Urease = neutralizes gastric acid

Flagella

Adhesins = bind Lewis antigens on host

Phospholipases

Vacuolating Toxins

CagA

Diabetics (hyperglycemia impairs neutrophil and macrophage function!)

Immunosuppressed individuals (AIDS, transplant patients)

Patients on broad-spectrum antibiotics (removal of normal flora)

Candida albicans, which is a cause of esophagitis, especially in AIDS patients in which oral thrush can progress to this more severe condition.

Herpesvirus is also a cause of esophagitis in AIDS patients

This is likely the result of Staph. aureus.  The quick onset means that it was likely a pre-formed toxin.  Staph. aureus produces an SE-A, heat stable enterotoxin that acts as a superantigen.  It binds neural receptors and triggers the vomiting center!

Staph preformed toxin is most often found in mayonaise and cream-containing foods.

It is SELF-LIMITING

A pre-formed enterotoxin (SE-A) encoded by a bacteriophage... it is heat-stable and has a short incubation period (1-6 hours)

give symptomatic Tx as it is self-limiting

This is likely a case of foodborne botulism.  Ingestion of the pre-formed neurotoxin (A, B, E toxins) results in the blockade of Ach release at neruomuscular junctions and causes flaccid paralysis.  Adequate heating destroys the botulinum toxin, as it is not heat stable.

Botulinum toxins = "honest ABE"  (toxins A, B, E)

How do you treat foodborne botulism?

Infant/adult botulism?

Wound botulism?

Treat foodborne botulism with antitoxin! (it is the pre-formed toxin causing the disease, not the bacteria, so antibiotics aren't necessary.

Treat infant/adult botulism with the antitoxin.  DO NOT use antibiotics, as this will only promote further release of the toxin!

Treat wound  botulism with antibiotics, antitoxin, and surgical debridement.

in other words: do not give antibiotics in cases of botulism food poisoning, only give them in wound botulism

Patients may need ventilatory support because the flaccid paralysis may lead to respiratory collapse!

Because of the long incubation period and the associated food (gravy and inadequately reheated meats), this is likely a case of C. perfringens food toxicity. 

C. perfringens produces type A-E enterotoxins after the bacteria is ingested and produces diarrhea but no vomiting.  It's incubation period is 8-16hrs. 

C perfringens produces the enterotoxin after it is ingested, and therefore has a longer incubation (8-16hrs).  Much the opposite, B. cereus preformed toxin has a short incubation period of 1-6 hrs.

Additionally, C. perfringens results in watery diarrhea without vomiting whereas, B. cereus preformed toxin results in vomiting without diarrhea.

B. cereus also has a long incubation form, which produces diarrhea.

Most commonly this results from ingestion of re-heated rice (ex: fried rice).  In these cases it involves a pre-formed toxin, which causes vomiting but no diarrhea within 1-6 hours.

It can also cause a diarrheal form after long incubation.

ETEC (enterotoxigenic)

It adheres to intestinal villi and then secretes its enterotoxin.  It is NOT invasive.  Therefore it causes watery, NON-bloody diarrhea.

ETEC, a common cause of traveler's diarrhea, secretes LT and ST toxins (heat Labile and heat Stable toxins)

They promote watery diarrhea by increasing adenylyl cyclase activity, which raises cAMP levels, which activates Cl- secretion, which pulls Na+ and water into the lumen.

The O1 serotypes are responsible for cholera epidemics.  These are subdivided into classic and "el tor" groupings.

However, in India and Bangladesh the non-O1 serotypes are responsible for cholera.

Shellfish!

Massive watery diarrhea, rice water stools (mucous flecks), metabolic acidosis, hypokalemia, hypovolemic shock leading to renal failure.

Tx= REHYDRATION!!!

ciprofloxacin antibiotic administration can reduce the duration of the symptoms

there is a vaccine!

The EPEC and EIEC strains (enteropathogenic and enteroinvasive) produce fever.

"the pathology of invasive organisms involves fever!" 

They can be distinguished by the fact that EIEC also has fecal WBCs in the stool.

EHEC (enterohemorrhagic E. Coli) is found in undercooked beef.  It is also known as Shiga-Toxin producing E. Coli because it contains a bacteriophage that produces shiga-like toxin. 

This strain is associated with Hemolytic Uremic Syndrome.  If antibiotics are given, the toxin levels increase, as does the likelihood of HUS.  So do not give antibiotics!

Shiga toxin damages the vascular endothelium, including that of the kidney, leading to acute renal failure.  It also activates platelets, causing thrombocytopenia.

Campylobacter jejuni, especially in patients with the HLA-B27 genotype.

Guillaine-Barre is an autoimmune condition associated with ascending paralysis.

Viral infections are also implicated

Clostridium difficile.  It elaborates two toxins: Toxin A is chemotactic for neutrophils, Toxin B causes cell death by interfering with actin polymerization.

Clostridium dificil is the cause of pseudomembranous colitis, which should be treated with oral metronidazole or oral vancomycin (oral metronidazole is preferred for cost reasons)

Listeria monocytogenes!  This bacteria carries a high mortality rate and is the cause of not only gastroenteritis, but meningitis and fetal stillbirth!

