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Micro 2 Flashcards

0
Q

What kind of virus is rotavirus?

A

Reoviridae

  • dsRNA genome - 11 segments
  • most important cause of gastroenteritis in young children
  • group A assoc. w/ human disease
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1
Q

What is orthoreovirus?

A

A member of reoviridae

Infects mammals, but not associated with serious disease in humans.

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2
Q

What cells do Rotavirus infect?

How long is incubation?

A

Tip of villi in sm. intestine

  • as few as 10 particles can cause infection
  • 1-4 days incubation period
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3
Q

Describe rotavirus pathogenesis

A

virus capsid proteins attach to glycolipid receptor on the apical enterocytes of sm. intestine villi.

  • Damage to sodium and glucose absorptive mechanisms -> increased luminal H2O volume. Viral replication -> acute onset of vomiting and diarrhea
  • Activation of intestinal nerves -> secretion of H2O
  • Fluid accumulation in lumen of sm. intestine, 10-20 diarrheal episodes / day and severe dehydration
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4
Q

Describe rotavirus structure

A

Unenveloped, icosahedral, 3 layer protein capsid
Segmented dsRNA genome
capsid contains all enzymes needed for replication
VP4 receptor protein - binds glycolipid of host cell

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5
Q

What are the major coat proteins of rotavirus?

A

VP4 - outer coat - binds receptor (sialic acid / integrins)
VP7 - outer coat - stripped during endocytosis
VP6 - middle coat - major protein that is tested for in antibody titer
VP2 - inner coat

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6
Q

How is rotavirus infection diagnosed in a lab setting?

A

Presence of virus particles in feces early in illness
- immune electron micoscopy, ELISA, immunoassay

Rise in titer of Ab to VP6

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7
Q

What are the two most important viruses contributing to diarrheal illness in children?

A

Rotovirus (reoviridae)

Adenovirus

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8
Q

What type of genetic material is carried by Adenovirus?

A

dsDNA

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9
Q

What is the most common cause of viral gastroenteritis in older children and adults?

A

Norovirus

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10
Q

How is norovirus transmitted?

A

fecal-oral

also contaminated food: shellfish and contaminated water

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11
Q

How long is the Norovirus incubation period and how long does it remain contagious?

A

incubation: 12-48 hours
From onset of symptoms: highly contagious until at least 3 days after symptoms recede - infectious viral particles may be shed as long as 2 weeks after illness

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12
Q

Norovirus symptoms

A

Acute onset of vomiting, diarrhea, stomach cramps, headache, fever, chills, myalgia

symptoms resolve 24-48 hours after onset.

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13
Q

How is norovirus spread prevented?

A

Handwashing - soap and water (alcohol hand-gel is inadequate)
10% bleach to clean surfaces.

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14
Q

What family of viruses is norovirus from?

A

Calicivirus

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15
Q

What is norovirus genome?

A

ss+RNA

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16
Q

What virus families do Hepatitis viruses A-E belong to?

A 
Hep A:  Picornavirus
Hep B:  Hepadnavirus
Hep C:  Flavivirus
Hep D:  satellite virus - undefined classification
Hep E:  Hepevirus (Hep - E - virus)
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17
Q

Genomes of Hepatitis A-E

A 
A:  ssRNA
B:  dsDNA
C:  ssRNA
D:  ssRNA (-)
E:  ssRNA
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18
Q

Which Hepatitis viruses produce chronic illness?

A

B and C

D in the context of association with B (is not infective on its own)

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19
Q

What causes hepatic cellular carcinoma

A

Chronic viral infection is leading cause (HBV, HCV)
course of chronic illness is 25-50 years
Ultimate cause: constant inflammation and constant stimulation of cellular replacement -> mutation and tumor formation

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20
Q

What was the first successful recombinant vaccine for a human disease?

A

Hep B vaccine

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21
Q

How is HBV spread?

A

sexual contact and parenteral exposure

most adults clear infection - 5% do not -> chronic infection
–May be asymptomatic

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22
Q

Describe the HBV genome

A 
Circular, partially double stranded DNA.  
Full length (-), 20-80% (+)
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23
Q

Describe the process of HBV replication

A

Genome is circular (-) DNA with partial (+) DNA. In nucleus, cellular DNApol -> full dsDNA
(-) DNA -> full length (+) RNA via host cell RNA pol II
(+) RNA is packaged in new core proteins
viral RNA/DNA dependent DNApol -> full length (-)DNA
(-)DNA copied by viral DNApol -> partial (+) DNA
HBsAg containing envelope acquired on exocytosis

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24
Q

How is HBV prevented / treated?

A

Recombinant vaccine
Interferon - alpha and/or inhibitors of HBV polymerase

These do not eliminate infection*

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25
Q

Describe Hep D’d genome and what it codes

A

Small (-)RNA genome (1.7kb)

codes one protein: delta antigen: RNA encapsidation

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26
Q

What is HDV superinfection?

A

Infection w/ HDV after host is already infected with HBV.
contrast w/ coinfection, where both acquired together
Superinfection -> high mortality (20%)

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27
Q

What family of viruses does HCV belong to?

A

Flavivirus

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28
Q

Describe HCVs genome

A

(+)ss linear RNA

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29
Q

How is HCV infection treated?

A

Combination of interferon-alpha and ribavirin
-can eliminate infection, but IFNa has unpleasant side-effects

2 new drugs w/ this mix -> 70-80% cure rate

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30
Q

How is HCV transmitted?

A

Contaminated blood products
Injection drug use
Mother to child (uncommon)
sexual contact

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31
Q

what is the leading cause for liver transplant necessity?

A

HCV infection

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32
Q

What is the course if HAV infection in humans?

A

Initial infection in intestinal mucosa -> liver -> lymphoid cells
Virus is excreted in large volume (10^8 infective units/ gm feces) in feces.

no chronic infection leading cause of jaundice world wide

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33
Q

Where is HEV infection most common? Who is most severely effected?

A

Mostly in developing countries - drinking water contaminated w/ feces. May be carried by rats, pigs, deer.
Pregnant women - 20% mortality rate

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34
Q

What are M cells?

