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Infectious Disease 1 > Exam Review 1 > Flashcards

Exam Review 1 Flashcards

1
Q

What are the 3 types of exotoxins?

A
  1. A-B toxins (cholera, tetanus toxins); 2. Membrane disrupting toxins (hemolysins, alpha toxin); 3. Superantigens (TSS)
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2
Q

What kind of bacteria can make spores?

A

Gram positive (gram negatives can’t make spores!)

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3
Q

What is LPS?

A

Essential component of Gram Negative bacterial survival and replication; Messes stuff up in the human body!

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4
Q

How is peptidoglycan made?

A
  1. Synthesis of water soluble, nucleotide-linked precursor in the cytoplasm; 2. Transfer of precursors to the membrane lipid; 3. addition of prefabricated block to the glycan chain; 4. Cross-linking to adjacent chain via transpeptidation
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5
Q

What are the typical bacterial reservoirs?

A

Endogenous (normal flora): skin, colon, oropharynx; Exogenous: water, air, food, ticks

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6
Q

What is the difference in the outbreak curve between common source outbreak and propagated epidemic?

A

Onset epidemic begins almost immediately, has a sharp peak, and comes back down (this is due to common source like food poisoning); propagated epidemic is more parabolic

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7
Q

Define: Infection

A

The ability of an organism to invade host tissue, replicate, and stimulate an immune response

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8
Q

Define: Intoxication

A

Agents that cause disease by elaboration of toxin sometimes without the presence of viable bacteria

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9
Q

Define: Incubatory stage of human infection

A

Subject incubating but w/out symptoms of disease - subject may be infectious

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10
Q

Define: Latent stage of human infection

A

Pathogen persists in tissue w/out symptoms for much of the time (eg HIV, TB, HSV)

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11
Q

What is horizontal transmission?

A

Transmission from infected individual to others through air, water, food, contact vectors, etc

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12
Q

What is vertical transmission?

A

Transmission to offspring through ovum, sperm, placenta, milk, contact

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13
Q

What is required for pathogen to establish infection?

A

Opportunity, adherence to and colonization of host surfaces, evasion of host defense mechanisms, adaptation to the host environment, invasion of tissue both locally or systemically (dissemination), host response (often responsible for tissue damage)

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14
Q

What are the differences in hemolysis for the streps?

A

S. Pyogenes is b hemolytic (complete), viridans strep is a hemolytic, enterocci are g hemolytic (no hemolysis)

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15
Q

Which strep grows in 6.5% NaCl? Bile esculin? Which is bacitracin susceptible? Optochin susceptible?

A

6.5% NaCl and bile: E. Faecalis; Bile: Nonenterococcal Gp D; nothing: strep viridans; Bacitracin susceptible: S pyogenes; Optochin: S pneumo

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16
Q

What is Group A Strep?

A

Strep pyogenes - what you think of as Strep Throat

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17
Q

What makes Group A strep virulent?

A

Hyaluronic acid capsule (anti-phagocytic); Gram + (peptidoglycan); Pili M protein type (VERY important in causing disease)

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18
Q

What does M Protein do?

A

Antigenic variations in M proteins are used to type Group A strep; strains lacking M protein are avirulent; M protein is anti-phagocytic and inhibits activation of complement via the alternate pathway

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19
Q

What are clinical features of Group A Strep pharyngitis?

A

Sore throat, sudden onset, fever, pain with swallowing, headache, lymphadenitis, tonsillar exudates, soft palate petechiae; sequelae can include abscess, sepsis, metastatic seeding

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20
Q

What findings are NOT suggestive of Group A Strep?

A

Conjunctivitis, nasal discharge, cough, diarrhea

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21
Q

How is Group A Strep diagnosed?

A

Culture is gold standard, rapid strep antigen kids can be used (treat if positive, confirm if negative), anti-streptolysin O reflects past (not present) infection

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22
Q

What is the epidemiology of Group A Strep Pharyngitis?

