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POD Exam 2 > Mirobiology > Flashcards

Mirobiology Flashcards

1
Q

Hansen’s Disease

A

Caused by Mycobacterium leprae and has two forms

Tuberculoid - Formation of skin plaques
Treated w/ Dapsone/Rifampin

Lepromatous- Highly contagious and primarily affects the limbs
Treated w/ Dapsone/Rifampin/Clofazime

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2
Q

Mycobacterium tuberculosis (Shootout at TB Corral)

A

GPR, non-spore forming, acid fast, obligate aerobe

Can be visualized w/ Auramine stain

Nitrate (+)

  • Acquired thru inhalation of respiratory droplets; will proliferate in alveolar macrophages
  • Treated w/

R(ifampin)
I(sonazaid)
S(treptomycin)
E(thambutol)

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3
Q

Stages of M. tuberculosis infxn

A

Primary- affects the lungs and forms calcifications that can be seen on an x-ray

Miliary- Causes multi-organ failure; usually happens in CF pts.

Latent- Occurs in immunocompromised pts due to decreased TNF-a release
*Hemoptysis and Night sweats=classic sign
Cachexia will occur

Treatment: Rifampin/Isonaizid/Ethambutol

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4
Q

Streptococcus pneumoniae (Knight “Numero Uno”)

A

GP diplococci, encapsulated, a-hemolytic

Bile solubility (+)

Catalase (-)

*Optochin (S)

Quellung Rxn: (+)

VFs: Pneumolysin- destroys ciliated epithelial cells
Adhesins
IgA proteases

*#1 cause of: Meningitis
Otitis Media
Pneumonia (community-acquired)
Sinusitis

Treatment- Penicillin G
-Vaccine available for immunocompromised

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5
Q

Streptococcus agalactiae

A

GPC, B-hemolytic, sialic acid on capsule

Bacitracin (R)

CAMP test (+)-will see satellite growth of S. aureus

Common cause of neonatal meningitis (NF of vaginal tract)
Early onset=»High mortality rate, common in premature infants
Late onset=» You’ll be alright, probably

Treatment: (Penicillin/Erythromycin,)

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6
Q

Streptococcus pyogenes (Pie Baker)

A

GPC, B-hemolytic, encapsulated

Contains M-protein that prevents phagocytosis and F-protein which mediates adherence to mucoepithelium by binding fibronectin

Streptolysin O => (+) ASO test

Bacitracin (S)

Common cause of: Scarlet-Fever, Erysipela, Pharyngitis, Necrotizing fascitis

Sequelae of pharyngitis: RHD (cross-reactivity w/ myosin in heart)
AGN

Treatment: Penicillin

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7
Q

Staphylococcus Aureus (Moses)

A

GPC, Coag (+) (activates fibrinogen), yellow-appearance on blood agar

Enterotoxins =»food-poisoning w/ rapid developing vomiting

TSST-1 =» Toxic-Shock Syndrome; assoc. w/ tampon use

Panton-Valentine Leukocidin: Causes lysis of macrophages and PMNs

Protein A-Component of cell wall that binds Ig

Mannitol Salt agar- grows yellow

*Common cause of acute bacterial endocarditis in IV drug users
And
Septic arthritis

*Can also cause scalded-skin syndrome w/ (+) Nikolsky’s sign

Treatment: Topical-cephalosporin or penicillinase-resistant penicillin; Blood- Vancomycin

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8
Q

Klebsiella pneumoniae

A

GNR, non-motile, common UTI cause

*Also a common cause of nosocomial pneumonia

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9
Q

Shigella (She-gorilla)

A

GNR, facultative anaerobe, acid-stabile

*most infectious intestinal pathogen

Lactose (-)

H2S (-)

Performs Type III secretion => release of inflammatory cytokines

*Shiga toxin causes HUS and `cleaves the 28sRNA of ribosome

Test: methylene blue stain of feces; look for PMNs

Treatment: Fluid and electrolyte replacement
-If sever enough, Ciprofloxacin

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10
Q

Reiter’s Disease

A

Caused by Shigella sp.

Will see arthritis, conjunctivitis, and urethritis

*Most pts are male and HLA-B27 positive

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11
Q

Salmonella sp. (Salmon dinner)

A

GNR, motile, encapsulated, and acid-labile

H2S (+)

Hektoen Agar => Grows black

Performs Type III secretion

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12
Q

Typhoid Fever

A

Caused by Salmonella typhi

Will see rose-colored spots appear on pt.

