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Pathology > To review, block three > Flashcards

To review, block three Flashcards

1
Q

List the methods used to diagnose infection with Bordetella pertussis in the laboratory

A
  1. Sample the nasopharyngeal aspirate
  2. Use charcoal blood agar
    a. Bordetella pertussis is a strict aerobe, nonmotile
    b. Slow growing, 3-7 days
  3. Antigen detection from nasopharyngeal smears by direct immunofluorescence
  4. Also PCR
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2
Q

List the diseases caused by non-typeable Haemophilus influenzae and by other Haemophilus species

A
  1. nontypeable/ unencapsulated Haemophilus influenzae:
    Otitis media, Sinusitis - acute and chronic, Bronchitis - exacerbates COPD
  2. Haemophilus parainfluenzae - respiratory
  3. Haemophilus aegyptius - conjunctivitis
  4. Haemophilus aphrophilus, H parainfluenzae - endocarditis
  5. H. ducreyi: chancroid = STD: genital ulcer, open sores
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3
Q

List (7) identification and virulence factors associated with Bordetella pertussis

A
  1. Gram negative coccobacilli
  2. No capsule
  3. Adhesins - Pertactin - surface protein; Filamentous hemagglutinin promotes intracellular survival
  4. Pertussis toxin AB
    a. B is binding portion that is an adhesin
    b. A is ADP ribosylation of inhibitory G protein: prevents inactivation of adenylate cyclase and increases cAMP, causing increased respiratory secretions and mucus production, lymphocytosis
  5. Tracheal cytotoxin = peptidoglycan fragment
    a. Causes extrusion of ciliated tracheal epithelial cells
  6. Dermonecrotic toxin
    a. Causes ischemic necrosis
  7. Endotoxin LPS
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4
Q

Describe the pathogenesis of infection with Bordetella pertussis

A

Bordetella pertussis attaches to ciliated cells by adhesins, tracheal cytotoxin and other toxins destroy ciliary cells, pertussis toxin causes systemic manifestations, mucus production, cough, lymphocytosis.

B. Pertussis does NOT invade respiratory tract - the TOXIN does.

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5
Q

List seven virulence factors associated with the Enterobacteraciae

A
  1. LPS = disease
  2. Capsule - protects from phagocytosis
  3. Antigenic phase variation bc of H and K antigens
  4. Type III secretion systems - secrete virulence factors
  5. Sequestration of growth factors (siderophores)
  6. Resistant to serum killing
  7. Antimicrobial resistance
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6
Q

Are any Enterobacteraciae oxidase positive? If so, which ones?

A

No, none of them are

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7
Q

What is the most communicable bacterial diarrhea?

A

Shigella

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8
Q

Key identifying features of Yersinia spp.

A

i. Pinpoint colonies on MacConkey at 24 hours

ii. Biochemical tests should be incubated at 25degreesC

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9
Q

Name the five groups of E. coli that cause gastroenterits

A 
ETEC = enterotoxigenic E. coli
EPEC = eneteropathogenic E. coli
EIEC = enteroinvasive E. coli
EHEC = enterohemorrhagic E. coli (caused by STEC, O157:H7)
EAggEC= Enteroaggregative E. Coli
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10
Q

Basic pathogenesis of and type of diarrhea caused by ETEC

A

a. Secretory toxins that DON’T damage mucosal epithelium

b. Profuse watery diarrhea. Travelers diarrhea. NO BLOOD, NO MUCUS

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11
Q

Basic pathogenesis of and type of diarrhea caused by EPEC

A

a. Adheres to epithelial cells in localized microcolonies and cause attaching and effacing lesions
b. Usually in INFANTS. No blood in diarrhea.