A

Found in mucus membranes of GI - antigen presenting cells

phagocytize bacteria and foreign particles and pass them to macrophages underlying the Mcell

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35
Q

What is MacConkey’s agar?

A

Selects for gram (-) organsisms
Bile salts and crystal violet inhibit gram (+) growth
pH indicator distinguishes between lactose fermenting (pink colonies) and non lactose fermenting organisms

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36
Q

3 types of secretory diarrhea and responsible organisms

A

Secretory Diarrhea: non-inflammatory, non-invasive

  1. Bacterial enterotoxigenic: Enterobacteriaceae and Vibrionaceae
  2. Bacterial neurotoxic: usually a preformed toxin is ingested: C.botulinum, B.cereus, S.aureus
  3. Non-inflammatory parasitic: G.lamblia, C.parvum
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37
Q

3 types of invasive inflammatory diarrhea and organisms responsible

A
  1. Bacterial cytotoxin caused inflammation: C.diff, EHECCCC
  2. Bacterial invasive infection: Shigella, EIEC, Salmonella
  3. Parasitic invasive: E.histolytica
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38
Q

Vibrio Cholerae: organisms of interest and characteristics

A

O1 and O139
Gram neg, oxidase pos, motile (single polar flagella), comma shaped rods
found in brackish water, fresh water ponds, can colonize shellfish
Two types of O1: Classic and El Tor
Classic - highly virulent, but does not survive freely in enviro well
El Tor - less virulent, but survives in environment for long periods

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39
Q

What are V.cholera’s virulence factors?

A

Motility - single polar flagellum
Adhesion - tcp pili (toxin co-regulated pili) and other adhesins - tight adhesion to intestinal epithelium
Cholera toxin

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40
Q

Describe Cholera toxin and its activity

A

AB type toxin (A is enzymatic, B is binding, consists if 5 identical units)
ADP ribosylating
B attaches to GM1 ganglioside, A1 is released to enter cell
A1 ADP-ribosylates Gs -> chronic activation of Gs -> massively increased cAMP -> hypersecretion of fluids, chloride ions, inhibition of Na absorption
End result is massive fluid loss

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41
Q

Describe the etiology / pathogenesis of cholera

A

ingestion of organism via contaminated water or food
10^8 organisms needed for infection - V.cholera sensitive to gastric acid
2-3 day incubation period, high replication
vomiting, high volume watery rice-water diarrhea no PMNs profound dehydration

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42
Q

How is Vibrio cholera identified in the lab?

A

Stool sample
Culture on TCBS (thiosulfate-citrate-bile salt-sucrose agar) - highly selective for vibrio species
Positive oxidase test
O antigens: O1 and O139 - assoc. w/ cholera toxin producing strains

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43
Q

5 classifications of E.coli and assoc. symptoms

A

ETEC (Enterotoxogenic): Watery d., cramps and low fever. Infants and travellers. Cytotoxins increase cAMP or cGMP
EAEC / EAggEC (Enteroadhesive): Persistent infant d., also AIDS pts. Sometimes gross blood. Low fever. Aggressive adherence to intestinal mucosa prevents fluid absorption
EPEC (enteropathogenic): copious watery d. w/ mucus in infants. Fever, N/V. Adhere and destroy epithelium of INTESTINE
EIEC (enteroinvasive): watery diarrhea then scant bloody stools. fever. invasion and destruction of epithelium of COLON
EHEC (enterohemorrhagic): watery d. then grossly bloody d. Hemolytic uremia (O157:H7). Cytotoxic verotoxin prevents protein synth.

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44
Q

What is ETEC and how is it identified

A

Enterotoxic E.coli - causes secratory diarrhea - traveler’s diarrhea, Montezuma’s revenge. Major cause of infant mortality worldwide.

ELISA or agglutination tests for the presence of toxins
DNA probes for LT and/or ST genes

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45
Q

What are the ETEC toxins?

A

LT - heat labile toxin - destroyed at 100deg C for 30 min, 75% similarity to cholera toxin (AB structure) and same mechanism (B binds GM1, A unit: ADP ribosylation of Gs -> increased cAMP or cGMP) new evidence: Type II secretion
ST - heat stable toxin - not destroyed at 100deg C for 30 min., family of small molecules. Bind membrane bound guanylate cyclase -> chronic elevation of cGMP -> fluid and electrolyte loss
note: both LT and ST are plasmid encoded

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46
Q

How is ETEC spread? What are symptoms?

A

contaminated food and beverages
most common in tropics and in young
Symptoms: N/V, weakness, dizziness, then watery diarrhea

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47
Q

How do ETEC adhere to a host?

A

Colonization Factor Adhesions (CFA) - plasmid encoded - allow binding to epithelium of sm. intestine

Bundle forming pilus - similar to Tcp pili of v.cholera

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48
Q

What is EPEC and how is it identified in the lab

A

Enteropathogenic E.coli: causes severe, often fatal, diarrhea in infants and children primarily in developing countries. Traveller’s diarrhea in adults.

Identified via ELISA and multiplex PCR

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49
Q

How does EHEC attach to host cells?

A

Bundle forming pilus - non-intimate attachment
Tir and intimin - closer, intimate attachment
-bacteria produce and secrete Tir (type III secretion), which embeds in host cell membrane and binds to bacterial intimin (in bacterial outer membrane), Tir interacts w/ actin cytoskeleton and forms pedestal-like structure beneath organism -> effacement: destruction of pili

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50
Q

Describe the etiology / pathogenesis of EPEC

A

Fecal - oral spread
Diarrhea not caused by toxin: caused by destruction of microvili (rearrangement of actin cytoskeleton) -> malabsorption and diarrhea

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51
Q

What is clostridium botulinum and how is it recognized in a lab?

A

Obligate anaerobe, gram (+) rod that produces botulism neurotoxin.
Spore forming
Usually clinical identification w/o culture
Can be grown in O2 free lab environment
Immune assay for toxin in food sample, blood, gastric contents

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52
Q

How does botulinum toxin work?

A

Usually ingested as a preformed toxin via contaminated food
sypmtoms 12-36 hrs after ingestion
AB toxin - B portion binds ganglioside receptors on nerve cells
Toxin blocks presynaptic release of ACh - prevention of muscle contraction and flaccid paralysis - death via respiratory collapse

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53
Q

Can botulinum toxin be inactivated?

