• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/144

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

144 Cards in this Set

  • Front
  • Back
Shape of helicobacter?

Get nutrition?
gram negative

spiral shaped

Ferment amino acids, but do not ferment or oxidize carbs
What are the three species of helicobacter that infect humans?
H. Pylori

H. cinaedi

H. fennelliae
H. Pylori pathogenesis?
lives in mucous gel that coats gastric mucosa and or between mucous layer and epithelium

may attach to gastric epithelium

Produces large amounts of urease

bacterial surface factors attract neutrophils and monocytes that contribute to epithelial cell injury

Bacterial proteases and phopholipases break down mucous gel that shields gastric epithelium from acid

Host inflammatory response causes additional gastric epithelial damage but doesn't resolve infection -- ulcers
Virulence factors of H. Pylori?
Cag A (cytotoxin associated gene protein)

Vac A (vacuolating cytotoxin)

Pic B (induces cytokine production)
Why does H. pylori produce urease?
catalyzes breakdown of urea

local neutralization of acid allows survival of bacteria

NH3 damages epithelial cells
What leads to ulcers in H. pylori?
combo of toxins, inflammatory responses and exposure to acid
What is gastritis and what causes it?
H. Pylori

infliltreation of neutrophils and mononuclear cells into gastric mucosa

acute: feeling of fullness, nausea, vomiting, decreased acid production in stomach

may develop into chronic
What is peptic ulcer disease and what causes it?
H. pylori

Ulcers develop at sites of intense inflammation -->
- junction between corpus and antrum - gastric ulcer
- proximal duodenum - duodenal ulcer

Epigastric pain randing from ill-defined sensation like hunger pain to burning, gnawing discomfort.
- relieved by antacids or eating with duodenal ulcers
- may be exacerbated by eating with gastric ulcers
What does chronic gastritis normally lead to?
replacement of normal mucosa with fibrosis and proliferation of intestinal type epithelium

this increases risk of gastric adenocarcinoma
H. pylori is also associated with infiltration of what kind of tissue into gastric mucosa?
lymphoid tissue

Monoclonal population of B cells develops in small percentage of pts

may evolve into MALT lymphoma
Shape of salmonella?
gram negative rod

enterobacteriaceae
Pathogenesis of salmonella enterica
Attach to intestinal mucosa and invade into microfold cells (M cells) in Peyer patches

Replicate within endocytic vacuoles

Can be released into blood or lymphatic circulation

Invasion process regulated by genes located in two pathogenicity islands

Inflammatory response confines most infections to GI tract

Inflammatory response also:
- mediates release of prostaglandins
- stimulates cAMP production and fluid secretion into lumen (diarrhea)
What is gastroenteritis? Caused by?
Salmonella enterica

Incubation period: 6-48 hrs

Nausea, vommiting, diarrhea (loose, non-bloody)

Low grade Fever, abdominal cramps, headache, and myalgias also common

Usually self-limiting (resolving in 3-7 days)

Neonates, elderly and IC pts susceptible to dehydration, disseminated infections
What are some of the localized infections that result from bacteremia as a result of salmonella?
Endovascular infections (arteritis, endocarditis)

Intraabdominal infections (rare)

Meningitis (mostly in infants)

Pulmonary infections

Bone and joint infections

Reiter's syndrome
What are the different types of salmonella?
Salmonella enterica - gastroenteritis

S. Typhi - typhoid fever

S. paratyphi - paratyphoid fever

others.
Pathogenesis of S. typhi and paratyphi?
Pass through cells lining intesting and engulfed by macrophages

Replicate after being transported to bone marrow, speen, liver

Colonize gall bladder and re-infect intestines
Transmission of S. typhi and paratyphi?
food contaminated by infected food handler or water contaminated with fecal material
Enteric fever? Caused by?
S. typhi and paratyphi

also called typhoid fever, paratyphoid fever

Incubation: 10-14 days

Most prominent symptom: prolonged fever which may last for 4 weeks if not treated

Headache, myalgias, malaise, anorexia common

Rash is an early finding (rose spots)

Hepatosplenomegaly
Symptoms of severe enteric fever? Caused by?
S. typhi, paratyphoid fever

