US

– diagnosed based on microscopic id of eggs or presence of adult pinworms

 

 

 

Pinworm

Prevention

strict personal hygiene

pinworm

treatment

  Pyrantel pamoate or mebendazole : both antihelminth drugs, two rounds of treatment at least two weeks apart, treat everyone in household

Categories: Microbiology