Invades lymphatics and is carried into the blood =» Facultative intracellular organism

Treatment: FQN
-Live attenuated vaccine available

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13
Q

Escherichia coli (E. cola’s Soda Fountain)

A

GNR, B-hemolytic

Lactose (+)

Indole spot test (+)

Nitrate (+)

Catalase (+)

*Contains p-fimbriae which binds to P-antigen on RBCs (Pyelonephritis pili)

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14
Q

EHEC

A

O157:H7

Cause of Hemolytic uremic syndrome
-Production of Shiga-like toxin that inhibits 60s ribosome
=»Bloody diarrhea, cramps

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15
Q

ETEC

A

Cause of WATERY diarrhea and is transmitted via infected h2o sources

Has a heat labile (inhibits cAMP) and heat stabile (inhibits cGMP) toxin

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16
Q

Bordetella pertussis (Board and Care)

A

GN cocco-bacillus

*Binds to mucocilliary escalator via hemaglutinnin

Oxidase (+)

DFA test => Sensitive but not selective

*Toxins: Pertussis- inhibits Gi via ribosylation
Invasive AC- increases cAMP opening ion channels and expelling intracellular materials

Treatment: Erythromycin

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17
Q

Pseudomonas aeruginosa (Pseudo Mona)

A

GNR, obligate aerobe, encapsulated

Green pigment=pyoverdin; Blue pigment=pyocyanin

Oxidase (+)

VFs: Exotoxin A => inhibits protein synthesis
Exoenzyme S- required for dissemination in burn patients
Alginate- Promotes adherence to respiratory epithelium
Elastase- Breaks down ECM proteins; under influence of quorum sensing process

Common causes folliculitis from contact w/ unclean water (hot tubs)

Common cause of Swimmer’s Ear, septicemia in burn pts, and ecthyma gangrenosum

Treatment: Piperacillin, Fluoroquinolones, AGCs

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18
Q

Mycobacterium Leprae (Good, Bad, and Lion-Faced)

A

GPR, non-spore forming, acid fast

  • diagnosed by AFB stain
  • person-to-person transmission

Reservoir = Armadillo

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19
Q

Staph MRSA

A

mecA gene responsible for resistance is located on the

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20
Q

Staphylococcus epidermidis

A

CNS

Transmitted thru infected catheter; commonly infects previously damaged or artificial heart valves

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21
Q

Staphylococcus saprophyticus

A

CNS

Novobiocin (R)

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22
Q

Anti-DNase B

A

Important marker in S. pyogenes infxns; depolymerizes cell free DNA in pus

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23
Q

Strep. viridans (Knight “Numero Uno”)

A

1 cause of acute bacterial endocarditis

GPC, a-hemolytic

Optochin: (R)

Central role in dental caries

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24
Q

Enterococcus (VRE)

A

GPC, can hydrolyze esculin

Bacitracin: (R)

Bile solubility: (-)

VFs: Aggregation substance
Carbohydrate adhesins
Cytolysins
Antibiotic resistance (AGCs, Beta-lactams, and Vancomycin)

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25
Q

Proteus mirabilis

A

Can cause UTI and large amounts of urease in the bacteria will cause the ppt. of calcium

=»Kidney stones

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26
Q

Pseudomonas infxn in CF lung

A

Type III hypersensitivity

=»Immune complexes stimulate macrophages excessively and cause tissue damage

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27
Q

Caveats of PPD test

A
  • Cross reactivity w/ other Mycobacterium species
  • IC pts. may not react
  • (+) test if received BCG vaccine
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28
Q

Most common Mycobacterium infxn in AIDS pts

A

Mycobacterium avium-intracellulare

-Readily diagnosed in blood

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29
Q

Mycobacterium kansasii

A

Forms yellow colonies; somewhat common in AIDS pts.

Found in the South

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30
Q

Neisseria meningitidis

A

GN-diplococci; non-motile, aerobic; grows best on chocolate agar

VFs: Porins A and B (B facilitates epithelial invasion and inhibits leukocyte fnxn)
LOS
Transferrin-Binding Protein

*Complement deficiences => Increased risk of infxn

Labs: Culture= Gold Standard
Growth on MTM agar
CTA: Can utilize glucose and maltose

Treatment: Ceftriaxone; prophylaxis of contacts also necessary

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31
Q

Meningococcemia

A

Severe circulatory collapse w/ DIC, purpuric rash, ischemia of the extremities, and fever

=>Can also lead to Waterhouse-Friderichsen syndrome

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32
Q

Chlamydia Trachomatis

A

Organism w/ cel membrane lacking muramic acid; visualized w/ Giemsa Stain

Serotypes A-C => Trachoma (most common cause of blindness worldwide)

Serotypes D-K => STD; can be asymptomatic in women but lead to PID and neonatal conjunctivitis if transmitted to a baby during childbirth

Serotypes L1-L3 => LGV; starts off as painless ulcer, progresses to tender lymphadenopathy