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12
Q

Basic pathogenesis of and type of diarrhea caused by EIEC

A

a. Invades epithelial cells

b. Inflammatory diarrhea like shigella: blood, mucus and many leukocytes in stool

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13
Q

Basic pathogenesis of and type of diarrhea caused by EHEC

A

a. Elaboration of cytotoxins Stx1 and Stx2 (shigatoxins)
b. Caused primarily by E. Coli 0157:H7
c. Signs: bloody diarrhea without WBCs.
d. Can progress to HUS: hemolytic uremic syndrome

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14
Q

Basic pathogenesis of and type of diarrhea caused by EAggEC

A

a. Adheres to epithelial cells like stacked bricks

b. Watery diarrhea with blood and mucus

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15
Q

Clinical presentation of STEC

A

a. 3-4 days nonbloody diarrhea with abdominal pain, then onset of bloody diarrhea and severe abdominal pain, and resolution in 4-10 days
b. Classic HUS, following diarrhea → death or sequelae (renal impairment, hypertension, or CNS)
c. Non-diarrheal HUS: occurs with pneumococcal infection, chemotherapy, transplant immunosuppression

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16
Q

How does the Shiga toxin attack (in severe Shigella and STEC)

A

Shiga toxin inhibits protein synthesis of commensal bacteria and host cells.
This damages microcirculation → vasculitis → mucosal damage. Infarction of mucosa → bleeding into bowel and bloody diarrhea.
Endothelial and epithelial cells in kidney and CNS are sensitive to cytotoxicity induced by shiga toxins–> HUS and CNS sequelae

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17
Q

Treatment of STEC

A

Rehydrate, monitor kidney function, dialysis if HUS
Don’t give antibiotics because this can release endotoxin
Don’t give antimotility agents or prophylactic cipro/bactrim

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18
Q

Lab diagnosis of STEC

A

a. Collect in early stages, when organism load is higher and before antibiotic treatment is initiated
b. Use whole stool
c. Use ProSpecT to detect antigens specific to STEC
d. PCR

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19
Q
  1. Compare the transmission and clinical manifestations of E. coli, Shigella, Salmonella and Y. enterocolitica
A

E. Coli- animals to people, Shiga toxin is in undercooked beef; non-bloody diarrhea, followed by bloody diarrhea (NO WBCs), can lead to HUS

Shigella - fecal-oral between humans;
dysentary - tenesmus, pus and blood in stool

Salmonella - usually chicken and eggs for non-typhi, humans carry typhi– secondary transmission is person to person; febrile gastroenteritis (3-5 days). Rarely: typhoid fever, septicemia, focal infections

Yersinia - pigs, usu. chitlings; usually infects children; mimics appendicitis, enterocolitis is 2/3 of infection. Diarrhea, fever, abdominal pain for 1-2 weeks

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20
Q

List the five clinical manifestations of Salmonella infection

A
  1. asymptomatic = carrier state
  2. Febrile gastroenteritis = most common presentation in humans. Malaise, nausea, vomiting, followed by abdominal pain and diarrhea. Duration is 3-5 days.
  3. Enteric Fever: prolonged serious illness. Typhoid fever, caused by S. typhi and S. paratyphi A and B. Incubation is 1-2 weeks, illness lasts 4 weeks. Increasing fever for 2 weeks (bacteremic stage) and then GI symptoms for 1-2 weeks. Reservoir of S. typhi is humans. Large inflammatory response.
  4. Septicemia: without major GI involvement. Found in patients with leukemia, lymphoma, AIDS, SLE, sickle cell crisis and alcoholic hepatitis.
  5. Focal infections: osteomyelitis, meningitis, brain abscess, endocarditis
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21
Q

List the major toxins produced by Pseudomonas aeruginosa and describe their principle effect on human cells.

A
  1. Exotoxin A blocks protein synthesis like diphtheria toxin, causing dermatonecrosis in wounds and tissue damage in lungs
  2. Exoenzyme S is an ADP-ribosylating toxin. Epithelial cell damage facilitates bacterial spread, tissue invasion and necrosis
  3. Elastase- 2 enzymes: Las A and Las B degrade elastin, leading to ecthyma gangrenosum. It also degrades compliment components and inhibits neutrophil chemotaxis and function
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22
Q

Why are pseudomonas infections so resistant

A

Altered porins
Efflux pumps

Need cell wall agent and aminoglycoside to treat serious systemic infections

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23
Q

How does cystic fibrosis make it easier for pathogens to infect lung

A

People with CF have no good copies of CFTR, leading to defects in innate immunity.

i. Can’t internalize bacteria in bronchial epithelial cells
ii. increased inflammation in CF airway
iii. abnormal electrolyte transport —> thick, dry, sticky mucus
iv. abnormal mucus reduces mucociliary clearance so IDEAL NICHE for chronic lung infection
v. Chronic pulmonary exacerbation causes recruitment of neutrophils, cytokine release, and neutrophil derived elastase causing lung problems

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24
Q

Hallmark of Stenotrophomonas maltophilia

A

Life-threatening systemic infections in debilitating patients. Oxidase negative. Highly resistant.

