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infection antimicrobials > Bacteria > Flashcards

Bacteria Flashcards

1
Q

Pathogenesis of stash areus

  • patient factors
  • interaction with host
A

Break in mucosa, inhalation, ingestion etc. Naturally found on skin and nares
Immuni compromised?
- coagulase: converts fibrinogen to fibrin
-spreads quickly: hyuronidase: breaks down hyularonic acid in CT
- exotoxins: proteases- DNA ribonuclease to break down host DNA

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2
Q

Staphylococcus areus

  • presentation
  • conditions
  • treatment
A

Often Immune compromised patients

  • skin lesions: impetigo, boils, ABSCESS
  • SPUR: severe persistent, unusual, recurrent
  • conditions: HAP pneumonia, meningitis, impetigo
  • complications: endocarditis (BSI), TSS SEPSIS

MRSA: glycopeptides- vancomycin (systemic) , erythromycin/Vancouver (local)
Others: amoxicillin

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3
Q

Clostridium difficile

  • pathogenesis
  • bacteria type?
  • interaction with host
  • risk factors
A

Gram positive anaerobic bacilli with spores

  • opportunistic infection when normal flora eliminated by antibiotics for another infection (amoxicillin, cephalosporins, clindamycin)
  • RF: age, pathological state etc
  • exotoxin A : causes inflammation = excessive histamine= fluid loss= widens intracellular spaces
  • exotoxin B: escapes though these gaps and kills host cells (disrupts protein synthesis)
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4
Q

Clostridium difficile

  • presentation
  • conditions
  • complications
  • treatment
A

Antibiotic associated DIARRHOEA
Pseudo membranous colitis
Complication: severe diarrhoea–> renal failure–> cognitive impairment
Perforated toxic mega colon–> peritonitis–> septic shock

Treatment: discontinue causative antibiotics, give metinodazole , vancomycin

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5
Q

Streptococcus pneumoniae
- type of bacteria
- patient factors? RF?
Mechanism of infection

A

Gram positive, pairs/chains. Capsulated

Direct contact. Normal flora in URT.
Patient factors: age, pathological state, (smoking HIV obesity, spleen, chemo) time: more common in winter,

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6
Q

How does streptococcus pneumonia lead to infection?
What conditions..
Treatment

A

Bacterial Pneumonia, - most common CAP
Can lead to meningitis/septicaemia , pericarditis, if enters blood stream
Pneumonia occurs when bacteria colonise lungs. Not easily phagocytosis (thick capsule)
Pus accumulates= symptoms

Treat: supportive. And broad spectrum antibiotics

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7
Q

Viridans strep- type, conditions, when

A 
Positive cocci
Breach in dental --> endocarditis
Occurs if there is poor dental hygiene --> Harmless bacteraemia--> accumulates on heart valves
Treat: penicillin, replace valve
Complication--> heart failure
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8
Q

Coagulase negative strep- conditions?

A

Positive cocci- clusters
Prosthetics infections malaise, fever etc
Localised infection and Inflammation = pain

Prosthetic >1 year then strep viridans, enterococcus faecalis, staph areus, candidia

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9
Q

Escheridia coli
Describe
Pathogenesis
Conditions

A 
Gram negative anaerobic, spore forming, rod
Faecal oral.
Different strains- some harmless.
Conditions: 
-gastroenteritis (colonises GI tract)
-Peritonitis(e coli from bowel perforation/surgery) 
= cramping, bloating, diarrhoea 
- cystitis: UTI

Other strains: travellers diarrhoea, shigella, cholera like illness

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10
Q

E coli infection
Treatment
Complications

A

Supportive: fluids, o2, immodium
Specific: board spec antibiotic,
Complications: peritonitis–> liver damage, septic shock, death :O
Prevention: gastroenteritis very infectious!

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11
Q 
Neissaria menigitidis.
Type
Virulence factors
Pathogenesis
Complications
A

Gram negative cocci
Direct contact with respiratory secretions- kissing, sneezing
Normal flora of URT
- colonises meninges (lining of brain) = headaches and non specifically I’ll
–> BSI = rash

Virulence:

  • potent endotoxins (immune over reaction = vasodilation and permeability= decrease TPR = SEPTIC SHOCK
  • renal and resp failure
  • And disseminated intra vascular coagulation–> Ischaemic necrosis –> multi organ failure
  • Also increase ICP
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12
Q