A

Humans are natural reservoir, mostly seen in 5-15 year olds, most common in temperate/cold climates (occurs in water, early spring), asymptomatic carriage is common, spread through droplets or nasal secretions (can also be foodborne)

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23
Q

What is the pathogenesis of Group A Strep?

A

Adhere to epithelial cells using adhesins (protein F1 and lipoteichoic acid), susceptibility to infection is determined by the presence or absence of type-specific antibody to M protein

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24
Q

What are nonsupperative sequelae of Group A Strep pharyngitis?

A

Rheumatic fever - carditis, polyarthritis, erythema marginatum, subcutaneous nodules, chorea; glomulonephritis

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25
Q

What is streptococcal TSS?

A

Pyrogenic exotoxins A-C have been implicated; similar mechanism of action to staph TSS (superantigen), but frequently also includes presence of infection; presentations w/ necrotizing fasciitis appear to be linked w/ specific M types

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26
Q

How is S pyogenes treated?

A

Penicillin; clindamycin can be added in invasive infections; soft tissue infections often require debridement; prophylactic antibiotics can also be given; NO VACCINE

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27
Q

What is strep pneumonaie/pneumococcus?

A

Gram + lancent-shaped diplococci; form a hemolytic colonies on blood agar; encapsulated; naturally competent (uptakes naked DNA from environment)

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28
Q

What is the epidemiology of strep pneumo?

A

Primarily causes diseases in the very young or very old; colonizes the nasopharynx of 5-10% of adults and 20-40% of children; transmitted by extensive close contact; often occurs in winter; mortality remains high

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29
Q

How does pneumococcal pneumonia invade?

A

Increased capsule expression, pneumolysin (cholesterol-dependent cytotoxin present in most invasive strains); adhere to alveolar type II cells and initiate an inflammatory response due to the cell wall; also has secretory IgA protease

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30
Q

What are the differences between the pneumococcal vaccines?

A

Children should get the polysaccharide protein conjugate vaccine (T cell dependent, more effective in infants

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31
Q

How do you identify the difference b/w staph and strep w/out a Gram stain?

A

Staph is catalase +, strep is catalase -

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32
Q

What are rifamycins?

A

Aka Rifampin! They block mRNA synthesis by binding to the bacterial DNA-dependent RNA polymerase; used in combo w/ other antimicrobials (only used alone as prophylaxis for N. Meningitidis)

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33
Q

How is sensitivity to a particular antibiotic determined?

A

Sensitivity is determined by the interpretation of the minimum inhibitory concentration

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34
Q

What is the minimum inhibitory concentration of antibiotics?

A

The lowest concentration of antibiotic that prevents visible bacterial growth after 24h of incubation in the appropriate culture media; it is organism and drug specific

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35
Q

What does susceptible mean?

A

Implies that the concentration of antibiotic that can be achieved at the site of infection is >MIC

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36
Q

What are the common causes of community acquired pneumonia?

A

1 is strep pneumo; “atypical organisms” are mycoplasma, chlamydia, etc; can also be viral

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37
Q

What can cause CAP in early childhood?

A

Group B Strep, gram negative enteric bacilli, cytomegalovirus, Listeria, HSV, Pertussis, RSV

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38
Q

What are weird exposures that relate to CAP?

A

Bats: histoplasma capsulatum; birds: chlamydophila psittaci, cryptococcus neoformans; contact with farm animals or outdoor cats: coxiella burnetii; exposure to rabbits: francisella tularensis; travel to southwest USA: coccidiodes immitis

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39
Q

What are common complaints in pneumonia?

A

Dyspnea (shortness of breath), fever, cough (productive or not), chills, chest pain, myalgia, headache

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40
Q

What are common physical exam findings in pneumonia?

A

Rales (clicking, rattling, and crackling noise), tactile fremitus (palpable vibration), decreased breath sounds, rhonchi (course rattling), grunting, nasal flaring

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41
Q

What are the major risk factors for pneumococcal pneumonia?