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25
Q

Disease associated with Burkholderia cepacia

A

CF and chronic lung disease

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26
Q

Disease associated with Burkholderia pseudomallei

A

Meliodosis -

a. Acute disease, septicemia with metastatic lesions - 95% mortality of untreated.
b. Subacute disease is most common = TB like pneumonia with cellulitis and lymphangitis
c. Chronic Disease = localized chronic cellulitis. Treat with antibiotics

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27
Q

Disease associated with Acinetobacter baumannii

A

45% of inpatient tracheostomy, often nosocomial, low virulence

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28
Q

Disease associated with Elizabethkingia

A

Breast pumps for premature infants. Neonatal meningitis.

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29
Q

Name the bacteria that are listed as potential bioterrorist agents and note non-fermenting

A

Category A:
Bacillis anthracis
Yersinia pestis
F. tularensis

Category B:
Burkholderia pseudomallei (non-fermenter!)
E. coli, Shigella, salmonella
Brucella

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30
Q

Identifying characteristics of erysipelothrix rhusiopathiae

A

gram positive rods, produces H2S on triple sugar iron agar, form long filaments (hair like)
microaerophilic or facultative anaerobe, slow growth - requires 2-3 days incubation, small, grayish alpha hemolytic colonies, catalase negative, non-motile, weakly fermentative,

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31
Q

Key characteristics of Arcanobacterium hemolyticum

A

non-spore forming gram positive rod producing irregular club shaped, curved or V formation. catalase negative. beta hemolytic, like Group A strep.

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32
Q

Key identifying characteristics of Nocardia

A

gram positive, strict aerobe, partially acid-fast rods, cell wall has mycelia acid, long incubation period (7days)

33
Q

Clinical presentations of anthrax

A

a. Cutaneous anthrax: painless papule, ulcer surrounded by vesicles, necrotic eschar, has 20% mortality
b. GI anthrax: upper GI (ulcers in mouth and esophagus), lower GI (terminal ileum most common, diarrhea) mortality is 100%
c. inhalation anthrax:
i. prolonged latent period - 2 months or more
ii. initial symptoms - nonspecific: fever, SOB, cough, hA, vomiting, chills, chest and abdominal pain
iii. second stage: fever, edema and enlargement of mediastinal lymph nodes - shown on x ray
iv. meningeal symptoms in 50% of patients
v. shock and death within 3 days unless treatment immediately

34
Q

Pathogenesis of Listeria?

A

Bacteria invade M cells and macrophages by internal protein - like salmonella.
**NEVER exposed to immune system bc goes cell to cell via ActA gene (actin to move bacteria between cells). Humoral immunity is thus not important

35
Q

Which two gram-positive rods are catalase negative?

A

Erysipelothrix and arcanobacterium

36
Q

Which two gram-positive cocci are catalase negative

A

Strep and enterococcus

37
Q

Clinical presentation of erysipelothrix

A

Cutaneous infection develop after organism gets through skin. Occupational- people who work with animals

38
Q

Pathogenesis of cory. diptheriae

A

Disease caused by exotoxin that inhibits protein synthesis of eukaryotes

a. A subunit of toxin shuts off proteins synthesis
b. B subunit of toxin binds to cell receptor
c. Toxin gene carried in bacteriophage (bacteria virus)

39
Q

Clinical presentation of Arcanobacterium hemolyticum

A

a. isolated from young adults symptomatic for pharyngitis, fever, occ. cutaneous rash, pseudomembranes pharynx/tonsils, submandibular lymphadenopathy (strep for 15-25 year olds)

40
Q

Epidemiology of Nocardia

A

Disease is most common in immunocompetent patients with chronic pulmonary disease of immunocompromised patients with T cell deficiencies (but not AIDS because it’s treated prophylactically)

41
Q

List two aerobic g+ rods that can cause food poisoning

A

Bacillis cereus, Listeria monocytogenes

42
Q

List the diseases associated with Nocardia, Rhodococcus and Tropheryma

A

Nocardia:

  1. pulmonary diseases
  2. primary or secondary cutaneous infections
  3. secondary CNS infections (abscesses)

Rhodococcus
- Pulmononary infections, opportunistic

Tropheryma
- Whipple’s disease (GI)

43
Q

How do you test VDRL

A

Must be done on cerebrospinal fluid

44
Q

Treatment regimens for primary and secondary and early latent syphilis

A

Use long acting formulation of Benzathine Penicillin G - gives LOW levels, but stays in blood stream for 1 month after injection. So single dose is effective. 30 days for tertiary infection.