A

Yes - boil 10-15 minutes

Spores are not destroyed (can withstand 100deg C for 3-5 hrs)

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54
Q

What are infant and wound botulism?

A

Infant botulism: infants have incomplete gut microflora. C. botulinum can colonize and produce toxin -> SIDS (v. rare)
-seen in cases of mothers giving infants honey

Wound botulism: colonization of deep wound (anaerobic) - organism found in nature, can contaminate wound, grow and produce toxin

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55
Q

What is the most common form of bacterial food poisoning?

A

Staph aureus

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56
Q

Describe S.aureus enterotoxin action.

A

Preformed toxin is ingested and absorbed. Assoc. w/ food being left out - potato salad, cold cuts.
Stimulation of neural receptors in gut - signal to emetic center -> projectile vomiting within hours
Enterotoxin is heat stable

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57
Q

What bacterial food-borne organism is associated with Chinese restaurants / fried rice?

A

Bacillus cereus

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58
Q

Describe B.cereus toxic effects

A

2 forms:

  1. Emetic: (1-6 hrs post ingestion) ingestion of preformed toxin (fried rice held at room temp for a long period). S.aureus like N/V, cramps
  2. Diarrheal: (8-16 hrs. post ingestion) toxin formed in vivo. Activation of intestinal AC -> elevated cAMP, fluid excretion, diarrhea. meat or veg. foods held at room temp after cooking.
    * ** both forms subside ~24 hrs. after onset ***
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59
Q

What is Clostridium perfringens?

A

Gram (+) rod, anaerobic spore-former.
Similar toxic effect to B.cereus
Assoc. w/ cooked food being left at room temp (meat, veg, gravy)
Abd cramps, N/V, diarrhea, no fever.
Symptoms 8-24 hours after consumption. Toxin produced in GI tract.

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60
Q

What are the symptoms of Giardia lamblia infection?

A

Acute watery diarrhea, cramping, flatulence.

May develop chronic diarrhea. Symptoms may wax/wane over a long period. Weight loss common.

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61
Q

What is Giardia lamblia and how is it identified?

A

Protozoan. Flagellated.
Two stage life-cycle: Trophozoite (free-living) cyst (infective)
Identified by microscopic examination of stool, duodenal aspiration, or duodenal biopsy - look for cyst
string test
Antigen test of stool

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62
Q

What is giardia’s incubation period?

A

7-10 days

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63
Q

What is Cryptosporidium parvum? Describe infection

A

Protozoan most often isolated in HIV patients w/ diarrhea
severe, prolonged, watery diarrhea in immunocompromised, less severe in normal
Oocyst ingested in contaminated water -> sporozoite in intestine -> Enters intestinal epithelial cells -> sexual / asexual reproduction -> oocysts released and shed in feces

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64
Q

What is Clostridium difficile and how is it identified?

A

Gram (+) rod, anaerobic, spore forming
Normal flora in ~5% of adults, but can cause inflammatory diarrhea (inflammation of colonic mucosa)
Culturing is not helpful to identification
Toxin test on stool is most helpful: EIA

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65
Q

What are C.diff’s virulence factors?

A

2 toxins
A: enterotoxin: -> accumulation of viscous bloody fluid in colon. Chemotactic for PMNs -> PMN lysis -> release of inflammatory mediators, fluid secretion, altered membrane permeability, Hemorrhagic necrosis of mucosa.
B: cytotoxin: disrupts actin polymerization and cytoskeletal organization, inhibits protein synthesis - similar in effect to diptheria toxin

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66
Q

What is pseudomembranous colitis?

A

Can be caused by C.diff infection
pseudomembrane forms at site of epithelial cell destruction - consists of fibrin, mucin, and dead PMNs, leukocytes
Produces watery, sometimes bloody diarrhea, may be mucus present. Abdominal pain and cramps, fever, nausea. In severe cases may be lethal.

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67
Q

What is EHEC?

A

Enterohemorrhagic E.coli (also STEC (shiga-toxin e.coli) and VTEC (verocytotoxin e.coli))

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68
Q

How is EHEC identified in the lab?

A

Gram (-) rod, facultative anaerobic
O157:H7 does not fement sorbitol, so can be selected for on sorbitol MacConkey agar
Serotype with anti-O157:57 serum
demonstrate pathogenic activity with vero cells
DNA probe for shigella toxin genes

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69
Q

EHEC virulence factors

A

Adhesion: Tir and intimin production - tight binding
Toxin: Shiga toxin
Type III secretion: attaching and effacing lesions

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70
Q

What is Shiga toxin?

A

Produced by EHEC also vero cytotoxin
AB toxin
B binds G3 ganglioside receptor. A subunit enzymatically modifies 28S rRNA of 60S ribosomal subunit - blockade of protein synthesis and cell death
Capillary thrombosis, inflammation of colonic mucosa, hemorrhagic colitis
Shiga Toxin I and II encoded by plasmids (Stx1, Stx2)

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71
Q

Describe the etiology of EHEC

A

Usually spread via contaminated food (Ground beef)
Small number of organisms can cause infection
Incubation period of 3-4 days - severe crampy watery diarrhea that evolves to grossly bloody diarrhea
Hemolytic Uremic Syndrome: 5-10% of patients - esp. children
-acute renal failure, thrombocytopenia, hemolytic anemia.
-shiga toxin damages renal glomerular cells

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72
Q

How is Shigella identifiable in the lab?

A

Gram (-), non-motile, lactose neg on MacConkey and Hektoen agars.
Serotyping - 4 groupings:
1. Group A: S. dysenteriae (Shiga bacillus - largest producer of toxin)
2. Group B: S. flexneri
3. Group C: S.boydii
4. Group D: S.sonnei (60-80% of US cases)

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73
Q

Describe Shigella infection and illness

A

Transmitted by food, fingers, flies, feces
Organisms multiply in sm. intestine, esp. lower sm. intestine.
First 12 hrs: abdominal pain, cramping, fever
12-72 hrs: organism is no longer in upper intestine. pain intensifies, dysentery, tenesmus, lethargy. Many PMN in mucoid stool.