A

Alcohol, smoking, asthma, hyposplenism or splenectomy, immunocompromised, antecedent influenza, defects in humoral immunity

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42
Q

What are risk factors for resistance to beta lactams?

A

Age >65, recently taking antibiotics w/in 3 months, alcoholism, immune suppression, multiple medical co-morbidities, exposure to child in daycare

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43
Q

How do you diagnose S. Pneumoniae?

A

Blood culture, urine antigen test, sputum culture (hard to get from a child); antimicrobial susceptibility testing is key!

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44
Q

How do you treat s. Pneumonia in a child?

A

Ampicillin or ceftriaxone (if resistant)

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45
Q

How do you treat S. Pneumonia in an adult?

A

Macrolide; if co-morbidity, fluoroquinolone or beta-lactam plus macrolide

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46
Q

What is different about mycoplasma?

A

Doesn’t have a cell wall; membrane contains sterols not present in other bacteria; lab cultures are rarely done (diagnosis usually by serology)

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47
Q

What is a vector?

A

An animal, most often an arthropod, which picks
up a pathogen and transmits it to a susceptible
individual

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48
Q

What is a reservoir?

A

an ecological niche where a pathogen
survives, lives and multiples (can serve as a
source of infection)

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49
Q

What is a host?

A

An organism that is infected with or is fed upon by

a parasitic or pathogenic organism

50
Q

What causes Rocky Mountain Spotted Fever?

A

Rickettsia rickettsii, small GN

coccobacilli (need special stain to see); obligate intracellular bacteria with minimal peptidoglycan and very weak LPS

51
Q

What is the reservoir and the vector for Rocky Mountain Spotted Fever?

A 
Hard ticks (Ixodidae family) are both the reservoir
and vector for RMSF – Dermacentor species: American dog tick, brown dog tick or RM wood tick, depending on location in U.S.
52
Q

Where is RMSF common?

A

“Rocky Mountain” is now a Misnomer:

most common in South East/South Central states

53
Q

When is RMSF common?

A

Most cases in the Spring, ~40% in June & July

54
Q

What are the risk factors for RMSF?

A

Exposure to dogs and residence in a wooded/high grass area may increase risk; Children ages 0-9 have
higher risk of fatal outcome; American Indians have more severe disease

55
Q

What are the symptoms of RMSF?

A

After ~1 week incubation: acute onset of flu-like
symptoms (i.e. fever, severe headache, malaise, myalgias/arthralgias, nausea/vomiting/abd pain); 2-5 days later a macular eruption appears on the wrists/ankles (rash in 90-95%). It becomes widespread and progresses
centripetally (proximally, starts on the extremities and
spreads inwards). The palms and soles are classically involved. With progression, petechiae and palpable purpura can develop

56
Q

What are the late symptoms of RMSF?

A

Full body petechial rash, multiorgan system failure, edema, ischemia, hypovolemia, thrombocytopenia, elevated liver enzymes

57
Q

What is the pathogenesis of RMSF?

A

Introduction @ tick bite site, travels via lymphatics to circulation where it invades the endothelial cells (OmpB mediates adherence), organism is engulfed but evades the phagosome, replication in the cytosol by binary fission; RickA activates the host cell actin, which pushes it to cell surface or nucleus, allowing cell-to-cell spread; increase vascular permeability from disruption of junctions between endothelial cells

58
Q

How do you diagnose RMSF?

A

clinical suspicion; immunocytochemistry on a skin biopsy (but this can take a week to get back!), serological tests and PCR (also takes time)

59
Q

How do you treat RMSF?

A

Treat w/ doxycycline immediately (even in children - short course) - do not delay treatment while waiting for lab work (could be deadly)

60
Q

What causes Rickettsial pox?

A

R. akari, transmitted by mite bite; mouse as reservoir; most commonly seen in NYC

61
Q

What are the symptoms of Rickettsial pox?

A

small bite that turns into an eschar (w/ black center), bad flu-like symptoms, diffuse macular rash that becomes papulovesicular, regional lymphadenopathy

62
Q

How do you diagnose Rickettsial pox?