  1. In later stage repeat the dose over 2 week period
  2. Could have reaction after - jarisch-herxheimer reaction. Caused by release of toxic products by spirochetes→ cytokine response

Alt, doxycycline, but doxy can’t be used for neurosyphillis or if pregnant. Must be desensitized first and then given penicillin.

45
Q

Describe the antigenic changes that Borrelia species undergo during clinical relapsing fever which result in immune escape, multiplication and relapse of clinical illness

A

PilS to PilE gene switch. Relapses caused by emergence and multiplication of antigenic variants

46
Q

Stages of Lyme disease

A

Early stage: erythema migrans: bullseye lesion at site of tick bite, w/ flu-like illness.
Early disseminated lyme disease: skin lesions, facial nerve palsy, joints, and heart block
Late stage:
arthritis, encephalopathy

47
Q

List the insect vectors and/or animal reservoirs of Borrelia and Leptospira species

A 
Borrelia Recurrentis:
Vector for epidemic: louse
Vector for endemic: tick
Reservoir: rodents
Transmission: tick bites! Or lice poop being crushed on body after biting.

Borrelia burgdorferi: **in US and Europe
Vector: tick, ixodes ricinus complex
Reservoir: deer and white footed mouse
Transmission: tick bites

Leptospira species:
Vector: rats, mice, rodents, dog, cattle
Reservoir: none
Transmission: water and food infected with animal hosts gross urine

48
Q

Clinical manifestations of leptospirosis

A

First stage: bacteremia: fever, chills, headache, myalgias. All over the patient

Second stage, immune: only in urine! But worse manifestations → aseptic meningitis, myalgias, headache, conjunctival stuff, involves the LIVER.

Severe: stages blend, weil’s disease. Liver failure, kidney failure. Hemorrhage.

49
Q

Vector and transmission for brucella

A
  1. Transmitted to humans by contact with animals or by ingesting contaminated milk or dairy products
  2. Vectors: goats, sheep, camels, pigs, cattle, dogs
50
Q

Vector and transmission for f. tularensis

A

infection in wild animals, transovarial transmission in ticks and flies. Acquired by humans through animal contact or deer fly or tick bites, inhalation of infectious aerosol in lab, consumption of contaminated meat or water, contact with domestic cat that caught an infected animal (rabbit)

51
Q

Vector and transmission for pasteurella

A

cat and dog bites/scratches. In normal flora of dogs and cats GI tract. Can inquire infection by respiratory route too.

52
Q

Vector and transmission for Y. pestis

A

Urban plague: reservoir is rats, spread to humans by fleas. Sylvatic Plague-endemic in western USA: carried by prairie dogs, mice, rabbits, and rats.
1. Transmitted by flea bite, direct contact with infected tissues, inhalation of infected aerosols or from a patient with pulmonary disease

53
Q

Growth requirements for brucella, f. tularensis, pasteurella, y. pestis

A

Brucellosis: blood cultures with extended incubation time, requires enriched media to grow and LONG incubation period

Francisella Tularensis: grow on chocolate agar, need sulfhydryl compounds and prolonged incubation time, strict aerobe (oxygen!)

Pasteurella Multocida: grows on blood and chocolate, NOT MacCONKEY AGAR
1. Oxidase POSITIVE and catalase POSITIVE

Yersinia Pestis: small pinpoint colonies, look like fried egg. Oxidase negative. Member of enterobacteriaceae.

54
Q

Describe the populations at risk for Zoonoses caused by Brucella, Yersinia, Francisella and Pasteurella and list measures used to prevent infection with these pathogens

A

Brucella: lab workers, veterinarians, farmers, those that consume unpasteurized dairy products, category B infectious agent. Avoid unpasteurized milk and dairy products, no human vaccine available, immunize livestock

Francisella Tularensis: men who hunt! Use insect repellent, wear gloves when handling animals, avoid mowing in areas where sick or dead animals reported

Pasteurella: people with pets? Cats and dog exposure

Yersinia Pestis: endemic in US - prairie dog exposure. Also domestic cats get exposed.

