Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infectious diseases > Gram negative organisms > Flashcards

Gram negative organisms Flashcards

1
Q

Gram negative encapsulated, oxidase positive diplococci.

A

Neisseria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which 5 serotypes make up most of meningococcal disease? Which is the most common? Which is the most virulent?

A

A, B, C, W135, Y
B most common
C most virulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the pathogenesis of neisseria meningitidis?

A

Nasal carriage common
Depend on virulence of serotype, host factors.

CAPSULAR POLYSACCHARIDE - enhances resistance
ENDOTOXIN (LIPOPOLYSACCHARIDE) - stimulates TLR4 receptor causing release of cytokines.
Bind to Human factor H (downregulates complement cascade)

Cytokines (TNFalpha, IL1, IL6, IL8 causes activation of intrisinc and extrinsic clotting cascade)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Complications of meningococcal menigitidis?

A

DEATH
DIC, hypotension, vasculitis, gangrene, adrenal haemorrhage, endophthalmitis, arthritis, pancarditis, pneumonia, avascular necrosis.
Deafness most common 5-10%
Cerebral arterial/venous thrombosis
Subdural effusion/empyema and other neuro problems.
Immune mediated problems - Arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are risk factors for meningococcal disease?

A 
Complement deficiency (+properdin deficiency)
Functional asplenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Is meningitis from complement deficiency more severe or less severe than normal immunocompetent hosts?

A

Usually less severe because they are infected with W135 or Y strains instead of B or C strain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What vaccinations can you give for meningococal meningitis? When do you give it?

A

MenCCV (conjugated meningococcal vaccination) Give at 12 months
MenPPV (Polysaccharide vaccine. Give at high risk groups)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What postexposure prophylaxis can you give?

A

Rifampicin
Ceftriaxone is better because it eradiates nasal carriage and safe in pregnancy. Also less problem with compliance. More expensive and hurts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which vaccine is associated with Guillain-Barre syndrome?

A

MenCCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fastidious, gram negative, pleomorphic coccobacillus.

A

Haemophilus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pathogenesis of haemophilus?

A

Pilus and non-pilus adherence factors - adhere to resp epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can haemophilus cause antibiotic resistance?

A
  1. Produce beta lactamase
  2. BLNAR (beta lactamase negative ampicillin resistant) isolates produce beta lactam insensitive cell wall synthesis enzyme called PBP3.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where were there a high incidence of HiB in pre-vaccination era?

A

Infants lack/low in antibody to PRP (polysaccharide polyribosylribitol phosphate). Helps opsonise. Both classic and alternative pathways important in defense against HiB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What postexposure prophylaxis can you give for HiB?

A

Rifampicin/cefriaxone (same as meningococcal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Unencapsulated gram negative diplococci?

A

Moraxella catarrhalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tiny fastidious gram negative coccobacilli?

A

Bordatella pertussis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How long does immunisation with pertussis last for?

A

3-5 years. Unmeasurable after 12 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What’s the difference between Bordetella pertussis from rest of bordetella species?

A

B. pertussis express pertussis toxin, the major virulence protein
- Releases histamine, leuocyte dysfunction. Causes lymphocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What’s the virulence factor of Bordetella Pertussis?

A 
Pertussis Toxin
Attaching factors:
FHA (Filamentous hemagglutinin
Agglutinongens
Pertactin

Tracheal cytotoxin inhibits clearance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What’s the incubation period of pertussis?

A

3-12 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What’s in the pertussis vaccine? What’s the difference between the childhood type and adolescent type?

A

acellular vaccine 3 components:

  1. FHA (filamentous hemaglutinin)
  2. Pertactin (PRN)
  3. Pertussis toxin (PT)

Boostrix have less of diphtheria and pertussis compared to tetanus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If a 10 month old child only has 2 and 4 months immunisations, how should they be given catchup dose?

A

Give all 3 catch up doses again (4 weeks apart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are side effects of pertussis vaccination?

A

Fever (20%) and local effects (10%) (lower incidence than whole-cell pertussis vaccines)
Local adverse effcts - limb swelling within 48 hrs of vaccination, gone by 1 week.
Febrile convulsions
Hypotonic-hyporesponsive episodes (HHE)
- episode of pallor, limpness and unresponsiveness 1-48 hrs post vacination (preceded by fever/irritability). No long-term effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Does DTPa vaccine cause SIDS?

A

No. Decreases risk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What’s are the virulence factors of salmonella typhi?

A

Survive low pH in stomch.
Enters M cells in small intestine
->Changes actin cytoskeletin -> produces IL8 -> destabilisation of tight junctions ->Salmonella containing vacuole ->Enters lymphoid system -> primary bacteremia (asymptomatic) -> seeding to RES, liver, spleen, GB, BM -> peyers patches re-exposed to S.typhi via bile -> secondary bacteremia (symptoms and end of incubation period)

  • More systemic effect and longer duration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the virulence factors of non-typhoid salmonella?