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74
Q

Explain Shigella virulence

A

Invasiveness: entry via M.cells, passed to macrophage, apoptosis induced, IL-1, inflammatory factors, PMN chemotaxis
PMN open tight junctions allowing Shigella to penetrate epithelium.
Escape from phagosome and movement to epithelial cells. Actin rearrangement “actin based motility” - allows bacteria to move through cell and enter neighbors.
Epithelial cells die after infectoin - ulcerative colitis
Product is bacillary dysentery. Only S. dysenteriae produces toxin which contributes to death of epithelium. Primary virulence is via cell invasion.

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75
Q

What is EIEC?

A

Enteroinvasive E.coli
Behaves like Shigella - cell invasion, actin rearrangement - cell death - dysentery. Symptoms the same.
No tests to differentiate from other E.coli strains,but can be differentiated from Shigella. Rare.

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76
Q

3 forms of Salmonella infection

A

Gastroenteritis: most common - 8-48 hour incubation, abrupt onset, low fever, diarrhea, N/V, 2-5 day duration.
Bacteremia: invasion of blood stream following oral ingestion. High spiking fever, septic. Usually no GI symptoms. Rare.
Enteric (Typhoid) Fever: 7-20 day incubation, chills, headache anorexia, myalgia, enlarged spleen and lymph nodes, gradual fever, insidious onset, early constipation followed by bloody diarrhea, lasts several weeks. 1/3 of patients develop maculopapular rash (rose spots) on trunk.

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77
Q

In chronic carriers of Salmonella, where is the organism reservoir?

A

Gall bladder

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78
Q

What size Salmonella inoculum causes illness?

A

10^4 - 10^8

Large inoculum needed.

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79
Q

Explain Salmonella’s virulence

A

Invasion: enter M cells or intestinal mucosa epithelial cells - multiplication within vessicles (phagosomes) -> cell lysis
Type III secretion: Actin rearrangement -> ruffled border
Endotoxin: Lipid A of LPS induces inflammatory response and contributes to mucosal dammage.

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80
Q

How is Salmonella identified in the lab?

A

Gastroenteritis: culture lactose neg, oxidase neg colonies, serological tests to determine serotype (there are many)
Bacteremia: blood cultures, stool cultures (usually negative)
Typhoid fever: early - blood culture, later - stool

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81
Q

How can Salmonella be differentiated from Salmonella in the lab?

A

Growth on Hektoen enteric (HE) agar

Salmonella grows distinct black colonies due to H2S production

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82
Q

What is campylobacter infection associated with?

A

Usually chicken consumption - undercooked

Sometimes other meats, raw milk

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83
Q

What are the symptoms of campylobacter infection?

A

Fever, malaise, abd. cramps, profuse watery / bloody diarrhea, mucosal inflammation.

84
Q

How is campylobacter identified?

A

Small, motile, flagellated bacteria. Comma shaped, gram (-), Oxidase pos (vs. Salmonella and Shigella neg)
Microscopy: stool sample - darting motility
Will not grow on MacConkey
microaerophilic and capnophilic (doesn’t ferment glucose)

85
Q

What are Campylobacter’s virulence factors?

A

Flagella - motile in mucus layer of sm. intestine, multiply in mucus
Toxins - enterotoxin, endotoxin, cytotoxin - destroy intestinal cells -> bloody diarrhea
Protein S - surface protien, blocks complement binding - serum resistance to phagocytosis
Autoimmune response: “Guillain-Barre” cross-reaction between host myelin and Campylobacter surface structure

86
Q

What is Guillain-Barré syndrome as it relates to Campylobacter?

A

cross-reactivity between organism surface proteins and host myelin
Self-reacting Ab formed -> inflammatory demyelinating polyneuropathy
Symptoms emerge 1-3 weeks post infection. Bilateral weakness,

87
Q

Yersinia enterocolitica - What and what does it cause?

A

belongs to family enterobacteriaceae - gram (+) cocci
Zoonotic - transferred from animals to humans (rabbits, rats, livestock)
Causes Enterocolitis with necrosis of Peyer’s patches
-bloody diarrhea, fever, abd. pain lasting 1-2 weeks
-inflammation of messenteric lymph nodes mimics acute appendicitis (esp. in young children)
- transfusion related septicemia (grows in blood at low storage temps)

88
Q

What bacteria is associated with transfusion related septicemia?

A

Yersinia enterocolitica

89
Q

How does H.pylori protect itself from stomach acid?

A

Urease: Converts urea to ammonia and CO2. Organism is surrounded by a layer of ammonia that protects from acid.

90
Q

How is H.pylori identified?

A

Small, gram (-), microaerophilic, motile, curved bacillus

Gastric biopsy for culture, and rapid urease - CLO (campylobacter like organism) test

91
Q

What toxins does H.pylori produce?

A

Cytotoxin and mucinase - contribute to tissue destruction and infiltration of inflammatory cells in ulcer formation

92
Q

How is Listeria monocytogenes identified?

A

Small, facultative anaerobes, non-spore forming, catalase pos, oxidase neg, B-hemolytic, gram (+) bacillus

93
Q

How are people infected by Listeria monocytogenes and what is the result?

A

Listeria is ubiquitous in nature, but usually infection through food - raw veg, raw milk, soft cheese, fish, poultry, meat (including ready-to-eat, like hot-dogs)
Motile bacteria crosses mucosal barrier of intestine and enters blood stream and:
1. is cleared by host immune system
2. infects other organs (esp. in immuno suppressed population) -esp. CNS - meningitis
3. crosses placenta to infect fetus - birth defects, spontaneous abortion

94
Q

What are 3 roundworms that can infect humans?

A

Ascaris lumbricoides - intestinal roundworm
Enterobius vermicularis - pinworms
Ancylostoma duodenale and Necator americanus - hookworms

95
Q

What are symptoms of Ascaris lumbricoides infection?

A

Often asymptomatic
GI upset, colic, loss of apetite
In heavy infestation worms can ball up in sm. intestine and cause obstruction

96
Q

What are Taenia saginata and Taenia solium?

A

Tapeworms
Taenia saginata - beef tapeworm
Taenia solium - pork tapeworm - can invade gut wall and migrate to other tissues and form cyst - cysticerocosis

97
Q

What are symptoms of peritonitis?