Gastrointestinal bleeding and intestinal perforation can develop in 3rd or 4th week

Possible neurologic manifestations: meningitis, GB syndrome, neuritis
Shape of shigella?
gram negative rod

enterobacteriaceae
What are the four GI pathogens of Shigella?
Dysenteriae

Flexneri

Boydii

Sonnei
Pathogenesis of shigella?
attach to and invade M cells in Peyer Patches

lyse phagocytic vacuole and replicate in cytoplasm

Invasion proceeds via cell-to-cell passage

Bacteria can induce apoptosis
Shigella: how does the invasion of the pathogen work? (mechanism)
cell-to-cell passage

Rearrangement of actin propels bacteria --> cytoplasm to adjacent cells (move directly from one cell to another)

Allows bacteria to avoid AB related clearance
Shigella: how does bacteria induce apoptosis?
release of IL-1B--> attracted of PMNs --> intestinal wall destabilization --> bacterial invasion of deeper epi cells)
Which strain of shigella uses Shiga toxin?
Dysenteriae

Similar to EHEC

Cleaves 28S rRNA in 60S subunit of ribosomes; disrupts protein synthesis

Primary effect: damage to intestinal epithelium

In small % of pts: damage to glomerular endothelial cells --> renal failure (HUS)
Populations that Shigella affects?
Peds

Homosexuals (males)
Transmission of Shigella?
person to person by fecal-oral route
- primarily on contaminated hands
- less often in contaminated food or water
What is Shigellosis?
caused by Shigella

Incubation: 1-4 days

Typical initial manifestations: transient fever, limited watery diarrhea, malaise, anorexia
- range from mild discomfort to severe cramps, diarrhea, fever, vomiting, tenesmus (straining to defecate)
- symptoms often more severe in children than in adults

May resolve or go to dysentery stage
What is the dysentary stage of shigellosis?
Acute collitis (mainly in distal colon and rectum)

Small volumes of bloody, mucopurulent stools

Increased tenesmus and abdominal cramps

Most cases self-limiting
What are the potential complications of Shigellosis?
Toxic megacolon: severe inflammation extends to colonic smooth-muscle layer --> paralysis and dilation

Hemolytic uremic syndrome
Shape of Vibrio?
gram negative curved rods
What are the medically important species of vibrio?
Cholerae (different serotypes) (water/food)

Parahaemolyticus (shellfish/seawater)

Vulnificus (shellfish/seawater)
Virulence factors for Vibrio cholerae.
Lysogenic bacteriophage CTXO encodes:

- Cholera toxin

- accerssoy cholera enterotoxin: increases intestinal fluid secretion

- zonula occludens toxin: increases intestinal permeability

- chemotaxin proteins: adherence to intestional mucosa

Adherence to intestional mucosa

Bacteria does not invade epitheliuml just attaches to surface and excretes toxins
What does the V. Cholerae cholera toxin do?
A-B exotoxin binds to intestinal epithelial cells

causes increase in levels of intracellular cAMP

Hypersecretion of water and electrolyes
Accessory cholera enterotoxin - bacteria and what does it do?
V. Cholerae

increases intestinal fluid secretion
Zonula occludens toxin - bacteria and what does it do?
V. cholerae

increases intestinal permeability
Chemotaxis proteins - bacteria and what does it do?
v. cholerae

adherence to intestinal mucosa
Transmission of V.cholerae?
contaminated food and water
What is cholera?
V. Cholerae

Incubation: 24-48 hours

Sudden onset of painless watery diarrhea that soon becomes voluminous
-Characteristic gray, cloudy fluid with flecks of mucous and no blood (rice-water stool)
- Somewhat sweet, inoffensive odor

Diarrhea often followed shortly by vomiting

Rapid and dangerous dehydration without fluid and electrolyte replacement
Shape of clostridium? Nutrition?
gram POSITIVE

spore forming rods

Mostly stricy obligate anaerobes
Species of clostridium important for humans?
Difficile

Perfringens

tetani

botulism
Virulence of C. difficile
Enterotoxin (toxin A)

Cytotoxin (toxin B)

Bacterial surface layer proteins (SLPs)
What does enterotoxin (toxin A) in C.difficile do?
stimulates infiltration of ileum by PMNs and release of cytokines