A

Diagnosis is clinical, but immunohistochemisty on a skin biopsy may be used

63
Q

How do you treat Rickettsial pox?

A

Disease is self-limited w/o treatment, but Doxycycline can be used

64
Q

What causes Epidemic Typhus?

A

R. prowazekii; Vector: human body louse; Reservoir: Humans; Humans infected after scratching infected louse feces into the bite; Outbreaks occur in crowded, unsanitary conditions and are associated w/ war

65
Q

What are the symptoms of Epidemic Typhus?

A

Main Targets: Brain and Lung; Fever, myalgia, cough, severe HA, delerium; +/- Cetrifugal, petechial rash (spreads outward), but spares the face, palms, soles; Multiorgan system failure, fatal 5-40%; typhus means smoky or hazy, which describes the experienced state of confusion often accompanied by stupor

66
Q

What is Brill-Zinsser disease?

A

Reactivation of Epidemic Typhus, disease is typically less severe

67
Q

What are Ehrlichioses?

A

Tickborne infections caused by members of the Anaplamataceae family; These are very small, obligate intracellular, Gram negative bacteria that generally have a coccoid appearance; They target either monocytes or granulocytes and are named accordingly

68
Q

What causes Human Monocytic Ehrlichioses?

A

Ehrlichia chaffeensis - targets monocytes

69
Q

What causes Human Granulocytic Anaplasmosis?

A

Anaplasma phagocytophilium

70
Q

Where is HME found and what is its vector?

A

S. Central, SE, mid-Atlantic states; Vector: Ixodes ticks (hard ticks), particularly the Lone Star Tick

71
Q

What is the reservoir for HME?

A

white-tailed deer

72
Q

Where is HGA found and what is its vector?

A

NE, mid-Atlantic, Upper Midwest, Pacific NW states + internationally; Vector: Ixodes ticks (hard ticks), particularly the I. scapularis (aka blacklegged tick or deer
tick) or Western Blacklegged tick

73
Q

What is the reservoir for HGA?

A 
small mammals (esp. whitefooted
mice)
74
Q

What are the symptoms of Ehrlichioses?

A

Can be a mild illness/asymptomatic to a severe, fatal infection (up to 3%); presents similarly to rickettsial disease, but less likely to get a rash

75
Q

What does Ehrliochioses cause?

A

Morulae inside WBC

76
Q

What is the treatment for Ehrlichioses?

A

Doxycycline

77
Q

How do you diagnose Ehrlichioses?

A

Clinical suspicion (fever/flu symptoms) in endemic region during tick season; PCR—acutely, diagnostic tool of choice; Serologic—look for 4x rise in antibodies – Most sensitive test; Examination of peripheral blood for morulae (very low yield)

78
Q

What causes Lyme Disease?

A

Borrelia burgdorferi, a Gram negative spirochete

79
Q

Where is Lyme Disease found?

A

Predominant in the NE

80
Q

What are the vector and reservoir for Lyme Disease?

A

Vector: I.scapularis—usually the nymph (must feed 24+ hrs); Reservoir: white-footed mouse or other small mammals (i.e. chipmunk)-fed upon by nymphs

81
Q

When is Lyme Disease common?

A

Peak transmission: June, July, August

82
Q

What are the stages of Lyme Disease?

A

Stage 1: early localized Lyme disease. The infection is not yet widespread throughout the body.; Stage 2: early disseminated Lyme disease. The bacteria have begun to spread throughout the body.; Stage 3: late disseminated Lyme disease. The bacteria have spread throughout the
body.

83
Q

What are the symptoms of Stage 1 Lyme Disease?

A

Erythema migrans (70-80%): a 5-12 cm “bull’s eye” rash or a flat or slightly raised red spot at the site of the tick bite. Often there is a clear area in the center. It can be quite large and expanding in size. There are also flu-like symptoms.