Treatment: Doxycycline

-Erythromycin in neonatal pneumonia/conjunctivitis

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33
Q

Mycoplasma pneumoniae

A

*Has no cell wall but membrane contains sterols (like a persons)

VF: P1 binds glycoprotein on cilia
=»Destruction of ciliated epithelial cells

*ACTS AS A SUPER-ANTIGEN; stimulates excess TNF-a, IL-1, and IL-6 release

Increased incidence in young people in close contact
-Military recruits

  • Can also cause erythema multiforme and Steven-Johnson syndrome
  • X-rays show severe, patchy infiltrate, however, patient only has walking pneumonia

Treatments: Macrolides

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34
Q

Neisseria Gonorrhoeae (not on exam 2)

A

GN-diplococci; non-encapsulated

Causes PID, DGI, and asymmetric arthritis

  • Opthalmia neonatorium in newborns
  • Pili are used to deter neutrophilic digestion and undergoes antigenic vriation

Treatment: Ceftriaxone and Azithromycin (for concurrent Chalmydia infxn)

35
Q

Haemophilus influenzae

A

tiny GNR that requires X and V factors

Non-typeable strains => Unencapsulated; produced minor infxns like sinusitis

Typeable strains => Encapsulated; produce major invasive infxns (Hib)

VFs: OMPs P2 and P5- bind bacteria to mucous
LPS
Pili
*Invades by separating tight jnxns of columnar epithelium

Labs: Staph-Spot Test => Satellite growth
Grows best on chocolate agar

Treatment: PRP vaccine
Ceftriaxone if serious

36
Q

Hib Meningitis

A

Most common cause of infant meningitis prior to immunization

Long term sequelae include developmental abnormalities, visual defects, and hearing loss

*Increased risk of infxn if…=> complement deficient
Post-splenectomy
No anti-PRP abs

37
Q

Hib Epiglottitis

A

Abrupt onset of fever, sore throat, and dysphagia

  • Pts. often DROOL too
  • May require emergency nasotracheal intubation
38
Q

Hib Arthritis

A

Often affects a single large joint; treatment requires surgical drainage

39
Q

Histamines

A

Source: Mast cells, basophils, platelets

Action: Increased vascular permeability, vasodilation, platelet activation

40
Q

Prostaglandins

A

Source: Mast cells, PMNs

Action: Vasodilation, Pain (PGE2), Fever (PGE2)

41
Q

Leukotrienes

A

Source: Mast cells, PMNs

Action: Increased permeability, Chemotaxis (LTB4), PMN Activation

42
Q

TNFa, IL-1, IL-6

A

Source: Macrophages, Mast cells, Endothelial cells

Action: Fever, Hypotension, Endothelial activation

43
Q

Platelet Activation Factor

A

Source: PMNs, Mast cells

Action: Increased vascular permeability, platelet activation, degranulation of platelets, vasodilation

44
Q

Kinins

A

Source: Liver

Actions: Pain, vasodilation, smooth muscle contraction, increased vascular permeability

45
Q

Facets of a Granuloma

A

Inner focus of granulomatous inflammation

Central collection of epithelioid cells* (characteristic)

Surrounding lymphs and possible caseating necrosis

*Epithelioid cells can combine to form giant cells

46
Q

CGD of Infancy

A

Deficiency off NADPH oxidase => chronic infxns

47
Q

Echinocandins

A

Inhibitors of glucan synthesis

48
Q

Nikkomycin

A

Inhibitor of chitin synthesis

49
Q

Sodarins

A

Inhibitors of fungal protein synthesis

50
Q

Candida albicans

A

Yeast @ 25 degrees; Mold at 37 degrees

VFs: Adherence to tissues
Germ tube production (proteinase)
Gliotoxin (immunosuppresant)
Dimorphic properties

Diagnosis: Calcoflour white prep. w/ KOH; should see pseudohyphae
*Germ-tube test faster

Treatment: Fluconazole OR mouthwash if only oral candidiasis

51
Q

Oesophageal candidiasis

A

Severe cottage-cheese appearance of fungi on tongue and down esophagus; occurs in IC

EXCEPTION- Women can get vaginal candidiasis on antibiotic therapy

52
Q

Chronic Mucocutaneous Candidiasis

A

Chronic, non-invasive infxns of mucous membranes, hair, and nails due to insufficient T-cell levels

-Requires multiple anti-fungal treatments

53
Q

Aspergillosis

A

Causes a variety of nosocomial acquired, invasive infxns

-Most common are of the bronchi or pulmonary parenchyma

Diagnosis: Rapid growth on potato agar
Histological ID of septate, dichotomously branching hyphae
Immunological ID

Treatment: Amphotericin-B or 5-flucystoine for invasive forms

54
Q

Mucormycosis (Rhizopus)