A

Abdominal distention, pain, decreased appetite, fever, nausea, thirst, vomiting, absence of bowel sounds.
May be other signs of shock

98
Q

Three types of peritonitis

A

Primary - develops without an evident source
Often associated w/ advanced liver disease
-Usually caused by gram (-) rods: E.coli, Klebsiella (>50%)
-~25 % by gram (+) organisms - streptococcus
Only facultative anaerobes - oxygen content of ascitic fluid prevents obligate anaerobes from living

Secondary: Trauma related - spillage of GI or UG organisms into peritoneal cavity. Usually polymicrobial.

Dialysis associated: often involves skin flora. Usually monomicrobial. usually: S. epidermidis, S.aureus, E.coli, Pseudomonas aeruginosa

99
Q

What are E.coli virulence factors

A

Adherence - 20 factors
Endotoxin - lipid A (LPS of outer membrane): activates complement -> inflammation; stimulates cytokine release -> septic shock
LPS -> LPS binding protein -> CD14 on monocytes and macrophages -> activation

100
Q

What organism is most frequently involved in CAPD peritonitis?

A

S.aureus

101
Q

What are the virulence factors of S.aureus?

A

Pili - adherence
Capsule - antiphagocytic, promotes adherence to tracheal epithelium
Endotoxin - LPS - may cause shock
Exotoxin A - increases tissue destruction by inhibition of protein synthesis (similar to diptheria)
Extracellular enzymes - pyocyanin: blue pigment, suppresses other bacterial growth, impairs function of nasal cilia

102
Q

How do intraperitoneal abscesses usually form?

A 
Complication of general or secondary peritonitis, appendicitis, diverticulitis, surgery or other intra-abdominal pathology.
Usually polymicrobial (~4, up to 12) consisting of endogenous flora
*Bacteroides fragilis
103
Q

What is Bacteroides fragilis and how is it identified?

A

Gram (-), anaerobic, encaspuslated bacillus
Normal flora of GI tract- causes infections when it escapes - major cause of intra-abdominal abscesses
Produces foul-smelling discharge from wound (anaerobic metabolites)

104
Q

What organisms are commonly associated with congenital infections?

A

Viruses spread mother -> fetus: HIV, CMV, rubella

Bacteria: L.monocytogenes, T.gondii

105
Q

What organisms are commonly associated with parinatal infection?

A

Perinatal: passage down birth canal
L.monocytogenes
E.coli
S.agalactiae (Group B strep )

106
Q

What organisms are commonly associated with post-natal infection of the newborn?

A

Organisms that can be spread through milk, saliva, physical contact
L.monocytogenes
S.agalactiae (Group B strep - B-hemolytic)
E.coli

107
Q

What is the leading cause of bacterial meningitis in newborns?

A

Group B strep

S.agalactiae - normal flora of female UG tract and GI

108
Q

How is Streptococcus agalactiae identified?

A

Gram (+), catalase neg, B-hemolytic, grow as diplococci or short chains in liquid.
In the case of bacterial meningitis - lab evaluation of CSF. Culture needed, but immediate gram stain should be done for empiric treatment.

109
Q

What are Early and Late Onset Diseases caused by GBS?

A 
EOD:  Within first week of birth (usually w/in 24 hrs)
-meningitis, pneumonia, bacteremia
LOD:  After first week of birth
-usually meningitis
-risk factors less well understood
110
Q

What are the risk factors for Early Onset Disease involving GBS?

A

Maternal carriage of GBS
Low anti-capsular IgA
Early delivery
Early / prolonged membrane rupture

111
Q

What are GBS virulence factors?

A

Capsule - most important - 9 serotypes (type 3 most assoc. w/ disease)
-sialic acid moiety on terminal sugar - limits C3b deposition and complement activation, thus phagocytosis
Invasion - can invade respiratory epithelium and cross BBB
B-hemolysin - damages respiratory epithelium, cytolytic for brain epithelium, enables crossing of BBB

112
Q

What E.coli strain is associated with newborn meningitis?

A

E.coli K1 - normal inhabitant of lg. intestine. Similar to GBS.

113
Q

Virulence factors of E.coli K1

A

K1 polysialic capsule: resistance to killing by neutrophils and normal serum, survival in blood and CSF
Invasins: IbeA and IbeB: needed to cross BBB
Type O antigen LPS
S.fimbriae - important for establishing infection

114
Q

What are symptoms of E.coli K1 meningitis in a newborn?

A

Variable, and possibly subtle
respiratory distress, fever, poor feeding, abdominal distension
Culture CSF and treat on suspicion

115
Q

How are Listeria infections of the newborn usually acquired?

A

From contaminated food.
Mother consumes and transfers to fetus.
Organism exhibits tropism for placenta and fetus.
Usually fatal - stillbirth, spontaneous abortion, premature labor.
Listeriosis of newborn usually acquired during delivery -> meningitis

116
Q

How is Listeria immunity mediated?

A

Cell mediated immunity - Listeria is intracellular pathogen

Initial infection: macrophages, then CD8+ Tcells

117
Q

What are Listeria’s virulence factors in the setting of fetal/newborn infection?

A

Internalins - allow cell invasion
Listeriolysin O - escape from vacuoles
ActA - recruits host-cell actin for motility and spread cell to cell w/o exposure to extracellular environment.

118
Q

What is the lifecycle of Toxoplasma gondii?

A

Oocyst consumed (fecal-oral)
Trophozoite is mature asexual proliferative form - infect cells, replicate, burst cells
Tissue cyst bradyzoite forms once immune response is initiated - cysts can exist in tissue for life of individual.

119
Q

What happens if a woman is infected with T.gondii for the first time during pregnancy?

A

Often stillbirth or spontaneous abortion.
Live births: microcephaly, hydrocephaly, motor disturbances, convulsion. May appear normal at birth, but develop problems later (retardation, chorioretinitis)
Subsequent births: no risk of transmission to fetus

120
Q

What is a primary histologic marker of chronic hepatitis?

A

Bridging fibrosis w/in hepatic lobules from central vein to portal triad

121
Q

What are the most common initial symptoms of viral hepatitis?