55
Q

Identify the areas within the USA where plague and tularemia are endemic.

A

Tularemia: OK, AR, MO. new cases in wyoming, SD, CO and nebraska
Plague: sylvatic plague is endemic in western USA.

56
Q

Describe the disease conditions associated with Brucella

A

Organisms survive intracellularly
Clinical symptoms: appear 2-8 weeks after exposure
a. Initial: nonspecific: malaise, chills, sweats, fatigue, weakness, myalgias
b. Fever: intermittent/cyclical
i. Orgs sequestered in granulomas in tissue and bone marrow
ii. Get a fever
c. Splenomegaly, lymphadenopathy, hepatomegaly
d. Advanced disease: GI symptoms, osteolytic lesions or joint effusions, respiratory symptoms, chronic infections

57
Q

Describe the disease conditions associated with F. tularensis

A
  1. Ulceroglandular infection: Get fever, chills, malaise 2-5 days after exposure.
  2. Oculoglandular : if touch eye with infected hand, one side, conjunctival inoculation
  3. Typhoidal infection: after ingest a lot, get fever, prostration (lie down), weight loss
  4. Pneumonic infection: from inhaling orgs
  5. Glandular form: adenopathy
  6. Oropharyngeal form: ingest infected meat or water, get pharyngeal ulcers
58
Q

Describe the disease conditions associated with Pasteurella

A
  1. Pain, swelling, and serosanguinous drainage at wound site
  2. Septic arthritis and osteomyelitis can occur
  3. Serious infections (fasciitis) requiring wide excisional debridement (removal of skin) can occur in compromised hosts like diabetics
  4. Pasteurella multocida is most common species in humans - facultative anaerobe
  5. Infection = skin lesion, bacteremia or exacerbation of chronic respiratory disease in patients with underlying pulmonary dysfunction
59
Q

Describe the disease conditions associated with Y. pestis

A
  1. Bubonic plague: fever and painful bubo (lymph node) 2-7 days after bite
  2. Septicemic plague: infection of blood, high fever, delirium, seizures, black hemorrhagic splotches
  3. Pneumonic Plague: plague bacillus → lungs. Cough purulent sputum
60
Q

Causative agent for each disease:

  1. Rocky Mountain Spotted Fever
  2. Rickettsialpox
  3. a. Epidemic typhus (louse-borne typhus) b. Brill-Zinsser disease
  4. Murine typhus
  5. Scrub typhus
  6. Ehrlichiosis: a. (HA): b. (HME)
  7. Q fever
A
  1. Rocky Mountain Spotted Fever: Rickettsia rickettsii
  2. Rickettsialpox: R. akari
  3. Epidemic typhus (louse-borne typhus): R. prowazekii Brill-Zinsser disease: R. prowazekii
  4. Murine typhus: R. typhi
  5. Scrub typhus: Orientia tsutsugamushi
  6. Ehrlichiosis: a. (HA): Anaplasma phagocytophilum, Ehrlichia ewingii b. (HME): E. chaffeensis
  7. Q fever: Coxiella burnetii
61
Q

Describe the mechanism of pathogenesis of these organisms, including the location of replication in host cells

A

Bacteria enter by endocytosis. This requires energy; bacteria is initially in membrane bound vesicle.

Bacteria replicate inside the host in EITHER through a cytoplasmic vesicle (membrane bound) (coxiella and ehrlichia and anaplasma) or free in cytoplasm (rickettsia and orientia)

Coxiella has Coxiella-containing vesicle (CCV) that fuses with phagosome. Requires low pH for growth. Delayed lysosome fusion.

Ehrlichia and Anaplasma are in phagosome - prevent lysosomal fusion with phagosome, large aggregates form morulae.