84
Q

When does Stage 1 of Lyme Disease occur?

A

3-30 days post-bite

85
Q

What are the clinical features of Stage 2 Lyme Disease?

A

Bell’s palsy: paralysis or weakness in the muscles of the face or other neurologic: meningitis, radiculopathy; Large joint (knee) arthritis, myalgias; Cardiac involvement: heart block or pericarditis

86
Q

When does Stage 2 of Lyme Disease occur?

A

days to weeks post-bite

87
Q

When does Stage 3 of Lyme Disease occur?

A

weeks to years post-bite

88
Q

What are the symptoms of Stage 3 Lyme Disease?

A

Recurrent bouts of large joint arthritis (in 60% of untreated); CNS and PNS complications (5% of those untreated)

89
Q

What is Post-Lyme Disease Syndrome?

A

No accepted definition; Chronic symptoms after receiving standard treatment regimens; May be an autoimmune issue without ongoing infection; Additional antibiotics not recommended; NOTE: reinfection can occur

90
Q

What is the pathogenesis of Lyme?

A

B. burgdorferi inoculated into the skin at the bite site, multiples, and spreads outward causing the characteristic rash; OspC variant helps facilitate transmission to human
& dissemination; lots of other surface proteins!

91
Q

How is Lyme Disease diagnosed?

A

If there is erythema migrans, diagnosis can be clinical; CSF examination may be indicated; Co-infection with HGA and babesia may occur (same vector)

92
Q

How is Lyme Disease treated?

A

Doxycycline (or alternative) for erythema migrans; Oral regimen may also be used for isolated Bell’s palsy, mild cardiac disease, arthritis; IV Ceftriaxone (3rd gen cephalosporin) for heart block, symptomatic cardiac
disease, other PNS/CNS disease

93
Q

How should you treat kids with Lyme Disease?

A

Amoxicillin

94
Q

What is the definition of diarrhea?

A

passage of 3 or more loose or liquid stools per day OR bowel movements more frequently than is normal for the individual

95
Q

Where is the problem if you have watery diarrhea?

A

Small intestine

96
Q

Where is the problem if you have bloody diarrhea?

A

Colon; NOTE: this is also called dysentery!

97
Q

What is the mechanism of watery diarrhea vs bloody diarrhea?

A

Watery: non-inflammatory (enterotoxin or neurotoxin); bloody: inflammatory (invasion or cytotoxin)

98
Q

Which diarrheal diseases require a small number of organisms (10-100)?

A

10-100: Shigella, EHEC;

99
Q

What are enterotoxins and what kind of diarrhea do they cause?

A

cause watery diarrhea by acting directly on secretory mechanisms in the intestinal mucosa (no cellular injury): Vibrio cholerae, ETEC, Clostridium perfringens

100
Q

What are cytotoxins and what kind of diarrhea do they cause?

A

cause destruction of mucosal cells and associated with inflammatory diarrhea; Shigella dysenteriae (Stx) or Shiga-like toxin (EHEC)

101
Q

What are neurotoxins and what kind of diarrhea do they cause?

A

act directly on central or peripheral nervous system; Staphylococcus aureus, Bacillus cereus

102
Q

How does the body fight diarrheal disease?

A

Normal flora, gastric acid, intestinal motility, immunity (secretory IgA, systemic IgG and IgM)

103
Q

What is Bacillus cereus enterotoxin?

A

Two enterotoxins: Emetic (heat stable toxin, elaborated in starchy foods): incubation period 1-6 hours; Diarrheal: Incubation period 10-12 hours

104
Q

What is Staphylococcus aureus enterotoxin?

A

Heat-stable toxin (incubation 2-4 hours); Increases peristalsis by autonomic activation, resulting in intense vomiting / diarrhea

105
Q

What is Vibrio cholerae?

A

Curved gram negative facultative bacillus with single polar flagellum; Susceptible to stomach acid so must ingest large quantities of bacteria; Over 200 serogroups, but only O1 (El Tor is a variant) and O139 are associated with epidemic and pandemic cholera; Transmission through contaminated food and water, person-to-person transmission is unusual

106
Q

What must a cholera strain have to be virulent?