Disrupts tight cell-cell junctions (increased permeability of intestinal wall --> diarrhea)
What does cytoxin (toxin B) in C.difficile do?
depolymerizes actin, causes destruction of cytoskeleton, damage to intestinal epithelium
What does SLPs in C.difficile do?
bacterial surface layer proteins

facilitate binding to intestinal epithelium
what is pseudomembranous colitis and what is it caused by?
C. difficile

pseudomembranes develop on colonic mucosa

1-2 mm whitish-yellow plaques (contain fibrin, mucous and inflammatory cells); converge and become confluent

Abdominal cramps, fever, and leukocytosis

May lead to toxic megacolon etc
Basic characteristics of hepatitis viruses
Hep A - infectious Hep

Hep B - serum hepatitis

Hep C - Non-A, Non-B post transfusion hep

Hep D - Enteric non-A, non-B hep
Which Heps have envelope?
B, C,D,G
Which Heps have + sense ss-RNA genomes?
A, C,E,G
Hep A and E pathogenesis
Hit and Run

Replicate in hepatocytes and Kupffer cells (released by exocytosis)

Large numbers of virions shed in stool 10 days before any obvious symptoms develop or ABs can be deteected (virions --> bile ducts --> intestines)

Liver pathology probably caused primarily by immune responses
What is the clinical presentation of Hep A and E?
Milder in children than adults

Incubation period 15-50 days

Initial symptoms (fever, fatigue, nausea, abdominal pain, loss of appetitie) occur abruptly and intensify for 4-6 days

Icteric phase: jaundice, dark urine, pale stools

Complete recovery in 2-4 weeks
Hep B pathogenesis
Replicates in hepatocytes with little cytopathic effect (released by exocytosis; not cytolytic)

Infection progresses slowly over relatively long time; can take 45 days or longer for symptoms to develop

Cell-mediated immunity, inflammation --> symptoms, but also work to resolve infection (highly effective but with severe symptoms)

Insufficient T cell response may lead to mild symptoms but inability to resolve infection and chronic disease)

Infections may be acute or chronic, symptomatic or asymptomatic
Clinical presentation of Acute Hep B infection
Less severe in children

Long incubation period

Subtle onset of symptoms

Prodormal period

Icteric period

Fulminant hep develops in 1% of icteric pts
Clinical presentation of Chronic Hep B infection
Occurs in 5-10% of HBV infections

there is chronic active and chronic passive
Three types of Hep C diseases?
Acute

Chronic Persistent infection
- initial disease asymptomatic
- usually progresses to chronic active disease in 10-15 yrs

Severe, rapid progression to cirrhosis
What is Hep D?
Delta agent

Incomplete virus that replicates and causes disease only in people with active HBV infections
-uses HBV and target cells proteins to replicate

Increases likelihood of fulminant hepatitis

Chronic infections possible
Rotavirus: enveloped? genome?
Non-enveloped

ds RNA
Pathogenesis of rotavirus
Diarrhea

Replicates in columnar epi cells covering villi of small intestine

Mucosal damage leads to malabsorption which leads to a net secretion of water and loss of ions = diarrhea
Transmission of rotavirus?
fecal-oral

survives well on fomites
Diseases that rotavirus can cause
Gastroenteritis
what is cryptosporidium?
protozoan parasite with worldwide distribute
What are the species of cryptosporidium that infect humans?
C. parvum and C. hominis
Transmission of cryptosporidium?
fecal oral
oral anal
cryptosporidium pathogenesis
invasion of tissues limited to epithelium

not alot known about it
What is cryptosoridiosis? Caused by?
cryptosporidium

presentation in IC hosts:

Incubation period 1 week

Watery diarrhea

some cases have prodome

Illness usually subsides in 1-2 weeks

Clinically significant dehydration

Biliary tract involvement can cause midepigastric or upper right quadrant pain
Life cycle of the pinworm
Ingestion of embryonated eggs starts infection

Larvae hatch in small intesting, migrate to large intestine, and mature into adults.