Neissaria menigitidis
Presentation
Treatment

A 
Fever chills sweats- quick onset- 24hrs
- then purperic rash, photophobia, fever, neck pain
Identification: 
Treat: o2, fluids, adrenaline
Measure lactate and urging
Blood cultures and 
Broad spec: cefriaxone
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13
Q

Salmonella typhi - basics

A 
Gram negative rod
Faecal oral
Typhoid fever
Gastroenteritis (food borne)
Pneumonia
--> sepsis and intestinal perforation/haemorrhage
--> endocarditis

Treat: supportive, antipyrexials,
Ciprofloxacin, cefriaxone

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14
Q

Legionella pneumophillia basics

A

Gram negative rod
Droplet- hot tubs air con, stagnant water

Fever, SOB, pneumonia, productive cough, death
Legionaries disease oft confused with:
Pointaic fever (no pneumonia )

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15
Q

Pseudomonas aerinoginosa
- type
- pathogenesis
Mechanism of infection

A

Gram negative bacilli, facultative anaerobes (prefers anaerobic but can be both)
- inhalation: respiratory infection
- other route e,g, UTI cystitis
RF: cystic fibrosis, HIV,neutropenia ,immunecomp etc,

Pathogenesis: opportunistic infection - needs disease to take hold. Can survive in thick cystic fibrosis mucus (facultative anaerobes)
Colonises bronchi first –> pneumonia

Most common HAP

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16
Q

Pseudomonas aerinoginosa

Virulence

A

Virulence factors

  • blocks eukaryotic protein synthesis= oncosis
  • biofilm like layer: mucopolysaccharide capsule- reduced phagocytosis = harder to destroy (especially if a splenic as spleen destroys capsule)
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17
Q

Pseudomonas aerinoginosa

Treatment

A

Supportive
Specific: tobamycin (IV)

Don’t let ct sufferers meet!

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18
Q

Mycobacterium tuberculosis

- features

A 
Gram stain resistant, obligate aerobes 
Has thick, mycolic acid capsule 
Slow growing - slow for cultures
Non motile
7 species
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19
Q

M. Tuberculosis

Mechanism of infection and virulence

A

Mycolic acids: resist phagocytosis
Frustrated phagocytosis–> multiplies inside –> destroys macrophage –> reduces host response
Produces IL 12–> (NK –> IFN A and CD4 cells –> TNF A) –> recruit macrophages –> langhans cells in granuloma

Intense immune response –> local tissue destruction –> cavitation
Systemic–> fever and weight loss etc

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20
Q

M tuberculosis
Patient: risk factors?
Transmission?
How does it develop into active to

A

Droplets. Long term exposure. Schools, families, overcrowding, prisons, hospitals,homeless,

Reaches lymph nodes = primary complex
–> active Tb (immune comp)
Or –> latent TB (Th contain infection) infected but not a case

  • -> post primary TB (mature and reactivation)
  • -> self cured, 95%
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21
Q

Investigating TB

MANAGEMENT

A 
investigate: varying symptoms, most have lung involvement
Military = systemic
- culture
- CXR
- NAAT, IGRA, TST

antibiotics: rifamycin, isoniazid (4mths), pyradizonamide, ethambutol (2 mth)
MDRTB, XDRTB
SE: liver toxicity, monitor compliance,, contract tracing

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22
Q

Norovirus
Structure
Transmission

A

Non enveloped
SsRNA
Isocahedral
Direct, indirect (air, facael oral)

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23
Q

Norovirus
- disease, presentation
Investigation

A

Gastroenteritis: vomiting

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24
Q

Noroviral infection: treatment and prevention

A

Fluids, supportive, at home if not too bad

Wash everything! Very contagious and veery dangerous in very old and very young
Normally only lasts 1-4 days
No high risk food prep in hospital etc, short cuts through kitchens, infection wards separate.

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25
Q

Norovirus, pathogenesis

A

Multiplies in small intestine and irritates lining

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26
Q

Adenovirus

Type of virus?

A

Ds DNA non enveloped
Isocahedral
Direct, faecal oral, droplet

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27
Q

Adenovirus
Mechanism of infection
Infections..

A

Respiratory tract to pharynx/URTI–> nasolacrimal duct
Or to –> GI tract

Leads to repiratory infection/conjunctivitis/gastroenteritis
- enlarged tonsils, inflamed pharynx ,fever, malaise etc

28
Q

Adenovirus

Treatment

A

Pain relief- paracetamol
Fluids
Antivirals if lethal strain

29
Q

Influenza A

Structure, mechanism of infection

A

-ssRNA
Circular capsid, enveloped
Different subtypes e.g. H1N1

30
Q

Influenza A

Pathogenesis? Diseases cause?

A

Surface proteins HA and NA
H: Haemagglutinin- Helps virus enter cell by binding to the envelope

N: neuraminidase- cleaves glycoproteins to allow viral release from a cell after replication = spreads

Symptoms - due to cytokine over reaction

Disease- flu. Fever, aches, pains, dry cough,
–> chest infection, siniusitis (meningitis)

31
Q

Influenza A treatment

A

Pain release, antipyrexials,

  • neuraminidase inhibitor (oseltamivir - tamiflu)
  • Antiviral (acyclovir)
32
Q

Influenza a prevention

A

Flu vaccine - but change raking fie to high mutation rate

  • antigenic drift (small changes)
  • antigenic shift (large changes, change in subtype and the therefore treatment)
33
Q

HIV
- structure?
Spread?

A

+ ssRNA
circular capsid
Enveloped
Bodily fluids

34
Q

HIV- mechanis, of infection

A 
Enters blood stream, 
Binds and fuses to CD4T cells, macrophages and dendritic cells
Binds using glycoproteins
Penetrates and releases enzymes
ssRNA--> DNA (reverse transcriptase)
--> host DNA (integrase)
Transcription and translation--> vesicle
Cell lysis
Mature (use viral proteases)

= decline in T cells. = more susceptible to infection

35
Q

HIV

- presentation

A

Often asymptomatic, any are non specific and 2-6 weeks later= Unknowningly spread infection
Fever malaise, headache, sore throat,
AIDS defining infections
- opportunistic oral Candida albicans
- TB - extra pulmonary
- pneumocystis pneumonia - caused by opneumocytis jirovecci
Kaposi sarcoma

Acute HIV: flu like, fevers, muscle ache etc, vomiting. –> AIDS illnesses –> weight loss, lymph enlargement, fatigue etc

36
Q

HIV treatment

A

Treat AIDS defining illness

- cd4 count checked. Take action if

37
Q

HIV - duration, complications,

A 
Asymptomatic and then stage 1 (CD4>500) --> 4(AIDS)
CAn live for years without it taking over- have class 1 MHCs that can present to CD8 T cells instead which destroy it

Most people have average life expectancy with treatment

38
Q

Hep B
Structure
Transmission

A

dsDNA
Isocahedral
Enveloped

Fluids and blood

39
Q

Hep B
Mechanism of infection

Pathogenesis, virulence factors
Presentation
How does it cause disease

A

Nucleocapsid core with envelope with surface antigen HBcAg

Virus enters blood stream
Surface antigen Binds to receptor on hepatocyte
Nucleocapsids: enter cell and reach nucleus
Replicate within
Tkillers recognise and destroy (and kill cell)

Hepatitis: liver failure, jaundice, fatigue, abdominal pain, Nausea, joint pain

40
Q

Hep B

Describe the duration of the illness and the serotypes you would see in the blood

A

Normally self resolves after 6 months but can become chronic

HBsAg- surface antigen, within 6 days (ALT/DNA levels rising too)= infections
HBsAg: e antigen: highly infections period
IgM released (1st antibody, immune system started to fight back)
HBsAb: antibody to e antigen= end of infections period. Virus inactive :) patient recovered
HbsAb: surface antigen antibody - memory cells in vaccinated/ resistant people
IgG- core antibody persists for life

41
Q

What is chronic HepB

Complications?

A

Hepatitis b infection >6mths
HBsAg persisted
Can lead to cirrhosis
Of hepatocellular carcinoma

42
Q

Treatment hepatitis b

Investigations

A

Stop drinking, non essential medications
Fever reducers , pain relief

Vaccinate- prevention better, or (within 24hrs infection)

Normally self resolves but can give antiretroviral drugs in chronic infection or pefinterferon Alfa 2a to stimulate immune system

FBC, u snd Es , LFTs, CRP, Hep C antibody test, PCRl

43
Q

Hepatitis c
Structure
Transmission

A

+ssRNA
Icosahedral
Enveloped

Blood NOT FLUIDS

44
Q 
Hep c
Pathophysiology 
Treatment
Investigations 
Complications
A

Virus travels to liver and replicates within hepatocytes but often asymptomatic. Most don’t know
Investigations: FBC, u snd Es , LFTs, CRP, Hep C antibody test, PCR
May have dark urine and RUQ pain, helatomegaly?

