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Bacteria Flashcards

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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
Norovirus, pathogenesis
Multiplies in small intestine and irritates lining
26
Adenovirus | Type of virus?
Ds DNA non enveloped Isocahedral Direct, faecal oral, droplet
27
Adenovirus Mechanism of infection Infections..
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
Adenovirus | Treatment
Pain relief- paracetamol Fluids Antivirals if lethal strain
29
Influenza A | Structure, mechanism of infection
-ssRNA Circular capsid, enveloped Different subtypes e.g. H1N1
30
Influenza A | Pathogenesis? Diseases cause?
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
Influenza A treatment
Pain release, antipyrexials, - neuraminidase inhibitor (oseltamivir - tamiflu) - Antiviral (acyclovir)
32
Influenza a prevention
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
HIV - structure? Spread?
+ ssRNA circular capsid Enveloped Bodily fluids
34
HIV- mechanis, of infection
``` 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
HIV | - presentation
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
HIV treatment
Treat AIDS defining illness | - cd4 count checked. Take action if
37
HIV - duration, complications,
``` 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
Hep B Structure Transmission
dsDNA Isocahedral Enveloped Fluids and blood
39
Hep B Mechanism of infection Pathogenesis, virulence factors Presentation How does it cause disease
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
Hep B | Describe the duration of the illness and the serotypes you would see in the blood
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
What is chronic HepB | Complications?
Hepatitis b infection >6mths HBsAg persisted Can lead to cirrhosis Of hepatocellular carcinoma
42
Treatment hepatitis b | Investigations
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
Hepatitis c Structure Transmission
+ssRNA Icosahedral Enveloped Blood NOT FLUIDS
44
``` Hep c Pathophysiology Treatment Investigations Complications ```
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
varicella zoster Structure Transmission
Herpes family Ds DNA Enveloped Trams,isisom: inhalation, direct contact with blisters
46
VZV Pathogenesis Who at risk
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
VZV | how does shingles occur?
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
Aspergillus fumigatus | Mechanism of infection
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
Aspergillus fumigatus | How does this body defend against this fungus
Cleared by mucocillary escalator --> pharynx --> swallowed Alveolar macrophages :) In ill patients: phagocyte deficiency--> multiplication of fungi :O
50
Aspergillosis- investigations and treatment
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
Plasmodium falcilarum | Structure, other strains,
Protozoa P. Vivax P. Ovale P. Malariae Via anopheles mosquito (saliva--> blood)
52
P falcilarum --> malaria?, how..
``` 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
Malaria, presentation investigate treat
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
HIV diagnosis
Blood culture PCR and antigen detection of genome ELISA: antibody screening tests Western blotting: antibodies
55
obligate anaerobes, where found in the body
``` Clostridium tetani (protective endospores) Bacteriodes - fragillis - oralis - melaniogenicus ``` Small bowel and COLON
56
Bacteria in colon
Anaerobes: clostridium tetani, difficile (antibiotics) perfringens (gas gangrene). Bacteriodes fragillis etc Enterococcus faecalis E. coli ``` Other Pseudomonas Klebsiella Salmonella Shigella Vibro cholera ```
57
In bowel/colon surgery what prophylaxis antibiotic would you give?
treat anaerobes, bacilli and cocci Metronidazole: anaerobes Gentamicin/cephalosporin: broad spec
58
Complications of bowel surgery and infections
``` Faecal peritonitis (peritoneum infected) Perinatal abscess (glands infected) ```
59
Most common UTI organisms
E.coli Enterococcus faecalis Gram neg: klebsiella, proteus, pseudomonas
60
Common mouth bacteria
Streptococci: gingivitis Staphylococci: Candidia Lactobacili Comps: infective endocarditis
61
Throat bacteria
``` Lots, think pneumonia and infections Staph strep Strep pyrogens--> tonsillitis (30% are bacterial) N. Meningitidis Haemophilius influenzae Candidia Lactobacilli ```
62
Nose bacteria
Staph Strep MRSA
63
Stomach
Helicobacter pylori in 50% pop Duodenal (and gastric) ulcers in 20% Other than that it's sterile
64
Vagina
Lactobacili | Turn acidic
65
Perineal skin
Aerobic so no obligate anaerobes e,g, bacteriodes | E. coli, lactobacili, enterococcus faecalis

infection antimicrobials (3 decks)

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