Fertilized females migrate to perianal area at night and deposit eggs in folds of skin there

The eggs mature rapidly and become infectious within a few hours.
What is enterobiasis? Caused by?
Pinworm

Severe pruritus in people allergic to worm secretions

Many asymptomatic
What are strongyloides?
infection form of the filaiform larvae penetrate human skin, enter circulatory system and migrate to lungs

larvae coughed up from lungs and swallowed, then develop into adults in small intestine

adult females burrow into mucosa of duodenum and produce eggs

Eggs hatch in mucosa and release rhabditiform larvae which is passed in stool
Direct infection cycle of strongyloides
Free rhabditiform larvae develop into infectious filariform larvae

invade through skin of new host
Indirect infection of strongyloides
free living adult worms live in soil and produce eggs and larvae

may lead to several generations as free living organisms before invading through skin of new host
What two pathogens cause gastroenteritis in a very short incubation period? (2 hrs)
Staph aureus

Bacillus Cereus (most often associated with fried rice)
Food poisoning on Florida's Gulf coast suggests?
Vibrio parahemolyticus
How does Vibrio parahaemolyticus get into food?
commonly present in marine and esturaine environments

can easily contaminate shellfish and other types of seafood

Filter feeders (like oysters) actually concentrate Vibrio and other bacteria in their bodies (E.Coli, Hep A, Polio etc)

Disease occurs when contaminated seafood is eaten raw or undercooked
What is kanagawa hemolysin? What pathogen does it belong to?
toxin of V. Parahaemolyticus

increases intracellular Ca in GI epithelial cells

increase Ca leads to Cl secretion and loss of water (different from cAMP mechanism)
What is indicated by the combination of fever with fecal leukocytes and RBCs?
an inflammatory diarrhea (as opposed to toxin-related food poisoning)
Shape of campylobacter jejuni?
small, comma shaped, gram negative rod
What are the species of campylobacter that affect humans?
jejuni - poultry, cattle sheep

coli - pigs, poultry, sheep, birds

upsaliensis - dogs and cats (not seen in US very often)

fetus - cattle and sheep (does not cause gastroenteritis)
How are humans infection with C. jejuni or C. coli?
by consuming contaminated milk, food or water

zoonotic infections

poultry responsible for more than half of the infections in developed countries
What is the most frequent cause of bacterial gastroenteritis in the US?
C. jejuni
What are the two most frequent viral causative agents of diarrhea outbreaks?
Rotaviruses

Noroviruses (Norwalk Virus) - more likely in adults
Norwalk - enveloped? genome?
+ sense RNA

Non-enveloped
How are norwalk viruses transmitted?
contaminated hands via fecal-oral route

Directly from person to person

contraminted food or water

by contact with contaminated surfaces (fomites)

May also be transmitted via aerosolized vomitus
What is the leading overall cause of gastroenteritis?
Norwalk virus
how is amebiasis transmitted?
fecal oral route
What does the involuntary flexing of the legs when the neck is passively flexed indicate?
Brudzinski Sign

Indicates inflammation of meninges
Brudzinski Sign
involuntary flexing of the legs when the neck is passively flexed
Neisseria: shape, nutrition?
Aerboic

Gram negative

diplococci
Virulence of N. meningitidis?
Pili

Capsule

Porin Proteins (PorA and PorB)

Lipooligosaccacharide (LOS): contains endotoxin
What are physicians looking for when they check for pailledema?
signs of increase ICP
What does the involuntary flexing of the legs when the neck is passively flexed indicate?
Brudzinski Sign

Indicates inflammation of meninges
Brudzinski Sign
involuntary flexing of the legs when the neck is passively flexed
Neisseria: shape, nutrition?
Aerobic

Gram negative

Diplococci
Virulence of N. meningitidis?
Pili

Capsule

Porin Proteins (PorA and PorB)

Lipooligosaccacharide (LOS): contains endotoxin
What are physicians looking for when they check for pailledema?
signs of increase ICP
Empiric therapy in childhood meningitis?
ceftriaxone and vancomycin
Pathogenesis of Neisseria meningitidis
Adheres to nonciliated epithelial cells in naspharynx

internalized into phagocytic vacuoles (but can avoid phagocytosis)

Replicates in epithelial cells

Migrates too subepi spaces then into the bloodstream and then to CNS
Transmission of N. meningitidis
droplet infection

asymp carriage faciliatates person to person transmission
What is meningococcemia?
bacteremia (without or without meningitis) --> thrombosis of small blood vessels and multiorgan involvement