A

Endocytose into small intestine wall. Induce local inflammatory response (TLR) - PMN infiltration.

-> diarrhoea.
They are unable to overcome defense mechanisms in immunocompetent hosts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Motile nonsporulating nonencapsulated gram negative rods that grow aerobically and capable of facultative anaerobic growth.

A

Salmonellae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are 2 important non typhoid salmonella species?

A

Salmonella typhimurium

Salmonella enteritidis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What host factors and conditions predispose to development of systemic disease with nontyphoid salmonella infection?

A 
Neonates and infants (<3months)
HIV
Other immunodeficiencies + CGD
Immunosuppressed (steroids)
Leukemias/lymphomas
Haemolytic anemia (sickle cell, chronic malaria, bartonellosis)
Collagen vascular disease
Inflammatory bowel disease
Achlorhydria or use of antacid medication
Impaired intestinal motility
Schistosomiasis, malaria
Malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which interleukin is important in clearance of Salmonella?

A

IL12 - induces IFN gamma by NK and T lymphocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the incubation period of salmonella?

A

6-72 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What complications can salmonella have in inflammatory bowel disease?

A

Toxic megacolon, bacterial translocation and sepsis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What can give you a prolonged carrier state after nontyphoidal salmonellosis?

A

Biliary tract disease + chronic cholelithiasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the treatment for nontyphoid salmonellosis

A

cefotaxime, ceftriaxone, ampicillin or cefixime.

35
Q

What is the incubation period of typhoid fever?

A

7-14 days

36
Q

What is the skin manifestation in typhoid fever?

A

Rose spot (macular/maculopapular rash around day 7-10 of illness. Usually on lower chest/abdomen, lasting for 2- 3 days.

37
Q

What is the most common extraintestinal manifestation of salmonella typhi?

A

CNS (3-35%)

38
Q

What are the typhoid vaccines? When do you take them?

A

Oral (live attenuated) - give 1 week before going (age >6) on days 1, 3 and 5.
Parenteral (Vipolysaccharide vaccine). >2years. (IM)

39
Q

What is the most common extraintestinal side effect of shigella?

A

neurotoxicity (seizures, delium)

Probably due to proinflammatory mediators (TNF alpha, IL1, NO)

40
Q

What ist eh most common complication of shigellosis?

A

Dehydration and electrolyte imbalance
SIADH
Hypoglycemia and protein losing enteropathy.

41
Q

What mediates HUS?

A

Shigatoxin (from s. dysenterae serotype 1)

E. coli can also produce shiga toxins (E. Coli O157:H7, E. Coli O111:NM, E. coli O26:H11)

42
Q

What nutritional factors do you have to complement in shigellosis?

A

Vit A and zinc.

43
Q

What are facultative anaerobic, gram negative bacilli that usually ferments lactose.

A

E. Coli

44
Q

What are the classes of E. Coli?

A 
ETEC (enterotoxigenic)
EIEC (enteroinvasive)
EPEC (enteropathogenic)
STEC (Shiga toxin-producing) or EHEC (enterohaemorrhagic)
VTEC (verotoxin producing)
EAEC or EggEC (enteroaggregative)
DAEC (Diffusely adherent)
45
Q

What is the most common cause of traveller’s diarrhoea?

A

Enterotoxigenic.

46
Q

What is curved, gram negative and nonspore forming rods that have tapered ends?

A

Campylobacter

47
Q

What is a neurological condition strongly associated with serotype C campylobacter jejuni?

A

Guillaine-Barre syndrome.
Molecular mimicry - especially miller-fisher variant (ataxia, areflexia, ophthalmoplegia)

1-12 weeks after infection

48
Q

What is the incubation period of campylobacter?

A

1-7 days.

49
Q

What focal extraintestinal infections can campylobacter cause in neonates/immunocompromised patients?

A 
meningitis
pneumonia
thrombophlebitis
pancreatitis
cholecystitis
terminal ileitisendocarditis
bone infections
Breast abscess
Periodontitis.

Others:
IgA nephropathy, other GN
Hemolytic anemia

50
Q

Who is likely to have severe prolonged campylobacter infections?

A

Immunodeficiencies (hypogammaglobulinemia)
Malnutrition
AIDS (correlates with CD4 count)

51
Q

Which group of people are likely to have reactive arthritis with campylobacter jejuni infection?

A

HLA B27

Can have Erythema nodosum.

52
Q

What group of people are at high risk of Yersinia infection?

A

Iron overload situations (because pathogenic strains need iron)
ie hemochromatosis
thalassemia
sickle cell disease

53
Q

What is the pathogenesis of yersinia?

A

Cause mucosal ulceration in the ileum, leading to necrosis of Peyer’s patches and mesenteric lymphadenititis.