A

~20 genes divided between two vibrio pathogenicity islands (VPI); Virulence regulated by ToxR which is a transmembrane protein that senses environmental conditions

107
Q

How do you treat cholera?

A

Rehydration: IV and/or Oral Rehydration Solution (glucose and electrolytes); Doxycycline

108
Q

What is the clinical course of cholera?

A

Variable: 75% Asymptomatic, 20% Abrupt watery diarrhea, 5% Severe watery diarrhea, vomiting, and dehydration; Duration 1-3 days; No tenesmus, strain or abdominal pain, or fever; Shed 7-14 days

109
Q

What is Shigella?

A

Small non-motile gram negative rod, member of Enterobacteriaceae, tribe Escherichieae; human host or non-human primates; VERY similar to E.coli, except no flagella and they are non-lactose fermenters

110
Q

What is the most potent Shigella?

A

S. dysenteriae type A1 is the most potent producer of Stx (shiga toxin); Usually found in tropical, developing areas

111
Q

What is the pathogenesis of Shigella?

A

Acid resistant; Invasion of intestinal epithelial cells, moving from small to large intestines, with multiplication and mucosal destruction including ulceration and abscess formation; Enterotoxin AND Cytotoxin elaboration (Stx)

112
Q

What are the symptoms of Shigella?

A

12 hours after ingestion, bacterial multiplication begins in the small intestines resulting in abdominal pain, cramping, watery diarrhea and fever; Onset of severe lower abdomen pain, accompanied by urgency, tenesmus, and bloody mucoid stools (dysentery); Resolution of fever in a few days; Illness lasts for average of 7 days; Colonic shedding for 1-4 weeks

113
Q

What is E Coli?

A

Lactose-fermenting GN rods, pili, flagella, many toxins (which may include shiga like toxins STX-1 and STX-2 toxins)

114
Q

What is the difference between ETEC and EHEC/STEC?

A

Enterotoxigenic (ETEC): traveler’s diarrhea; Enterohemorrhagic (EHEC or STEC): hemorrhagic colitis, associated with HUS in children (example O157:H7)-but no invasion

115
Q

What is Hemolytic Uremic Syndrome?

A

Due to circulating Stx; Hemolytic anemia with fragmented erythrocytes, Thrombocytopenia, Acute renal injury; Can cause capiliary thrombosis & inflammation/damage colonic mucosa and hemorrhagic diarrhea

116
Q

What is Salmonella?

A

Microbiology-member Enterobacteriaceae; Gram negative, facultative anaerobic rod

117
Q

What is Non-Typhoidal Salmonella?

A

colonizes virtually all animals: human and many other animals (chickens, turtles, etc) so transmission is usually through contaminated food, sometimes animal handling; causes gastroenteritis for 3-7 days and fever, abdominal cramping; bacteremia can occur; can cause localized infections and Arterial infections, cholecystitis, osteomyelitis, septic arthritis

118
Q

What is Typhoidal Salmonella?

A

strict human pathogens, transmission is fecal-oral; causes enteric fever (Fever begins 5-21 days after ingestion and persists 4-8 weeks in untreated patients), Rose spots (30%), hepatosplenomegaly (50%)

119
Q

What are complications of Typhoidal Salmonella?

A

death in 1-30%; intestinal perforation, abscesses, endocarditis; relapse in 10%.

120
Q

What do you do if patient has diarrheal disease?

A

Observe clinical symptoms; ask questions about travel, contact, consumption, oral-anal contact, underlying medical conditions

121
Q

What tests should you run for diarrheal disease?

A

Stool PCR, fecal leukocytes, bacterial culture, toxin evaluation, parasite evaluation

122
Q

Which diarrheal disease should NOT be treated by using antibiotics?

A

EHEC - you might make it worse

Infectious Disease 1 (10 decks)

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