Small petechial lesions on trunk and lower extremities may coalesce --> large hemorrhagic lesions

Possible overwhelming DIC and shock, with bilateral destruction of adrenal glands
What is Waterhous-Friderichsen syndrome?
possible overwhelming DIC and shock with bilateral destruction of adrenal glands brought about by meningococcemia

N. meningitidis
What are the 6 causative agents of bacterial meningitis?
Strep pneumoniae: most frequent >20 y/o

N. meningitidis: 25% of all cases; up to 60% in children and young adults

Enteric Gram-negative rods: mostly in pts with chronic and debilitating diseases like diabetes, cirrhosis, alcoholism

Group B Streptococcus: primarily associated with meningitis in neonates, but no reported with increasingly frequency in adults

Listeria monocytogenes: important cause of meningitis in neonates

Hawmophilus influanzae B
Clostridium: shape, nutrition?
Gram positive

spore forming rods

Mostly strict obligate anaerobes

PART OF NORMAL GI FLORA
Types of clostridium?
difficile: AB associated diarrhea, pseudomembranous colitis

perfringens: soft tissue infections (cellulitis etc) food poisoning, enteritis, necroticans, bacteremia

tetani: tetanus

Botulinum: botulism
Virulence of C. tetani
Tetanus toxin
What is tetanus toxin?
C. tetani

AB toxin encoded on plasmid

Binds specifically to sialic acid receptors and adjacent glycoproteins on surfaces of motor neurons

Internalized and transported in axon to motor neuron soma in spinal cord

Enzymatically cleaves proteins that regulate release of inhibitory NTs glycine and GABA

Unregulated excitatory activity in motor neurons --> spastic paralysis of muscles

toxin damage irreversible, so recovery depends on whether new axonal terminals form
Why do you get spastic paralysis from tetanus?
unregulated excitatory activity in motor neurons caused by enzymatic cleavage of regulatory proteins for inhibitory NTs
Where can clostridium tetani be found? (environment?)
Inhabitant of soils

Vegetative form killed by O2 but spores are not

Spores from soil enter through would, germinate and produce toxin

Tetanus quite rare in US since use of vaccine

Most cases now in elderly with waning immunity
What is tetanus?
Clostridium tetani

incubation period: days to weeks

Usual presenting symptom: sardonic "smile" (risus sardonicus) from sustained contraction of masseter muscles (lockjaw)

Other early signs: drooling, sweating, irritability, and persistent back spasms

Severe cases can involve ANS which lead to:
- cardiac arrythmias
- fluctuations in blood pressure
- excessive sweating
- dehydration
What are opisthotonos?
persistant back spasms
C. botulinum virulence?
Botulism toxin
Botulism toxin
binds to specific sialic acid receptors and glycoproteins (not those targeted by tetanus toxin) on surfaces of motor neurons

Toxin internalized and stays at neuromuscular junction

toxin enzymatically inactivates proteins that regulate release of AcH

Neurtransmission at peripheral cholinergic synapses (required for excitation of muscle) blocked

Results in flaccid paralysis of muscles controlled by affected motor neurons

Recovery requires regeneration of nerve endings
Why does C. botulinum cause flaccid paralysis?
Neurotransmission at cholingeric synapses blocked - these are required for excitation of muscle

Results in flaccid paralysis of muscles controlled by affected motor neurons
What is the recommended first line therapy for treatment of clinical tetanus?
Metronidazole

It stops bacterial replication to reduce production of toxin
Why is penicillin no longer first line for treatment of tetanus?
It is structurally similar to GABA the effect would be potentiation of the effect of tetanus toxoid
Where can clostridium botulinum be found?
common resident of soil and aquatic environments

Foodborne
4 types of botulism?
Fooborne

Infant - SPORES (not toxin)

Wound botulism

Inhalation
Foodborne botulism: incubation period
C. botulinum

Incubation period: 1-2 days after consuming toxin
Fooborne botulism: initial signs
blurred vision

dry mouth

constipation

abdominal pain

no fever
Foodborne botulism: other signs (not initial)
bilateral descending weakness of peripheral muscles