54
Q

What are extraintestinal complications of Yersinia?

A
  1. Abscess formation - in spleen and liver
  2. Reactive arthritis, uveitis, erythema nodosum (especially in HLAB27 groups)
  3. Kawasaki
55
Q

What is the treatment for Yersinia?

A

Bactrim

56
Q

What is the typical presentation of yersinia pseudotuberculosis?

A

Pseudoappendicitis

57
Q

What is a complication of yersinia pseudotuberculosis mediated by superantigen release in 8% of cases?

A

Kawaski disease

58
Q

Gram negative rod. Strict aerobe

A

Pseudomonas

59
Q

What are virulence factors of pseudomonas?

A
  1. Pilli - attachment
  2. Extracellular proteins, proteases, elastases, cytotoxins.
  3. EXTOXIN A (cause local necrosis and facilitate systemic invasion)
  4. Type III secretion system (TTSS)
  5. Biofilm.
60
Q

What is the characteristic skin lesion of pseudomonas?

A

ecthyma gangrenosum

- pink macules, progressing to haemorrhagic nodules and ulcers with gangrenous centres and eschar formation.

61
Q

Aerobic, non spore forming, unencapsulated gram neg bacilli that stains poorly with gram negative stain

A

Legionella.

62
Q

What is the environmental reservoir of legionella?

A

Warm water (fresh water)

63
Q

Gram negative, oxidase negative fastidious aerobic rods that ferment no carbohydrates. Usually motile.

A

Bartonella

64
Q

What is oroya fever

A

Severe febrile hemolytic anemia caused by bartonella bacilliformis. Associated delirium.

65
Q

What is verruca peruana?

A

eruption of hemangioma-like lesion caused by bartonellosis. Get

66
Q

How do you get bartonella bacilliformis (bartonellosis)?

A

Through sandfly bite. Living in endemic areas (Andes mountains)

67
Q

What is the bug that causes cat-scratch disease?

A

Bartonella henselae.

68
Q

What do you see on histopathology of cat scratch lesion/LN?

A

Central avscular necrotic area with lymphocytes, giant cells and histiocytes.
Granuoma formation.

69
Q

What is the incubation period of cat scratch disease?

A

7-12 days.

70
Q

What is a complication of cat scratch disease?

A

Parinaud oculoglandular syndrome - unilateral conjunctivitis followed by preauricular lymphadenopathy.
Hepatosplenomegaly
Dissemination in bones - granulomatous osteolytic lesions
Neuroretinitis.
Encephalopathy
Stellate macular retinopathy
Hematologic manifestations - ie leukocytoclastic vasculitis.

71
Q

How do you treat cat scratch disease?

A 
Azithromycin
Bactrim
Rifampicin.
Cipro
Aminoglycosides.
72
Q

What causes trench fever?

A

Bartonella quintana. Body louse as vector.
Fever, conjunctivitis
Crops of macules.
Epidemic.

73
Q

What is bacillary angiomatosis?

A

Bartonella infection in immunocompromised hosts (AIDS/post transpolant).
Look like kaposi sarcoma - red papules. Can be found in any lesion (like bone).

74
Q

What is bacillary peliosis

A

Vasoproliferative lesions (usually in liver) caused by bartonella henselae and quintana in immunocompromised hosts.

75
Q

How do you treat bacilla angiomatosis?

A

Macrolides/tetracyclines.

76
Q

What do you see on histopathology of cat scratch lesion/LN?

A

Central avscular necrotic area with lymphocytes, giant cells and histiocytes.
Granuoma formation.

77
Q

What is the incubation period of cat scratch disease?

A

7-12 days.

78
Q

What is a complication of cat scratch disease?

A

Parinaud oculoglandular syndrome - unilateral conjunctivitis followed by preauricular lymphadenopathy.
Hepatosplenomegaly
Dissemination in bones - granulomatous osteolytic lesions
Neuroretinitis.
Encephalopathy
Stellate macular retinopathy
Hematologic manifestations - ie leukocytoclastic vasculitis.

79
Q

How do you treat cat scratch disease?

A 
Azithromycin
Bactrim
Rifampicin.
Cipro
Aminoglycosides.
80
Q

What causes trench fever?

A

Bartonella quintana. Body louse as vector.
Fever, conjunctivitis
Crops of macules.
Epidemic.

81
Q

What is bacillary angiomatosis?

A

Bartonella infection in immunocompromised hosts (AIDS/post transpolant).
Look like kaposi sarcoma - red papules. Can be found in any lesion (like bone).

82
Q

What is bacillary peliosis

A

Vasoproliferative lesions (usually in liver) caused by bartonella henselae and quintana in immunocompromised hosts.

83
Q

How do you treat bacilla angiomatosis?

A

Macrolides/tetracyclines.

Infectious diseases (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions