Brainscape's Knowledge GenomeTM

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


See full index

Path > Micro > Flashcards

Micro Flashcards

1
Q

Adverse effects of antimicrobials

A 
GI upset
Fever & Rash (SJS)
Renal dysfunction
Anaphylaxis (very rare)*
Hepatitis (more common to have derranged LFTs than full blown hepatitis)

*don’t let the fact that someone has a mild allergy disuade you from using that abx if it is the best abx for that patient.

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

What determines what abx we should choose

A

CHAOS
Choice
Host factors
- E.g. Age (can’t use tetracyclines in kids cos they deposit in bone. Also kids, don’t give 6x/day) Pregnancy (can’t use folate antagonists e.g. trimethoprim), Immunocompromised, Renal failure, Liver failure, severity of disease, interactions with other drugs e.g. statins and fusidic acid -> liver failure, warfarin, SSRIs and lineozlid,.

Antimicrobrial susceptibilities
Trust policies

Organisms
E.g. pneumonia - pneumococcus, haemophilus, moraxella (g-ve) (Amoxicillin is broad and covers pneumo and haemophilus)

Site
Some sites are difficult to treat e.g. bone, CNS, some abx are difficult to get into the blood and wouldn’t be good for a septicaemia

ALWAYS LOOK AT LOCAL POLICIES.

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

How do we identify the infective organism?

A

Gram stain the joint aspirate, CSF or pus

PCR/immunoflorescence - rapid antigen detection

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

When do and don’t we change from IV to po abx?

A

We change from IV to PO asap i.e. 48 hours after pt is stabilised.
Exceptions: meningitis as PO doesn’t reach csf, endocarditis and osteomyelitis

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

Why is it important to measure the serum level of abx (less in clinical context and more in research context)

A

The level of the peak of the drug predicts how successful the drug will be (adjust dose if too high or lose)
The level of trough predicts elimination (concern if it isn’t being eliminated) (adjust interval if too high or low)
TYPE 1- This is important for aminoglycosides as they have a dose dependent effect. therefore they usually have a OD regimen where you try to maximise the peak.
TYPE 2 - For pencillins, the time above the MIC is important and therefore the regimens are usually 3-4tds.
TYPE 3 - Clinda, Vancomycin - its the area under the curve i.e. the total amount your body receives over time that determines efficacy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What specific time recommendations exist for antimicrobials?

A

Generally, short as possible a part from:
N meningitides meningitis - 7d
Acute osteomyelitis in adults - 6 weeks
Bacterial endocarditis - 4-6 weeks
Gp A Strep (pharyngitis) - 10 d (rheum and glom)
Simple cystitis - 3d

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

Generalisations for abx indications for specific diseases

A

Skin/soft tissue - worried about strep/staph - fluclox (unless MRSA or worried about pen allergy)
Mild CAP - pneumococcus hib and moraxella - amoxicillin
Severe - clina + coamoxiclav (worried about resistance)
Pharyngitis - ben pen 10d
HAP - tend to be g-ve e.g. pseudomonas - cephalosporin, ciclosporin, tazobactam
Meningitis - Neisseria menigitids, S pneumoniae - Ceftriaxone (listeria if neoatae, lederly or pregnant - add amoxicillin)
UTI - Trimethoprim 3d
Hospital UTI - (trimeth resistance high) so cephalexin or co-amoxiclav

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

What is the eagle effect?

A

Effect that bacteria are only susceptible to abx when dividing so if they are in the stationary phase e.g. in group a strep there is a high burden and they stop replication (May be due to lack of nutrition) and increase the dose of abx won’t be effective

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

C dif colitis mx

A

Stop the offending abx (usually ceph)
If severe treat with oral metro
If that fails use vanco.

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

What do you do if there is no response in 48 hours?

A

Does the pt really have a bacterial infection
Is there a persistent focus/source present e.g. urinary catheter
Is there a deep seated collection that requires drainage e.g. abscess
Could the patient have bacterial endocarditis
Am i using the right dose?
Is there another infection present e.g. candida?

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

Causes of acute meningitis

A 
Causes:
Neisseria meningitidis (A, B & C serotypes) (GRAM NEGATIVE- ATTRACTS NEUTROPHILS)
Streptococcus pneumoniae (GRAM POSTIVE, DIP)
Haemophilus influenzae (GRAM NEGATIVE, COCOBACILI, oxidase and catalase positive)

Streptococcus pneumoniae meningitis has a bimodal distribution (mainly in children/young people and elderly patients)

Other causes:
Listeria monocytogenes (key cause of meningoencephalitis) (GRAME POSITIVE, RODS)
Group B Streptococcus (can cause neonatal meningitis)
Escherichia coli (biphasic - old people and neonates)

Rare causes:
TB (ZN IS BLUE BACKGROUND RED CHAINS)
S. aureus, T. pallidum,
Cryptococcus neoformans (fungal) (HIGH OPENING PRESSURE, ORBIT STRUCTURE - circles with mass in the middle, india ink stain which is red) (HIV is RF)

Neisseria meningitidis- Enters the body through the nasopharyngeal mucosa in a susceptible individual. Causes infection in < 10 days

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

Chronic Meningitis

A

This is TB Meningitis
Similar presentation to acute meningitis (fever, headache, neck stiffness)
• More common in immunosuppressed patients
• Takes weeks to present
Involves the meninges and basal cisterns of the brain and spinal cord
Cx: Tuberculous granulomas, asbcesses and cerebritis
Also, there is leptomeningeal enhancement
Chronic meningitis needs to be managed by specialists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Aseptic Meningitis

A

MOST COMMON infection of the CNS
Presentation: headache, stiff neck, photophobia
A non-specific rash may accompany these symptoms MOST COMMON Organisms
• Coxsackie group B
• Echoviruses
o Usually occurs in children < 1 year
o Self-limiting disease that resolves in 1-2 weeks

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

Risk factors for bacterial meningitis

A

Complement deficiency, hyposplenism (susceptibleto encapsulated organisms), hypogammaglobulinaemia

S.pneumoniae specifically: Immunodeficiency (alcoholic), infection (pneumonia), entry #, previous head trauma w/ CSF leak

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

Encephalitis causes

A

Viral: Coxsackie, M & M, VZ, EBV, CMV
IMPORTANT: West Nile Virus is becoming a leading cause of encephalitis worldwide

Bacterial - Listeria
Amoebic Encephalitis (Naegleria fowleri)
Parasitic Encephalitis (Toxoplasma gonadaii)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Most likely route of infection of brain abscess and causative organism

A

Tend to occur due to direct extension (e.g. otitis media, mastoiditis, paranasal sinuses)
Can occasionally spread haematogenously (e.g. endocarditis). Common ENT pathogens are staph and strep.

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

Most likely route of infection of spinal infection and causative organism

A

Pyogenic vertebral osteomyelitis is a common form of vertebral infection (e.g. staph and strep)
It can spread via direct open spinal trauma from infections in adjacent structures or it can spread haematogeously
If untreated, it can lead to:, Permanent neurological deficits, Significant spinal deformity and Death
Risk Factors
• Age
• IV drug use
• Long-term systemic steroids
• Diabetes mellitus
• Organ transplantation

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

Meningitis Mx

A

Ceftriaxone 2g IV BD is good at killing meningococcus, pneumococcus, haemophilus and E. coli
However, Ceftriaxone does NOT cover Listeria monocytogenes- This requires amoxicillin. Therefore add amoxi if immunocompromised or >50 (2g IV 4 hourly)

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

Meningoecephalitis Mx

A

Aciclovir 10mg/kg IV TDS

Ceftriaxone 2g IV BD

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

Staph Aureus

A

Gram positive coccus, catalase positive, coagulase positive, bunch of grapes
Preformed toxin -> rapid onset of symptoms
Prominent vomiting, watery, NON BLOODY diarrhoea
Self limiting

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

B cereus

A

Heat labile diarroheal toxin, heat stabile emetic toxin, gram positive, rod-spores,
Watery non bloody diarrhoea
self limiting
rare cx cerebral abscess

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

C diff

A
  1. Pseudomonas colitis (abx induced diarrhoea*) (can be any abx - apart from aminoglycoside - that caused it but usually the 4Cs cipro cef clina coamox)
    Stop abx. Metro is first line for mild, oral vanco is second line. Infection control.
    f-o transmission via spores
    *abrupt, with explosive, water, foul-smelling diarrhoea
    Rf
    o Administration of antibiotics
    o 65+ years
    o Duration of hospital stay
    o Severe underlying diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Anaerobic organisms

A

C diff species
Actinomyces species
Lactobacillus species

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

Listeria

A

Listeria monocytogenes - GRAM POSITIVE, RODS
V or L shaped, ß haemolytic, aesculin +ve, tumbling mobility
GI watery diarrhoea, cramps, headache, fever, little vomiting.
Perinatal infection, immunocompromised patients Outbreaks of febrile gastroenteritis
Refrigerated food (unpasteurised dairy, vegetables)
Mx: 1st Ampicillin. Ceftriaxone, Cotrimoxazole

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

Enterobacteriaceae

A

Enterobacteriaceae includes, along with many harmless symbionts, many of the more familiar pathogens, such as Salmonella, Escherichia coli, Klebsiella, and Shigella. Other disease-causing bacteria in this family include Enterobacter and Citrobacter.

Members of the Enterobacteriaceae can be trivially referred to as enterobacteria or “enteric bacteria”, as several members live in the intestines of animals.

In fact, the etymology of the family is enterobacterium with the suffix to designate a family (aceae)—not after the genus Enterobacter (which would be Enterobacteraceae)—and the type genus is Escherichia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

E coli

A

Facultative anaerobes, oxidase negative

  1. ETEC - the main type
    Toxigenic, Travellers diarrhoea (fo)
    Heat labile LToxin stimulates adenyl cyclase and cAMP
    Heat stable SToxin stimulates guanylate cyclase.
    Acts on the jejeunum, ileum not on colon.
2. EIEC - invasive
Invasive dysentery (bloody diarrhoea)
  1. EPIC - paeds
    Infantile diarrhoea

4.EHIC - haemorrhagic
Caused by verotoxin

4b. 0157: H7 subtype Anaemia, thrombocytopenia, renal failure

Mx: Self limiting - can treat with ciprofloxacin (avoid Abx)

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

Salmonella

A

Antigens: O, H, Vi Ag’s
H2S producers (black colonies), TSI agar, XLD agar
Motile
3 main species we are worried about: typhi (paraptyphi), enteriditus, cholerasuis

  1. Typhi/Paratyphi
    Only transmitted by humans
    Multiplies in Peyers patches,
    Slow onset fever + CONSTIPATION, relative bradycardia Splenomegaly and rose spots, anaemia and leukopaenia
    Spreads via ERS -> bacteraemia will occur, 3% will become carriers (in gallbladder)
    SCD pts are particularly at risk, as our any pts with bone grafts
    Ceftraixone or ciprofloxacin
  2. Enteritides
    Poultry, eggs and meat, invasion of small and large bowel Bacteraemia is infrequent. Stool is positive.
    Invasion of epithelial and subepithelial tissue
    Enterocolitis i.e. loose stool Self limiting non-bloody diarrhoea
    Management usually not needed
    Rose spots

Recurrent infections are associated with salmonella being carried by reptillian pet

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

Shigella

A

Non-lactose fermenters, non H2S, non motile
Mainly affects the distal ileum + colon -> mucosal inflammation, fever, pain, BLOODY diarrhoea.
Shiga enterotoxin
Most effective enteropathogen (low ID 50)
No animal reservoir or carreir state
Also has cell wall O antigens and polysaccharide (groups A-D)

Avoid abx (Cipro if required)

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

Vibrios

A

Late lactose fermenters Oxidase +ve, COMMA SHAPED, ‘beautiful’ lol
Two groups O1 - most lie in here, associated with epidemics. The non O1 group: sporadic, non pathogens.

  1. Vibrio cholerae
    Rice water stool. T: Human faeces (e.g. water borne foods in shellfish)
    Path: ↑cAMP opens Cl channel at apical membrane of enterocytes -> efflux of Cl to lumen (loss of H2O and
    electrolytes).
    Massive diarrhoea without inflammation
    Mx: Electrolye replacement, fluid resus
  2. Vibrio parahaemolytics
    Raw/uncooked fish
    Self limiting (lasts 3 days)
    Difficult to pick up, have to use salty agar
  3. Vibrio vulnificus
    Cellulitis in shell fish handlers/divers cut by coral can cause shock and be fatal, thorough hx needed
    Doxy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Campylobacter

A

Campylobacter- (curved, comma or S shaped)
Microaerophilic, Oxidase +ve, motile, sensitive to nalidixic acid (first quinolone).

Drinking unpasteurised milk, food eg: poultry
Prodrome of headache and fever, debilitating abdo cramps, bloody (foul-smelling) diarrhoea

Assoc with Guillain-Barre, reactive arthritis (Reiter’s)

Mx: Erythromycin or Cipro if first 4-5/7 but mostly get better by the time you diagnose

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

Yersinia enterocolitis

A

Enterocolitis, mesenteric adenitis w/ necrotising granulomas, assoc reactive arthritis & eythema nodosum.
Transmitted via food contaminated with domestic animals excreta. Prefers 4oC “cold enrichment”

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

What have we forgotten?

A

TB - IT CAN ALWAYS BE TB

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

Non0bacterial causes of diarrhoea

A 
Viruses: Secretory Diarrhoea
• Rotavirus - <6yrs
• Adenovirus – Types 40,41 cause non bloody diarrhoea (<2yrs)
• Norovirus – Adult outbreaks, vomiting.
• Poliovirus
• Enteroviruses (coxsackie, ECHO)
• Hepatitis A

Protozoa

Entamoeba Hystolytica
Motile trophozoite in diarrhoea
Non-motile cyst in non-diarrhoeal illness
4 nuclei and no animal reservoir. Colonize colon
Makes a flask-shaped ulcer on histology
Symptoms: dysentery, wind, TENESMUS. Chronic weight loss + RUQ pain due to liver abscess !
Stool microscopy
Rf camping and didn’t boil water
Metro + paromycocin if luminal disease

Giardia
Pear shaped trophozoite 2 nuclei Trophozoites/cysts found in stool
rf: travellers, hikers, day care,MSM, mental health hospital
Get it by ingesting cysts from faecally contaminated H2O
Malabsorption of protein + fat - FOUL SMELLING non- bloody diarrhoea
Metronidazole
Dx = ELISA string test
Mx = Metro

Cryptocsporidium Parvum
DONT GO SWIMMING POOL IF YOU’VE HAD D&V BECUASE OF THIS BAD BOI
Infects the jejunum. Severe diarrhoea in immunocompromised.
Oocysts seen in stool by modified Kinyoun acid fast stain
Lecturer said self-limitng, meded says Paromomycin, Nitazoxanide in kids

34
Q

HIV epidemiology

A
  • The vast majority of cases occur in Sub-Saharan Africa
  • 1 in 10 people living with HIV are children
  • HIV is a massive contributor to under-5 mortality rates across the world
  • HIV accounts for 35% of deaths in children < 5 years old in Sub-Saharan Africa
  • There is an increasing proportion of cases appearing in teenagers with undiagnosed perinatally-acquired HIV
  • Over 90% are due to mother-to-child transmission
  • However, child sexual abuse is also a major risk factor for vulnerable children
35
Q

HIV Manifestations

A

• Chronic swelling of the parotids is an early indication of HIV infection
• Molluscum contagiosum is also associated with HIV (if it is recurrent or chronic)
• Lymphadenopathy is an important and common presenting feature
• Dental caries, gingivitis and upper respiratory infection are also very common
• Lymphoid interstitial pneumonitis is a lung condition associated with HIV that is characterised by lymphoproliferation due to immune activation
o NOTE: if the lymphoid tissue contracts, you will end up with bronchiectasis and chronic suppurative lung disease
• Shingles is usually uncommon in children, however, seeing shingles in more than one dermatome raises suspicion of immunodeficiency
• HIV Encephalopathy
o Basal ganglia calcification
o White matter changes
o Atrophy
o Vasculopathy/stroke
• Severe failure to thrive is another key feature of HIV in childhood
• CMV coinfection (which is transmitted perinatally) usually causes no consequences but can cause sight-threatening retinitis
• Kaposi sarcoma is associated with co-infection with HHV8

36
Q

Risk factors for vertical transmission of HIV

A
  • Vaginal birth
  • the first twin
  • something that can damage the placenta and impair its barrier (e.g. malaria,toxoplasmosis)
  • PROM
37
Q

Should HIV mothers breast feed?

A

o NOTE: however, the difference in mortality was not that big because formula-fed babies were more likely to develop diarrhoea
o Therefore, the decision to avoid breastfeeding is dependent on the context of the society - if infant mortality is high, then it would be better to exclusively breastfeed
o I.e. consider whether formula feeding is accessible, affordable and safe
o WHO recommends that if infant mortality rate > 40/1000 live births, recommend:
• Exclusive breastfeeding
• ARVs for mother and baby

38
Q

Barriers to treating HIV in africa

A

o Malnutrition
o Multiple co-infections (especially TB)
o Risk of immune reconstitution inflammatory syndromes (IRIS)
• Revamping the immune system can lead to a severe inflammatory response which leads to deterioration in clinical state
o Family disruption (Children as caretakers)
o Stigma in school
o Depression
o Poverty

39
Q

Arrow trial showed what?

A

o Showed no difference in outcome when clinical monitoring is compared to laboratory monitoring

40
Q

Prion diseases

A
  • Prion stands for protein-only infectious agent
  • Rare transmissible spongiform encephalopathies in humans and animals
  • They do contain DNA but they are only made of protein
  • When they enter the brain they can trigger a cascade where existing prion proteins become rapidly affected and develop the abnormal isoform of the prion protein
  • This leads to the development of spongiform vacuolisation of the brain
  • Results in rapid neurodegeneration
  • Currently UNTREATABLE
41
Q

Prion Pathogenesis

A

All of us have a normal prion gene found on chromosome 20. It encodes a prion protein. The normal function of prion protein is poorly understood but it is thought to have some role in copper metabolism. The normal protein does NOT cause any issues - it is only when we get the abnormal isoform that it causes neurodegeneration. On Codon 129 there are THREE polymorphisms that we can find: MM - this predisposes to prion disease (methionine).
Problems occur when the normal prion protein transforms into the abnormal version (PrPSc)
This has a beta-pleated sheet configuration and is RESISTANT to proteases and radiation so it is difficult to get rid of (e.g. surgical instruments contaminated with diseased prions are impossible to clean)
Once you get a seed of the abnormal prion protein (PrPSc) it seems to act as a template which promotes conversion of PrP into insoluble PrPSc
This is what results in rapid neurodegeneration
The trigger for this process is unclear in sporadic cases

42
Q

Sporadic CJD

A 
Rapid dementia with: Myoclonus, Cortical blindness, Akinetic mutism, LMN signs 
Mean age: 65 years (range 45-75 years)
Incidence : 1/million/year 
Death within 6 months 
Cause is uncertain
o	Could be due to somatic PRNP mutation 
o	Spontaneous conversion of PrP to PrPSc
o	Environmental exposure to prions

Diagnosis
EEG (2/3 pts will have abnormal one)
MRI (Increased intensity in basal ganglia)
CSF (Raised 14-3-3 protein and S100 (these are markers of rapid neurodegeneration)
Brain biopsy - definitive, done at autopsy
Histology -spongiform vacuolisation

43
Q

vCJD

A

Younger age of onset (median = 26 years)
Median survival time = 14 months
Psychiatric onset (Dysphoria, Anxiety, Paranoia, Hallucinations)
Followed by neurological symptoms (Peripheral sensory symptoms, Ataxia, Myoclonus, Chorea, Dementia)
MRI - shows pulvinar sign (high intensity in the putamen)
EEG - non-specific slow waves
CSF - 14-3-3- and S100 are NOT useful
Tonsillar biopsy is 100% specific and sensitive

44
Q

Iatrogenic CJD

A

o Human cadaveric growth hormone
o Corneal transplants
o Neurosurgical procedures (e.g. corneal grafts)
o Blood transfusions
o Other surgical procedures (e.g. appendicectomy, tonsillectomy)
(NB there is no blood test)
o Starts with a progressive ataxia
o Dementia and myoclonus occurs at a later stage
o Speed of progression depends on route of inoculation (CNS inoculation is the fastest)

45
Q

Familial Prion Disease

A

Autosomal Dominant mutations
1. GSS (Onset age 30-70 years, Survival 2-10 years, PRNP P102L (MOST COMMON mutation))

  1. Fatal familial insomnia
    o PRNP D178N
46
Q

CJD treatment

A

o Clonazepam for the myoclonus

o Quinacrine, tetracycline, pentosan for delaying prion conversion

47
Q

PCP presentation and treatment

A

• Widespread, bilateral ground glass shadowing with reduced exercise tolerance and low saturations is suggestive of Pneumocystis jirovecii pnuemonia
Ix • This is visualised using a silver stain (Grocott-Gomori stain)
• This is treated with co-trimoxazzole

48
Q

Actinomyces

A

o Gram-positive rod that branches
o Causes lung abscesses in immunocompromised patients (alcoholics and chronic illness such as DM)
o Closely associated with Nocardia (g+ rod)
o These infections tend to be indolent and go on for a long time
o They are slow-growing and very difficult to treat
o As it is slow-growing, it is hard to grow in the labs so you should notify the histopathologist and microbiologist that you are worried about actinomyces
Histological features of actinomyces
• Basophilic sulphur granules
• Gram-positive rods that form branches as they grow

49
Q

Rifampicin

A
  • One of the TB drugs
  • Part of the rifamycin group under inhibit DNA synthesis class but actually inhibits RNA synthesis
  • Good at disrupting biofilms and has good penetrance
50
Q

Osteomyelitis management approach

A

o Antimicrobial therapy alone is NOT curative in most cases of osteomyelitis
o Continuous drug over a long period of time will lessen the amount of discharge, but it will not cure the disease because it cannot sterilise dead bone or cavities with necrotic content and rigid walls
o Removal of devitalised tissues and the prevention of extension of infection by providing adequate drainage is extremely important (debridement)
oThis is because immune system forms fibrous capsules can form around bacteria which makes it impenetrable to antibiotics and it becomes a chronic source of infection
Always always always be aware of an external source of infection e.g. prosthesis, implant, picc line, catheter. Their removal an adequate debridement is second to none.

51
Q

When stool samples are sent what are they tested for?

A

All faecal samples will be tested for:
o Salmonella
o Shigella
o Escherichia coli O157

Clostridium difficile testing is performed automatically in anyone > 65 years

52
Q

C Diff colitis management

A

o Isolate in a single room
o Assess severity
o Stop offending antibiotics if possible
o Wash hands with soap and water before and after each patient contact and use gloves and aprons
• NOTE: alcohol gel isn’t effective against the spores
Commence C. difficile care pathway, fluid balance chart and Bristol stool chart
Non-Severe Disease - Metronidazole 400 mg PO TDS 14 days. If no response in 72 hrs -> classed as severe
Severe: vancomycin 125 mg PO QDS 10-14 days ±metro

53
Q

What counts as severe c diff

A 
>38.5
HR>90
WCC>15
Rising creatinine
Signs of colitis 
Failure to respond in 72 hrs
C. difficile Ribotype 027
54
Q

C. difficile Ribotype 027

A 
o	Associated with a severe outbreak in 2005
o	Associated with increased severity of disease 
o	Identified by PCR ribotyping 
o	Produces:
•	16 x more toxin A
•	23 x more toxin B 
•	Compared to control strains 
assoc with high mortality
55
Q

Path of C diff

A

C. difficile is a Gram-positive spore-forming anaerobe
• The organism produces two toxins:
o One toxin damages the epithelial cells (cytotoxin)
o The other disrupts the tight junctions
• This leads to a lot of inflammation with neutrophil infiltration of the tissues
• The disruption of tight junctions leads to lots of fluid loss into the bowels
• It is called pseudomembranous colitis because you are left with plaques of fibrous and damages material which looks like membranes
• NOTE: high WCC + low CRP is common in C. difficile infection

56
Q

Hep C

A

Enveloped FLAVIVIRUS, positive sense ssRNA genome
1. Acute and chronic disease
2. Mainly blood product spread (apart from MSM) rf are blood transfusions, egyptian, 60-80% chronicity (worse for men)
Complications: Cirrhosis, Cryoglobulin Ax disease* +
glomerulonephritis.
- Genotypes 1 (40-50% of HCV UK burden), Treatment less successful
- Genotypes 2 and 3 – (40-50% of HCV UK burden) Treatment more successful

*Within the past decade, it has been recognised that a majority of patients with essential mixed cryoglobulinemia (MC) are chronically infected with hepatitis C virus (HCV). Although the underlying mechanisms have not been fully elucidated, cryoglobulin formation is clearly linked to the attempt of the host to clear the significant quantities of virions generated daily by the chronic infection.

57
Q

Hep C treatment

A
  1. Vaccine: Recombinant vaccine, purified HbSAg
  2. Initially interferon therapy (Peg INF ⍺ 2b/2a)
  3. NS3/4 protease inhibitors (-previrs, block translation): telaprevir, boceprevir, simeprevir, asunaprevir (learn one or two)
  4. NS5A inhibitors (-asvirs, block release): ledipasvir, daclatasvir
  5. Direct polymerase inhibitors (- buvirs, block replication): Sofosbuvir, dasabuvir
58
Q

Hep D

A

Deltavirus, enveloped virus, negative sense, single-stranded circular RNA
Always coinfection with HBV
Transmission: Sexual, parental, perinatal (only possible in combination with HBV)
Peginterferon-⍺

59
Q

Hep E

A

Unenveloped positive sense ssRNA genome
1. Acute hepatitis – India
2. Faeco-oral transmission
Rare complications: CNS disease – Bell’s palsy, Guillain Barre, other neuropathy; Chronic infection
Largely supportive care
Vaccine - Effective in trials- recombinant HEVg1

60
Q

Hep A

A

Unenveloped, picornavirus, positive sense ssRNA genome*
Acute hepatitis – 2-6 weeks incubation, severe in elderly Faeco-oral transmission
Incubation 2-6 weeks
Dx: Acute - Anti-HAV IgM (IgM persists up to 14w)
Supportive Tx, Vaccine
Live attenuated and inactivated preparations
* Positive-sense ssRNA viruses have genetic material that can function both as a genome and as messenger RNA; it can be directly translated into protein in the host cell by host ribosomes

61
Q

Hep B

A

Enveloped, hepadnavirus genome is mixture of DNA and RNA
Incubation 2-6 months
90% of those >5y clear the virus, only 10% of neonates do
t: vertically, sexually and blood(ily)
In immunocompromised there is a risk of re@ e.g. rituximab usage
Ix: ALT and AST raised
HBsAg - infection and vaccination
HBeAg - infectivity
HBcAb (acute IgM)

Mx:

  1. Inf a
  2. Lamivudine
  3. Entecavir
  4. Telbivudine
  5. Tenofovir
Treatment goal – Prevent progression to cirrhosis + HCC. Maintain serum HBV DNA level as low as possible &amp; attain histology improvement, ALT normalization. 
Loss of HBVeAg and seroconversion to HBVeAb
Pegylated Interferon (INF) Alpha 2a (subcut) – Direct antiviral effect + upregulates expression of MHC on cell surfaces
62
Q

epidemiology of surgical site infections

A

15.7% of HAI were SSIs

S Aureus E coli Pseudomonas Aeruginosa

63
Q

How much bacteria is needed to cause an infection?

A

> 10^5 microorganisms/ gram of tissue increases the SSI risk. But, the threshold is reduced if there is metal work.

64
Q

Septic Arthritis (aet/causative organism, PC, Ix, Mx)

A

Remember this is a JOINT infection
Aet: Abnormal joint (eg RA) or Immunosuppression & bacteraemia (eg diabetes, IVDU)
Bugs: Staph aureus(46%), Streptococci (22%)
Bug adheres to synovial membranes and proliferates in fluid.
• Px: Unwell febrile patient with red hot swollen joint (50%: knee, 90% monoarticular, unable to weightbear). Host inflammatory response damages joint.
• Dx: Blood culture before Abx, joint aspirate (>50,000cells/mm3), inflammatory markers. Imaging shows effusion
• Rx: IV antibiotics (cephalosporin or flucloxacillin) MRSA - Vanc. Drain joint.

65
Q

Osteomyelitis

A

Remember this is an infection of BONE or B/MARROW
• Ax: Local or haematogenous spread!! (doesn’t originate within the bone and this is a relatively isolated site) Brodie abscess (subacute) > frank osteomyelitis
• Bugs: Staphylococcus aureus
• Px: Pain, fever, local swelling
• Dx: MRI best imaging, bone biopsy for culture/histology
• Rx: Antibiotics treat most cases. Second-line = Debridement. Remove sequestra and infected bone

66
Q

Prosthetic Joint infection

A

• Ax: Local (wound infection);
Systemic bacteraemia (eg UTI)
• Bugs: Staphylococcus, Gram negatives eg Enterobacteriaceae
• Px: Pain, failure of joint, sinus, patient complains joint was ‘never right’
• Dx: Radiology – ‘loosening’, Joint aspirate – done with caution as risk of introducing
infection if joint is not infected.
• Rx: Remove metalwork and revise joint replacement: single or two stage revision. Use
Abx-impregnated cement.

67
Q

types of osteomyelitis

A

Acute
Chronic (brodie abscess, sinus tract, pain)
Vertebral (older population) -most likely lumbar region, MRI, back pain and fever, 1/3 have neuro impairment
Metaphyseal (kids)

68
Q

Septic arthritis bugs

A

Staph (recognises host factors such as fibronectin)
Strep pyogenes, agalactiae, pneumoniae), less commonly various gram -ve organisms e.g. E-Coli, Hib, nesssiera g, salmonella
Others: • Kingella kingae , Lyme, brucellosis,

69
Q

SSI Prevention

A

Pre op - Stop DMARDs 4 weeks before and taper off steroids and radiotherapy, ensure DM is well controlled, treat all remote infections, proph abx
During op - skin prep, normothermia

70
Q

Brucella granuloma Mx

A

Rifampicin, cirpofloxacin and doxy

71
Q

What is Brodie’s abscess

A

Brodie’s abscess is a rare form of osteomyelitis. It involves a subacute or chronic infection of the bone with development of a localized abscess, usually within the metaphysis of long bones. The tibia is the most common bone involved and staphylococcus aureus is the most common organism identified.

72
Q

What antibiotics breakdown beta lactamase? ESBL?

A
  1. Fluclox
  2. Cephalosporins
  3. Merpenems (ONLY ONE THAT DOES ESBL)
  4. Coamoxiclav / Piptazobactam
73
Q

What are the abx in spectrum of narrow to broad?

A

Ben pen
Flucloxacillin*
Amoxicillin
Co amoxiclav* (amoxi + the beta lactamase i clavulonic acid)
Piptaz/ tazocin (piperacillin + tazobactam)
Carbapenem

It’s impossible to put cephalosporins as a whole in there because each once is different and each generation has different breadths

74
Q

Categories of abx

A
  1. Protein Synthesis i
  2. DNA synthesis i
  3. Cell wall synthesis i
  4. Others
  5. MALT
  6. Fluoroquinoloes, Nitroimadazoles, Rifampicyin
  7. Beta lactams and glycopeptides
  8. Cell membrane toxins, Anti folates
75
Q

Protein Synthesis inhibitors

A

ALL of these inhibit the step when ribosomes come together and translate
GOOD FOR ATYPICALS

MALT
Macrolides - good for G+ve, atypicals
- Clari, Azithro, Erythro
- Clari - safe in pregnant

Aminoglycosides

  • Gentamicin - very negative - knackers you kidneys, deafness but also good for gram negatives e.g. pseudomonas
  • Not good for anaerobes

Linezolids
- Good for G+ve and MRSA/ other R strains

Tetracyclines- good atypical
-Doxcycline - atypical pneumonia, do’t give to pregnant women or children

76
Q

DNA synthesis inhibitors

A 
Fluoroquinoloines - good for g-ve, shit against anerobes 
Floxacins
Ciprofloxacin
Works against pseudomonas 
Not that good against anaerobes

Nitroimadzoles (2s)
1. Metro
2. Nitrofurantoin - not a nitro but similar
Only forms active inhibitory complex under anaerobic conditions -> used to treat gut and UTI

Rifamycins
Rifampicin (TB drug) (RNA synthesis)

77
Q

Cell wall synthesis inhibitors

A

Originally good for gram positive but the later generations are good at both!

  1. Beta lactams (cephalosporins and carbopenems)
  2. Glycopeptides
    • Ben pen - very narrow, group A strep for pharyngitis
    • Flucloaxcilin - can break down beta lactamase
    • Amoxicillin - relatively broad, good against some g+ (listeria) and G- but can be broken down by beta lactamase
    • Piperacillin - same as amoxicilin but can work for pseudomonas
    • Co- amoxiclav - Amoxi combined with clavulanic acid, now can’t be broken down by beta lactamase
    • Piptaz/tazocin - Piperacillin combied with tazobactam - can’t be broken down be beta lactamase
    • Carbapenems - can only be broken down by carbapenamses
78
Q

Glycopeptides

A
  1. Glycopeptides -> Vanco
    GOOD FOR G+VE that are resistant (never use for g-ve)
    NOT ORALLY ABSORBED exception is c dif colitis (needs to stay in gut)
79
Q

Antifolates

A

Antifolates (mostly UTIs)
Sulfonamide
Diaminopyrimidines - Trimethoprim used in UTI, PCP 2 classes of anti-folate e.g. co-trimoxazole (combo 1 from each class)

80
Q

Cell membrane toxins

A

Cell Membrane Toxins:
Daptomycin - G+ve
Colistin - G-ve e.g. acinetobacter
Very toxic, last resort

“HAIL MARYS”

81
Q

Psuedo monas tx

A

Fluoroquinolones - g-ve (puts pesudomonaz)
Gentamicn - g-ve
Ceftaz
Meropenem

82
Q

What is post primary TB?

A 
This is reactivation or exogenous re-infection
o	Happens > 5 years after initial infection 
o	5-10% lifetime risk 
Risk Factors for Reactivation
•	Immunosuppression
•	Chronic alcohol excess 
•	Malnutrition 
•	Ageing

Clinical Presentation can be Pulmonary or extra-pulmonary

Path (10 decks)

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