Death usually from respiratory paralysis
Infant botulism: why do they get it?
infant <1 year of age lack sifficient intestinal flora to compete with C. botulinum if spores ingested

C. botulinum becomes established and produces toxin (doesnt happen in adults)
What are initial signs of infant botulism
constipation

weak cry

failure to thrive
Signs of infant botulism (not initial)
progressive flaccid paralysis if not treated (floppy baby syndrome)

Low mortality rate with proper treatment
Typical symptoms of brain abscess
Dull, aching, and poorly localized headaches

Focal neurologic symptoms; specific features depend on location of lesion

Fever

Papilledema

WBC counts: normal

Blood cultures are positive only in 10% cases
First step in treatment of botulism. Anything different for infants?
admin of anti toxin

Infants CANNOT receive antitoxin because their disease is a result of the actual bacteria/spores and not just the toxin. Treat with botulism antibody (Ig)
Routes of infection for brain abscess
Direct spread from contiguous cranial infection (otitis media, dental infection, sinusitis)
Treatment options for brain abscess
AB therapy alone: multiple, small or deep seated anscesses or if pts general condition does not allow surgery

Abscess aspiration (often by sterotaxic surgery)

Open craniotomy and evacuation of abscess cavity or excision of abscess
What is the most frequent cause of gas gangrene associated with a dirty wound?
clostridium perfringens

Gram positive

spore forming rod
Where is clostridium perfringens found?
soil and fecal matter
C perfringens virulence factors
at least 12 toxins and enzymes

ALPHA TOXIN

Phospholipase C lyses RBCs, platelets, endothelial cells

massive hemolysis, increased vascular permeability, bleeding, massive tissue destruction
Pathogenesis of C. perfringens?
Wound infection starts as cellulitis with gas bubbles

Suppurative myositis

Clostridial myonecrosis (gas gangrene)
Suppurative myositis
first stage of gas gangrene

Systemic symptoms (fever)
accumumlation of pus in muscle plains
no destruction of muscle tissue
Clostridial myonecrosis (gas gangrene)
second stage of gas gangrene
What would be the first line recommended treatment C. perfringens?

If pt is allergic to pen?
Pen G

Clindamycin (good for anaerobes)

Allergic: metronidazole and clindamycin
C. perfringens affects what parts of the body?
gangrene anywhere

GI track (food poisoning)
What is suggested by acute onset of pain with warmth, erythema and pain on passive movement? (Bacterial)?
Infection of joints

Sinovitis
What are the most likely causative agents of joint infections?
infections of joint replacements now fairly rare

But urgent empiric treatment required prior to ID of causative agent by lab

Most of these infections acquired intraoperatively or postoperatively as a result of wound infections
What is the recommended empiric treatment for a pt with a joint infection?
You want to think about what the bug could be: P. aeruginosa, staph, strep

Vancomycin, Clindamycin, or a 3rd gen cepahlo

The pt has a high probability of being infected with staph or strep introduced into the pt during surgery

Since this would be a nosocomial infection, the organism is presumed to be a resistant strain.
Coagulase negative staph?
Staph epidermidis

Staph aureus is coag+
What is the appropriate treatment for S. epidermidis is identified as the causative agent?
Vancomycin or Clindamycin
What is associated with fever, chills, swelling, tender, boils on neck and chest (can be scarred and crusted)?
osteomyelitis
What organism is isolated from more than 50% of osteomyelitis patients?
staph aureus
Microbes enter bones by one of three routes:
- hematogenous route

- direct spread from contagious focus of infection

- Direct introduction by penetrating wound
what are sequestra?
progressive ischemic necrosis of bone which leads to separation of large devascularized bone fragments - this occurs in chronic osteomyelitis
What are Involucrum?
elevated periosteum deposits new bone tissue
Reiter's syndrome?
reactive arthritis that sometimes develops following certain types of bacterial infections

Classic: asymmetric poly arthritis, balanitis, urethritis, conjunctivitis, uveitis, oral ulcers, and rash

Not all pts have all symptoms; some may present only with polyarthritis

Follows 1% of NGU cases

Known to follow other kinds of mucosal infections (GI):
- Yersinia enterocolitica
- Campylobacter jejuni
- Salmonella