Rickettsia and Orientia replicate in cytoplasm:

  1. Rickettsia and R Typhi use actin to move (like listeria)
  2. R. prowazekii and Orientia exit through lysis.
62
Q

List the vectors and reservoirs of each of the four rickettsia organisms

A
  1. Akari: vector: mites, reservoir = mice
  2. Rickettsiae: vector: mites, reservoir = small rodents and dogs
  3. Prowazekii: vector: lice, reservoirs: humans and flying squirrels
  4. Typhi: vector flea, reservoir are rodents
63
Q

List the vectors and reservoirs of orientia, ehrlichia, anaplasma, and coxiella organisms

A

Orientia: vector: mites, reservoir is mite
Ehrlichia: vector: tick, reservoir is rodent and deer
Anaplasma: vector: ixodes tick, reservoir: chipmunks, mice, voles
Coxiella: mammals: cattle, sheep, goat

64
Q

List the distribution of each disease in the U.S. and/or world

A

Rickettsia:

  1. Akari: russia, africa, korea, northern USA
  2. Rickettsiae: worldwide, SE atlantic and South central states
  3. Prowazekii: central, SA, africa, US rural areas
  4. Typhi: temperate and subtropical coastal areas of Africa, Asia, Australia, Europe, and South America

Orientia: SW pacific, SE asia, japan

Ehrlichia: in US in SE mid atlantic and South central states. Oklahoma.

Anaplasma: in US in northern and central midwestern states and northeast and central atlantic states

Coxiella: found world wide

65
Q

Main virulence factor of C. perfringes

A

Alpha toxin: lecithinase - lyses inflammatory cells, tissue destruction

66
Q

Toxins involved in C. diff

A

Toxin A = brush border enterotoxin → inflammatory response

Toxin B = cytotoxic, actin

67
Q

Main virulence factor of B. fragilis

A

Polysaccharide capsule

68
Q

Is propionobacterium acnes involved in single or mixed infections

A

Single

69
Q

Key features of C. perfringes

A

G+, non-motile, encapsulated, box car, spore-forming, double zone hemolysis

70
Q

Does tetanus germination cause necrosis (in adults)?

A

No! Toxicity is caused by the preformed neurotoxin that blocks the release of GABA

71
Q

Media for bacteroides

A

Enriched

72
Q

Key features: prevotella

A

gram negative, requires enriched media, non-motile, non-encapsulated, STRICT anaerobes (like botulism)

73
Q

Which antibiotics that have good/excellent activity against anaerobes

A

C. perfringens - for gas gangrene: penicillin, clindamycin; for food poisoning: self-limiting

C. tetani - treat with IVIg and give 3 doses DPT, revaccinate every 10 years

C. botulinum - antitoxin, avoid contaminated food

C. diff - Stop antibiotics, metrinidazole, oral vanc. if severe, cholestyramine binds toxin

Bacteroides, fusobacterium, peptostrepto - metronidazole

74
Q

Distinguish the unique life cycle and structure of Chlamydia from those of other bacteria

A

a. Elementary body is infection form, binds to receptor on surface of epithelial cell and enters phagosome inside the cell
b. Then turns into reticulate body (NOT infectious). The reticulate body replicates, forms large group of RBs called inclusion bodies
c. Then condense back into smaller elementary bodies which burst the cell and disperse into the body.

75
Q

Distinguish the unique structural and microscopic characteristics of Mycoplasma and Legionella from those of other bacteria

A

Mycoplasm: no cell wall, smallest bacteria

a. Single triple layered cell membrane = sterols
b. Needs cholesterol for growth and eaton agar
c. Fried egg

Legionella

a. Obligate aerobe
b. Gram negative rod
c. Non-fermentative, derives energy from amino acids

76
Q

Lab culture: chlamydia

A

PCR is best
Giemsa stain
Can use antigen detection
Nucleic acid hybridization probe of ribosomal RNA

Culture must be taken from epithelial cells, which is difficult

77
Q

Lab culture: Legionella

A

Buffered charcoal yeast extract agar, with cysteine and iron
Diagnose with silver stain
PCR won’t work

78
Q

Mycoplasma diseases

A
  1. Mycoplasma pneumoniae: spread by resp droplets
    a. Flu like symptoms, cough, rhinorrhea, chest pain, sore throat, bad chest x ray, secondary complications: paralysis, meningoencephalitis, rashes, arthritis
  2. Mycoplasma hominis: PID and UITs in women (urogenital tract)
  3. Mycoplasma genitalium: urethritis, in men (urogenital tract)
79
Q

Legionella reservoirs and risk factors

A

Man-made water reserviors, warm temperature and stagnation

Older men, smokers, organ recipients, chronic lung disease

Pathology (17 decks)

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