Brucella is also found in these circumstances

Rotavirus is a naked dsRNA virus

Rotavirus is the most common cause of viral diarrhea and vomiting.

it is self limiting, but you must ensure proper hydration.

Astrovirus is a naked, (+)ssRNA virus

an asterix (*) symbol looks like a (+)

All of these viruses cause watery diarrhea and nausea predominantly in CHILDREN.  Rotavirus has a short incubation, astrovirus has an intermediate incubation (1-4 days) and adenovirus has a long incubation. 

Astrovirus has less severe symptoms than rotavirus, and adenovirus has the longest duration of symptoms.

Adenovirus is a naked dsDNA virus

Adenovirus has DNA i its name...

Calicivirus (a norovirus) is a naked, (+)ssRNA virus.

*all the GIT viruses are naked!  Recall, this allows them to survive longer outside the host and permits fecal-oral transmission!

Hepatitis A and E are naked viruses

recall: hepatitis A and E only cause Acute disease and are transmitted Enterically (fecal-oral, meaning they must be naked)

In your mind, group Hep A and Hep E together!

Enveloped, gapped dsDNA virus

annoying, confusing structure: Hep B is a bitch to remember

or B looks like two D's on top of eachother= dsDNA

Vibrio cholera

Rotavirus

Calicivirus

Hepatitis A virus

In the acute infection, you would see anti-HAV IgM.  Approximately 3 months later, the serum would contain anti-HAV IgG, which grants lifelong immunity to the virus

recall HAV only causes acute hepatitis

Ground glass nuclei (both chronic and acute)

Bridging fibrosis (chronic)

The younger you are when you acquire HBV, the more likely it will lead to chronic hepatitis.  Therefore, children that acquire it perinatally from an infected mother have a greatly increased risk of chronic HBV infection! this is because the immune system is still developing when the baby is infected, and this may lead to tolerance to the virus.  This results in a decreased ability to clear the infection and leads to chronic HBV.

Adults that acquire HBV are more likely to clear the virus and suffer just from the acute disease.

the HDV virus is an enveloped, (-)ssRNA virus

recall, HDV is special because it requires an HBV infection to be infective itself.  (can only infect those with HBV)  perhaps the (-)ssRNA structure has something to do with this?

HCV and HBV coinfection is common... HCV infection often overshaddows the HBV infection, so that the HBV infection is occult.  Therefore, you must test for these two viruses at the molecular level (PCR). 

It is even more important to check for both HCV and HBV because coinfection leads to more severe disease and a higher risk of hepatocellular carcinoma.

Greatly simplified:

if HBcAb is up and HBsAb is up there was an infection but it was cleared (Acute)

if HBcAb is up and HBsAb is not up, there is an infection and it's not cleared (Chronic)

HPV 6 and HPV 11 are 'low risk' viruses that are the cause of genital warts (condyloma acuminata) and laryngeal papillomas.

HPV 16 and HPV 18 are 'high risk' viruses that have a greater chance of producing high grade dysplasias and cervical carcinomas.

The HPV E7 protein inhibits pRB, thereby causing the release of E2F transcription factor and promoting cell cycle progression.

E7 also inactivates p21, another cell cycle repressor

The general rule of thumb is "HSV1 above the belt (orolabial cold-sores) and HSV2 below the belt (genitals)" according to Hawley.

however, HSV1 also causes genital disease. 

The difference is that HSV2 genital lesions are more severe and recur more frequently.  According to bergeron "if you're going to get genital herpes, get HSV1"

The normal vaginal pH is 4.5-5

Trichomoniasis, caused by Trichomonas vaginalis, increases the pH to 5-6

bacterial vaginosis (Gardnerella vaginalis) also causes a slightly increased pH.

Diabetes, Aids, Antibiotics, Diaphragms, COCPs and foley catheters are predispose women to vaginal infection by candidiasis.

Tx = imidazoles or nystatin

Chlamydia can cause PID in women that go untreated.  This can result in salpingitis, leading to scarring, infertility, and ectopic pregnancy!

Treat chlamydia with Azithromycin or doxycycline

D-K serotypes are sexually transmitted
("a four letter word that starts with a D and ends in a K is involved in sexual transmission" -Hawley)

L1-L3 serotypes are found in lymphogranulosum venereum

(L for lymphogranulosum)

Skin lesions/petechiae and arthritis

a young sexually active woman with arthritis should be checked for lyme disease, disseminated gonorrhea, or juvenile arthritis...

Gonorrhea can lead to PID and infertility/ectopic pregnancy

It can also cause neonatal blindness!

Gonorrhea requires a special culture medium.  This can either be Thayer-Martin chocolate agar or NYC agar.

primary syphilis = hard, painless chancres.

diagnose with Darkfield Microscopy

secondary syphilis = condylomata lata/ maculopapular rash

diagnose with Non-Treponemal antibody test (VDRL, RPR), confirm with Treponemal test (FTA-Abs)

tertiary = Gumma, syphilitic aortitis, neurosyphilis

diagnose/confirm same as secondary

Toxoplasmosis

Rubella

CMV

Herpes

Rubella infection causes an increased risk of Diabetes Mellitus type I

(as well as cataracts/blindness, deafness, and heart defects)