A

Malaise, weakness, N/V, anorexia, vague dull RUQ pain, low grade fever - all precede jaundice if it occurs (50-80% of pts do not experience jaundice)
Jaundice and dark urine usher in icteric phase - bring pt. to doctor.
Also - smokers lose appetite for smoking.

122
Q

what is the effect of circumcision on STI transmission? Why?

A

Reduces risk of acquiring HIV by 51-76% (hetersexual)
Large population of macrophages, CD4+ cells in nonkeratinized inner mucosal cells of foreskin.
Also: decreased incidence of HPV, HSV - 2, syphilis, and trichomonas.
No effect: N.gonorrhoeae, C.trachomatis
Female partners: decreased risk for HSV, BV, trichomonas

123
Q

What symptoms are associated with urethritis?

A

May be asymptomatic
Urethral discharge - purulent / mucopurulent
Dysuria, burning, pain, pruritus (itching)

124
Q

What are the causes of urethritis?

A 
Most involve N.gonorrhoeae
Often polymicrobial
Chlamydia (if gon, at least 30% likliehood of having Chlamydia)
Mycoplasma genitalium
etc
125
Q

Arthritis-dermatitis is the classic presentation for what?

A

Disseminated Gonococcal Infection

Bacteremial spread of Gonorrhea

126
Q

What are the symptoms of Neisseria gonorrhoeae infection?

A 
Urethritis - mucopurulent discharge
Mucopurulent cervicitis - vaginal discharge
dysuria
Pelvic Inflammatory disease in 10-20%
Disseminated gonococcal infection
pharyngitis, conjunctivitis
127
Q

How is Gonorrhea diagnosed?

A

Gram stain of urethral, cervical, or anal swab
-Gram (-) diplococci within or associated w/ PMNs
-sensitive and specific
Culture - Modified Thayer Martin media (2-3 days)
-can test susceptibility
-preferred for pharynx and rectum
DNA probe, PCR, NAAT (nucleic acid amplification test)- best (very highly sensitive and specific - near 100%)

128
Q

What medium is N.gonorrhoeae grown on?

A

Modified Thayer Martin

129
Q

What is treatment for Gonorrhea?

A

Cephalosporins - resistant to FQ, Penicillin, tetracycline
Ceftriaxone 250mg IM or
Cefixime 400 mg (single dose PO) or
Cefpodoxime 400mg (single dose PO)
Always include treatment for chlamydia - azithromycin or doxycycline

130
Q

Who is more likely to be an asymptomatic carrier of gonnorhea: male or female?

A

Female

131
Q

Who is more likely to be an asymptomatic carrier of chlamydia: male or female?

A

Common in both

132
Q

What can be said about women w/ positive cervical culture for chlamydia?

A

Probable upper genital tract infection

133
Q

Who should be screened for chlamydia?

A

All young women, annually (<25) regardless of sexual risk.
Older women w/ risk factors
No routine screening in males

134
Q

How is chlamydia diagnosed?

A

Women: urine or swab from endocervix or vagina
Men: urine or urethral swab, anal swab
Culture, immunofluorescence EIA - no longer used
Nucleic Acid Hybridization
NAAT - best sensitivity, modern standard

135
Q

What is therapy for chlamydia?

A

1g single dose of azithromycin - preferred
or - doxycycline 100mg bid 7days

amoxicillin in pregnant patients

136
Q

What is the most likely cause of urethritis if non-gonococcal?

A

Mycoplasma genitalium - most often (10-25%)
then Chlamydia trachomatis

No identifiable pathogen - frequent finding

137
Q

How is non-gonococcal urethritis treated?

A

1g single dose azithromycin - preferred
or - doxycycline 100mg bid 7 days

M.genitalium often fails with doxy, and increasing resistance to azithromycin

138
Q

What bacteria are commonly associated with PID?

A

N.gonorrhoeae 30-50%
C.trachomatis 25-40%
Mixed bacteria 25-50%

Natural vaginal flora also common - reduction in lactobacilli -> overgrowth, infecton

139
Q

What organism is associated with chancroid?

A

Hemophilus ducreyi

140
Q

What are the symptoms of Syphilis?

A

Slow development (12-40 days incubation)
Primary painless ulcer at site of inoculation (penis, vagina, vulva, mouth)
No purulence
Painless inguinal lymphadenopathy

141
Q

What are the stages of syphilis?

A

Primary infection: painless ulcer, painles lymphadenopathy
Secondary (6weeks - 6mos): multiple mucocutaneous lesions, fever, alopecia, lymphadenopathy, meningitis
Tertiary (months - years): gumma (necrotic sores)

142
Q

What is the modern algorithm for identification of Treponema pallidum (syphilis)?

A

EIA or CIA -> if pos: quantitative RPR -> if pos, syphilis

if neg: TP-PA (treponema pallidum particle agglutination assay) -> if pos: syphilis, if neg: syphillis unlikely

143
Q

How is syphilis treated?

A

Early: Benzathine Penicillin - IM
Latent / asymptomatic neurosyphilis: Benzathine Penicillin - IM weekly, for 3 weeks
Neurosyphilis: IV Benzyl Penicillin X 10days (IV Cephtriaxone)

144
Q

How do we know if syphilis treatment is working?

A

4 fold drop in titer in 6mos (early syph) or in 24 mos (latent/ late)

145
Q

What causes gential herpes?

A

HSV 1 and 2
2 primarily, but 1 is on the rise
2 does not infect mouth

146
Q

What are the symptoms of genital herpes?

A 
Multiple painful, shallow genital ulcers
May be missed
Constitutional changes (F>M)
Fissures (F)
lymphadenopathy, cervicitis, urethritis
147
Q

What is treatment for genital herpes?

A 
7-10 days treatment:
acyclovir
famcyclovir
valacyclovir
can't eradicate virus, but goal to decrease viral shedding and recurrences.
148
Q

How is Herpes diagnosed in the lab?

A

Direct Fluorescent Antibody test
Culture (specific, not sensitive)
PCR
Type specific IgG serology - commercial kits

149
Q

What is the most frequently reported infectious disease is the US?