A

Aseptate, non-staining, ribbon-like hyphae that bend at right angles

*Outbreaks assoc. w/ use of infected bandages or taping

Clinically similar to Aspergillus

*Seen w/ hospital construction exposure, organ transports, immunosuppression theraopy

Treatment: Amphotericin-B

55
Q

Rhinocerebral mucormycosis

A

Invasive disease common in severely burnt patients that is accompanied by facial pain, headache, dilated pupil, and a change in mental status

  • Due to fungi infecting the nasal cavity and spreading to the nearby soft tissue
  • Terminal event in patients with acidosis or diabetes
56
Q

Cryptococcus neoformans

A

Major opportunistic organism in AIDS pts. and most common cause of fungal meningitis

*Pulmonary infections will appear nodular

Diagnosis: India Ink (+)
Niger-seed agar (+)
Urease (+)
Phenol oxidase (+) - blocks Epinephrine
Budding, encapsulated yeast cells
*Latex agglutination test (most common)

Treatment: (Induction Therapy) Amphotericin-B + Flucystosine -2 weeks
(Consolodation Therapy) Oral fluconazole or itraconazole - 8 weeks
*If AIDS pt, should take follow-up CSF samples at the end of therapies and for a year; CULTURE THESE

57
Q

Pneumocystis Carinii

A

Resembles protozoa and fungi; often the first infxn to present in AIDS pts

Diagnosis: Methenamine Silver-stain => Cup-shaped organism
*Often presents as walking pneumonia

Treatment: Trimethoprim-Sulfamethoxazole

58
Q

Viral ether sensitivity

A

Enveloped viruses EXCEPT Poxvirus

59
Q

Non-infectious viruses

A

Either have empty capsids or under-go faulty maturation

60
Q

Pox Virus Envelope

A

Is not received by budding; is more complex and synthesizes its envelope in the cytoplasm

61
Q

Defective Interfering Proteins

A

Produced after high MOI cells and cannot replicate on their own due to lack of all of their NAs

=» Require “helper virus” to complete its defective genome

*Interacts more strongly with polymerase than the full-length helper virus and leads to persistent infections

62
Q

Viral destruction of cell polysomes

A

Poliovirus

63
Q

Negri bodies

A

Inclusion bodies formed from rabies virus

64
Q

Guarnieri bodies

A

Inclusion bodies formed from smallpox virus

65
Q

Only single-stranded DNA virus

A

Parvovirus

66
Q

Only Double-stranded RNA virus

A

Reoviridae

67
Q

Active Trachoma

A

Presence of yellow follicles on the upper conjunctiva along w/ the presence of Herbert’s pits in the cornea

68
Q

Cicatricial Disease

A

Evidence of pannus, trichiasis, and corneal opacity

=»blindness

69
Q

Chlamydia cervicitis

A

Visible mucopurulent discharge along w/ erythematous and febrile cervix

*Can present alongside Fitzburgh-Hugh Syndrome

70
Q

Fitzburgh-Hugh Syndrome

A

Perihepatitis w/ inflammation of the liver capsule that is seen w/ C. trachomatis infxns

71
Q

Parinaud oculoglandular Syndrome

A

Conjunctivitis alongside periaucular, submandibular, and cervical lymphadenopathy

-Caused by LGV serotypes of Chlamydia

72
Q

Herpes family

A

a= HSV, VSV

b=CMV

y=EBV

73
Q

Herpesvirus structure

A

Double-stranded, enveloped, iscosahedral

74
Q

Four configurations of Herpes DNA

A

Prototype, Inverted Short (IS), Inverted Long (IL), Inverted short and long (ISL)

*Only one type of DNA per viral particle

75
Q

Extracellular receptor for HSV

A

Heparan sulfate

76
Q

Immediate herpesvirus protein synthesis

A

a =»regulatory proteins

77
Q

Early herpesvirus proteins

A

b =»enzymatic and needed for DNA replication

78
Q

Late herpesvirus proteins

A

y =» structural and used to synthesize the progeny virus

79
Q

EIEC

A

Invades at the M-cells and produces dysentery-like diarrhea

80
Q

Hemadsorption

A

RBCs attach to the surface of infected cells via the viral antigens of hemagluttinin that are being presented

81
Q

TCID50

A

The dilution of virus at which 50% of tissue cultures are showing CPE

82
Q

Herpes virus DNA replication

A

After moving into the nucleus, the DNA circularizes at internal redundancies and undergoes rolling replication

83
Q

Where does formation of the herpes virus capsule occur?

A

The nucleus

84
Q

Common CPE of herpesvirus

A

Multi-nuclear end giant cells

POD Exam 2 (3 decks)

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