Treat: smoking, drinking, excercise, antiviral (ribavirin), interferon (stimulates immune system)

–> cirrhosis, liver failure, liver cancer

45
Q

varicella zoster
Structure
Transmission

A

Herpes family
Ds DNA
Enveloped
Trams,isisom: inhalation, direct contact with blisters

46
Q

VZV
Pathogenesis
Who at risk

A

Immune compromised
Young children very common (chicken pox) much more serious in adults

Normal immune response:
Class 1 MHC –> cd8 T cells –> cytotoxic T cells
IgG antibodies persist = lifelong immunity

47
Q

VZV

how does shingles occur?

A

Reactivation of the dormant virus
- lies dormant in dorsal ganglion of sensory nerves–> dermatome formation
- if immunecomp
Shingles : red rash (pox raised and itchy)

48
Q

Aspergillus fumigatus

Mechanism of infection

A

In the air normally spores always present and inhaled
Rod shaped
Causes disease I’m immunocomprimised patients - opportunistic

Likes high O2 areas, carbon rich surfaces - starchy foods, organic material
Communised in the lungs–> chronic pulmonary aspergillosis

49
Q

Aspergillus fumigatus

How does this body defend against this fungus

A

Cleared by mucocillary escalator –> pharynx –> swallowed

Alveolar macrophages :)
In ill patients: phagocyte deficiency–> multiplication of fungi :O

50
Q

Aspergillosis- investigations and treatment

A

FBC, u snd Es , LFTs, CRP, PCR, CXR, sputum culture,

Antifungals: ampotericin
Colony stimulating factors in some cases
Ant pyrexials, pain relief
Avoid abundant spores

51
Q

Plasmodium falcilarum

Structure, other strains,

A

Protozoa
P. Vivax
P. Ovale
P. Malariae

Via anopheles mosquito (saliva–> blood)

52
Q

P falcilarum –> malaria?, how..

A 
Blood stream by sporozites
To liver
Divide and rupture hepatocytes
Thousands of merozites released
--> rbc (hb used)--> oncosis and burst --> gameocytes released = haemolytic anaemia

Gameocytes adhere to endothelium in bra in–> cerebal malaria –> coma :O

53
Q

Malaria, presentation investigate treat

A

Fever chills sweats 3 day cycle
Travel hx

Splenomegaly
3 blood smears, identify parasite strain,
FBC, u snd Es , LFTs, CRP, coagulation studies, head CT scan, PCRmof nucleic acid but too slow

Treat depends on strain: quinine/atovaquone-progunail
Or chloroquine in non resistant

Coma convulsions death

54
Q

HIV diagnosis

A

Blood culture
PCR and antigen detection of genome
ELISA: antibody screening tests
Western blotting: antibodies

55
Q

obligate anaerobes, where found in the body

A 
Clostridium tetani (protective endospores)
Bacteriodes 
- fragillis 
- oralis
- melaniogenicus

Small bowel and COLON

56
Q

Bacteria in colon

A

Anaerobes: clostridium tetani, difficile (antibiotics) perfringens (gas gangrene). Bacteriodes fragillis etc
Enterococcus faecalis
E. coli

Other
Pseudomonas
Klebsiella 
Salmonella
Shigella
Vibro cholera
57
Q

In bowel/colon surgery what prophylaxis antibiotic would you give?

A

treat anaerobes, bacilli and cocci
Metronidazole: anaerobes
Gentamicin/cephalosporin: broad spec

58
Q

Complications of bowel surgery and infections

A 
Faecal peritonitis (peritoneum infected)
Perinatal abscess (glands infected)
59
Q

Most common UTI organisms

A

E.coli
Enterococcus faecalis

Gram neg: klebsiella, proteus, pseudomonas

60
Q

Common mouth bacteria

A

Streptococci: gingivitis
Staphylococci:
Candidia
Lactobacili

Comps: infective endocarditis

61
Q

Throat bacteria

A 
Lots, think pneumonia and infections 
Staph strep
Strep pyrogens--> tonsillitis (30% are bacterial)
N. Meningitidis
Haemophilius influenzae
Candidia
Lactobacilli
62
Q

Nose bacteria

A

Staph
Strep
MRSA

63
Q

Stomach

A

Helicobacter pylori in 50% pop
Duodenal (and gastric) ulcers in 20%

Other than that it’s sterile

64
Q

Vagina

A

Lactobacili

Turn acidic

65
Q

Perineal skin

A

Aerobic so no obligate anaerobes e,g, bacteriodes

E. coli, lactobacili, enterococcus faecalis

infection antimicrobials (3 decks)

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