A

Chlamydia

Gonorrhea is #2

150
Q

Lymphogranuloma venereum

A

Caused by Chlamydia trachomatis (serotypes L1-3)
More common in developing countries
Persistent Chlamydia infection - begins with small papule on genitalia, anus, or rectum - heals in a few days
Regional lymphadenopathy - systemic symptoms (fever, rash, nausea)
No treatment

151
Q

How is chlamydia cultured?

A

Indirectly. Can’t culture the organism itself, but can culture the cells that it inhabits
epithelial or reticular cells

152
Q

Describe Chlamydia’s lifecycle

A

Two stages:
Elementary Body - infectious - enters cell to form RB
Reticulate Body - non-infectious, metabolically active

EB enters epithelial cells, inhabits endosome and converts to RB which multiplies extensively. Under stress, can remain in RB stage. Otherwise, binary fission -> EB which are released.

153
Q

What happens in persistent Chlamydia infection?

A

Under stressful conditions, remains in cell as RB
Downregulation of major outer membrane protein (MOMP),
Increased production of stress factors (hsp60, hsp10) -> chronic inflammation
Refractory to Abx

154
Q

How is chlamydia treated?

A

Tetracycline, erythromycin common treatments

Erythromycin and amoxicillin used in pregnant women and infants

155
Q

Are B-lactams effective against Chlamydia?

A

No - may drive infection into persistent state

156
Q

Are men or women more likely to be asymptomatic Chlamydia carriers?

A

Women

157
Q

What are Opa genes in Gonorrhea?

A

Outer membrane proteins -> opaque cell appearance
Involve in binding host cells - close contact, possibly invasion
Several Opa genes - constantly transcribed, only translated if start codon is in frame
CTCTTT segments added/ lost - may shift start codon out of frame - control mechanism of expression

158
Q

Does infection with N.gonorrhoeae confer immunity?

A

No

159
Q

Describe pathogenesis of Treponema pallidum

A

Infection: sexual contact w/ active lesion (primary or secondary)
Invasion of mucus membranes - multiplication and spread -> lymphatics
systemic spread before primary lesion forms
3-4 weeks: primary chancre forms and heals in 4-6 weeks
2-10 weeks after healing: 2ndary syph: fever, sore throat, rash, lesions on hands and feet and face
Clear infection or latency
Tertiary syph - months later: granulomatous lesions (gumma) of skin, bones, joints. Neurosyphilis, CV syph. organism rare in tertiary lesions.

160
Q

When can a fetus become infected with T.pallidum? How diagnosed?

A

Infection can occur at any stage of pregnancy.

Fetal anti T.pallidum IgM is diagnostic

161
Q

How does congenital syphilis usually present?

A

Normal at birth and for 3-8 weeks. then fail to thrive, rhinitis, pneumonia
25% mortality

162
Q

What are P-pili, what do they bind? mannose sensitivity?

A

Primary virulence factor in Uropathogenic E.coli
Bind globobiose (glycosphingolipids) and P group antigens on RBC -> agglutination in lab
Mannose insensitive
Induces IL6,8, PMN chemoattractive -> inflammation

163
Q

HIV treatment goals

A

Reduce moridity and improve survival
Restore and maintain immunologic function
Maximal, durable viral load suppression
Prevent vertical transmission (Mother -> child)
Improve quality of life

164
Q

What is first line treatment for HIV?

A

2 NRTIs
1NNRTI
1 “boosted” PI
Raltegravir - integrase inhibitor

165
Q

What is the preferred NNRTI used in HIV?

A

Efavirenz
except in 1st trimester of pregnancy or women with high pregnancy potential

Preferred alternative: Nevirapine

166
Q

What is Ritonavir?

A

Is a protease inhibiting drug, but not used as such. Is a potent inhibitor of CYP3A4, which is used to extend the life of other protease inhibitors.
–BOOSTING

167
Q

What is the preferred NRTI combo used in HIV treatment?

A

Tenofovir and Emtricitabine

-available as co-formulation

168
Q

Uropathogenic E.coli virulence factors

A 
P-pili
Type-1, Type-S fimbriae
Adhesins (AfaD, AfaE, Dr)
Toxins (Hemolysin, cytotoxic necrotizing factor-1)
K antigen
LPS (endotoxin)
169
Q

What are S.saprophyticus virulence factors?

A

S.saprophyticus surface-associated protein (Ssp) - adhesin
Hemagglutinin / Fibronectin Binding Protein - adhesin
Hemolysin - not in all strains
Urease - stones

170
Q

What is the etiology/ pathogenesis of S.saprophyticus?

A

UTI pathogen - cystitis, not pyelonephritis
Natural inhabitant of colon - self infection
More common in females
Sexual activity increases risk of UTI
Increased risk w/ spermicide nonoxynol-9

171
Q

Klebsiella pneumoniae virulence factors in UTI

A

Type 1 and 3 fimbriae
Capsule
LPS
Urease

172
Q

Proteus mirabilis virulence factors in UTI

A

MRP - mannose resistant proteus like hemagglutinin
PMF - proteus mirabilis fimbriae
flagella
urease - high concentration of ammonium - alkalinize urine, stones

173
Q

What is Bile esculin used for?

A

Differentiation of Enterococcus from Streptococcus

Enterococcus grows - blackens medium

174
Q

What are the virulence factors of Enterococcus in UTI?

A

Aggregation substance (Asa1)- plasmid exchg and adhesion
Cytolysin - lyse RBC -> iron for growth
Sex pheromone - Neutrophil chemoattractant (can enter PMN)

175
Q

What are host defenses against UTI?

A 
normal flora
flushing effect of urine
sloughing epithelium
high osmolality, low pH of urine
insignificant immune defense
176
Q

In what infections should anti-GI motility agents not be used?

A

In infectious diarrhea w/ the following:

bloody diarrhea, Shiga-toxin producing E.coli, C.diff

177
Q

How is Salmonella treated?

A

Treatment generally not recommended except extreme cases or certain morbidities
-Cipro, Amp/Amox, TMP/SMX, 3rd gen ceph, Azithro

check susceptibility!

178
Q

Treatments for E.coli GI infection?

A

FQ, TMP/SMX, Cephalosporins

  • usually 3 days
  • check susceptibilities!!
179
Q

V.cholera treatment?

A

1 dose - 300mg Doxycycline

180
Q

Giardia treatment

A

-10 days of Metronidazole

181
Q

Diarrhea in ped patients - avoid what drugs? What is preferred?

A

Tetracyclines and FQ

- TMP/SMX, penicillins / cephalosporins are better

182
Q

What are the symptoms of CMV infection?

A

90% asymptomatic

Infectious mononucleosis, hepatitis, thrombocytopenia, myocarditis

183
Q

What is the risk of transmission from pregnant mother to fetus of CMV?

A

40%

184
Q

How is CMV isolated for testing and how is diagnosis made?

A

Virus isolated from buffy coat, urine, or cervical secretions
Tests used:
IgG titer (rapid 4x increase in specific titer)
PCR rapid diagnosis
Measurement of specific IgM (persists 4-8 months after infection)

185
Q

What is the treatment for congenital CMV?

A 
gancyclovir (IV)
or valgancyclovir (oral)

Not recommended if asymptomatic!!!

186
Q

How is congenital CMV diagnosed?

A

virus isolated from saliva or urine in first 2 weeks of life

187
Q

What are the symptoms of congenital CMV? Mortality rate?

A

10% asymptomatic
Petechiae, jaundice, hepatic and splenic enlargement, thrombocytopenia, conjugated hyperbilirubinemia
Neurologic abnormality: microcephaly, seizures, hypotonia, intracranial calcifications
Sensorineural hearing loss (30%)
Eye abnormalities
Neurodevelopmental delay
Dental abnormalities
15-30% mortality. Survivors: long-term sequelae

188
Q

What are the symptoms of perinatal CMV infection?

A

Most subclinical / asymptomatic.
Most common illness is self-limited pneumonitis (severe if infant premature)

No long-term deficits

189
Q

What are three ways in which neonatal HSV infections present?

A

SEM : skin, eyes, mucus membranes (40%)
Localized CNS involvement (w/ or w/o SEM) (34%) - seizures, lethargy, apnea. In CSF: pleocytosis, elevated protein
Disseminated: (22%) - adrenal glands, liver, kidneys, heart, etc. Mortality for disseminated - 55% (80% w/o therapy)

190
Q

Treatment for neonatal HSV infection?

A

Acyclovir or vidarabine (unusual, but eye-drop formulation available)

191
Q

Fetal Varicella syndrome

A

Occurs when mother contracts varicella (not shingles) in first 20 weeks of pregnancy (small risk - 1.2%)

  • scarring of infant (cutaneous)
  • hypoplastic extremities (usually unilateral, usually lower limbs)
192
Q

Neonatal varicella

A

contracted from mother during last 3 weeks of preg

-If maternal infection occurs w/in 5 days before or 2 days after delivery - lesions at 5-10 days of age.

193
Q

Neonatal varicella treatment

A

Acyclovir

If mother develops varicella 5 days before or 2 days after delivery - VZV Immunoglobin ASAP

194
Q

What results from Parvovirus B19 infection?

A

20% asymptomatic
Fifth disease
Erythema infectosum - skin rash - slapped cheek
In adults - flu like, symmetric polyarthropathy
Chronic - anemia, transient aplastic crisis (virus shuts down RBC production - problematic in sickle cell patients)

195
Q

Fetal Parvovirus B19 infecion

A

Can result in hydrops fetalis or death (risk cardiac dysfunction

196
Q

Toxoplasma gondii infection

A

80-90% asymptomatic
may be flu-like - muscle aches, lymphadenopathy
responsible for 1-5% mononucleosis cases
Complications - myocarditis, hepatitis, encephalitis, deafness, pneumonia

Tissue bound cysts - latent phase of infection - life long

197
Q

Treatment of maternal toxoplasmosis

A

spiramycin - attempt to prevent fetal infection

If fetal infection confirmed - folic acid antagonists - pyrimethamine and sulfadiazine

198
Q

What organisms are most commonly responsible for sepsis neonatorum?

A 
Group B strep
Coagulase neg staph
Other strep
E.coli
H.influenzae
C.albicans
199
Q

In early onset GBS sepsis, what is the usual focus of inflammation?

A

Usually lungs

Meningitis can also occur

200
Q

In late onset GBS sepsis, what is the focus of infection?

A

No focus of inflammation.
Bacteremia is most common presentation
followed by development of meningitis.

201
Q

Common presentation and cause of mononucleosis

A

Fever, exudative mononucleosis, lymphadenopathy, hepatosplenomegaly, atypical lymphocytes in peripheral blood

Usually caused by EBV
Also CMV
T.gondii (1-5%)

202
Q

Treatments for infectious mononucleosis

A

Bed rest in acute phase
Avoid sports until spleen is no longer palpable
Steroids may be used for some symptoms: massive splenomegaly, tonsillar swelling, hemolytic anemia, hemophagocytic syndrome

203
Q

Describe the course of HHV-6

A

Incubation 9-10 days, transmitted via respiratory secretion
Roseola (exanthem subitem, sixth disease)
Fever >102deg F for 3-7 days then macular or papular rash for 2 days (spread from trunk outward)

204
Q

What organism(s) cause Impetigo?

A

Usually Group A Strep

Also S.aureus

205
Q

What causes scalded skin syndrome?

A

soluble exotoxin of S.aureus

206
Q

What antibiotics are used for CA-MRSA?

A 
Vancomycin - doesn't penetrate lungs
Daptomycin - limited lung pen.  inactivated by surfactant
Linezolid
TMP/SMX
Clindamycin (~15% resistant)
Doxycycline/minocycline
207
Q

What is Kawasaki disease?

A

Unknown etiology - vasculitis of all vessels most severely affecting med. sized arteries
Must have 4 of these:
-bilat. non-exudative conjnctival infections
-changes of oral mucosa
-changes of hands and feet
-rash
-cervical lymphadenopathy >1.5cm
AND
disease not explained by any other process
Presents with fever >39C, always cardiac involvement

208
Q

How is Kawasaki disease treated?

A

IV Immunoglobin - 2/kg over 10-12 hrs.
repeated if fever persists
Aspirin 80-100 mg/kg/day divided q6 hrs.

M2 (19 decks)

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