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Phase 3 > Week 7 > Flashcards

Week 7 Flashcards

1
Q

Describe campylobacter:

A
  • Curved G-ve bacilli
  • Large animal reservoir
  • Infection transmitted via contaminated food
  • Inflammation, ulceration and bleeding in small and large intestine
  • Bacteraemia can occur, and campylobacter can farley cause post-infection demyelination syndrome
  • Treatment: fluid replacement is sufficient in most cases, clarithromycin in severe disease
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2
Q

Describe salmonella:

A

Microbiology: G-ve bacilli
Epidemiology: found in animals, only S typhi and paratyphi do not have an animal reservoir
Pathogenesis: Acquired by contaminated food/water (less common), diarrhoea due to invasion of epithelial cells in the distal SI and subsequent inflammation
Treatment: fluid replacement, abs in severe infection

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3
Q

Describe Shigella:

A

Similar to salmonella
Pathogenesis: organisms attach to and colonise mucosal epithelium of terminal ileum and colon; no systemic invasion
Shigella dysenteriae produces protein exotoxin (Shiga toxin) causing haemolytic uraemia syndrome (HUS)
Treatment: fluid replacement

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4
Q

Describe cholera:

A

Microbiology: comma shaped G-ve bacilli
Pathogenesis: flagella and mucinase facilitate penetration of intestinal mucous, diarrhoea due to production of exotoxin
Treatment: oral or IV rehydration, tetracyclines may shorted duration of diarrhoea in severe disease

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5
Q

Describe staphylococcus aureus:

A

Microbiology: G+ve cocci
Pathogenesis: 50% of SA produce enterotoxins, bacteria multiply at room temperature and produce toxins. Infection via contaminated foods
CFs: Incubation 30mins-6hours, profuse vomiting and abdominal cramps
Tx: illness usually self-limiting so FRx
Control: hygienic food prep and refrigerated storage

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6
Q

Describe E. coli:

A

Microbiology: G+ve bacilli with six different diarrhogenic groups; though three main: EPEC, ETEC, EHEC

EPEC: adheres via pili, then formation of lesion mediated by intimin protein with disruption of microvilli. Incubation is 1-2 days and causes watery diarrhoea with a fever

ETEC: diarrhoea due to action of 1 or 2 plasmid-encoded toxins (heat labile and heat stable). Incubation period of 1-7 days, causes watery diarrhoea with fever

EHEC: attaching and effacing lesion (like EPEC), production of shiga-like toxins: EC,O157:H7. Causes bloody diarrhoea with no fever. and HUS in severe cases

Treatment is adequate rehydration. Abs not indicated and can worsen HUS, anti motility agents not indicated

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7
Q

Describe bacillus cereus:

A

Micro: aerobic, spore forming G+ve bacilli

Pathogenesis: spores and vegetative cells contaminate wide range of foodstuffs. 2 types of disease-

  • emetic (associated with fried rice, after boiling protein enterotoxin produced during sporulation) and,
  • diarrhoeal (spores in food survive cooking, germinate and organisms multiply in food

CFs:

  • Emetic disease; incubation 30mins-6hours, causes profuse vomiting with abdominal cramps and watery diarrhoea
  • Diarrhoeal disease; no vomiting. Neither have fever

Tx: self-limiting disease

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8
Q

Describe clostridium perfingens

A

Micro: anaerobic, spore-forming, G+ve bacilli

Pathogenesis: spores and vegetative cells in soil and animal gut, organisms contaminate food (often in bulk cooking of meat) and multiply and produce enterotoxin in large intestine

CFs:

  • Incubation 6-24 hours
  • 12-24 hour duration
  • watery diarrhoea and abdominal cramps, no fever and no vomiting

Tx: self-limiting disease, control by rapid chilling/freezing of bulk-cooked foods and thorough re-heating before consumption

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9
Q

Describe clostridium botulinum:

A

Micro: anaerobic, spore-forming G+ve bacilli

Pathogenesis:

  • uncommon in UK, spore and vegetative cells in soil and animal gut produce powerful heat-labile protein neurotoxinF
  • food-borne, infant and wound botulism
  • forms of entry for toxin with spreads via bloodstream to enter peripheral nerves where they cause neuromuscular blockade at the synapses

CFs:
- paralysis and progressive weakness, involvement of muscles of chest/diaphragm causes respiratory failure

Tx:

  • urgent intensive supportive care to address swallowing and breathing
  • treatment with antitoxin

Control: Hygienic food preparation, proper cooking

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10
Q

Describe clostridium difficile:

A

Micro: anaerobic, spore forming G+ve bacilli, spores resistant to heat, drying, disinfection and alcohol. CFs due to production of potent toxins

Pathogenesis:

  • spores and vegetative cells in environment
  • carried by 3-5% of the community, though up to 30% in hospital
  • infection requires disruption of the normal protective gut flora (commonly due to abx)

CFs:

  • mild to severe abdominal pain
  • severe cases may develop pseudomembranous colitis
  • fulminant cases may progress to colonic dilatation and perforation
  • relapses are common

Tx:

  • stop abx
  • oral metronidazole (if not severe), oral vancomycin (if severe or no improvement on metronidazole
  • recurrent disease may need fecal transplant

Control: Antimicrobial stewardship. Infection prevention and control methods. Cleansing/disinfection with hypochlorite disinfectants

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11
Q

Describe listeria monocytogenes:

A

Micro: G+ve coccobacilli

Pathogenesis:

  • widespread in environment
  • especially affects pregnant, elderly and immunocompromised
  • infection associated with contaminated foods, unpasteurised milk and soft cheese, pate, cooked meats, smoked fish and coleslaw
  • invasive infection from GIT results in systemic spread via bloodstream

CFs:

  • incubation 3 weeks
  • duration 1-2 weeks
  • initial flu-like illness with or without diarrhoea, majority of cases present with systemic infection (septicaemia, meningitis)

Tx: IV abx (usually ampicillin and gentamicin)

Control: Susceptible groups should avoid high risk foods

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12
Q

Describe h. pylori:

A

Micro: G-ve spiral shaped bacilli

Pathogenesis:

  • faecal-oral or oral-oral spread
  • humans only reservoir
  • acquired in childhood and lifelong unless treatedP
  • pathogenesis involves cytotoxin production and a range of factors to promote adhesion and colonisation

CFs: Infection is asymptomatic unless peptic ulceration develops, gastric cancer risk

Tx: combined treatment with PPI and combination of abx such as clarithro and metronidazole

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13
Q

What viruses cause GI disease and what age groups are most susceptible to them?

A
  • Norovirus and sapovirus (calciviridae family) can affect all ages and healthy individuals but often most serious in young and elderly
  • Rotavirus, adenovirus and astrovirus affects mainly children under 2 years, elderly and immunocompromised
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14
Q

Describe norovirus:

A

Transmission: person-peron, food-borne, water

  • Very small infectious dose and very stable, being able to remain viable in environment for a long time
  • 24-48 hour incubation period
  • Causes vomiting and diarrhoea
    • also nausea, abdominal cramps, headache and muscle aches, fever (rare) and dehydration in young and elderly
  • Treated with symptomatic therapy (rehydration)
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15
Q

Describe immunity to norovirus:

A

Immunity developed only lasts 6-14 weeks, may be link between blood group and norovirus infection

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16
Q

Describe rotavirus:

A
  • Double stranded, non enveloped RNA virus with 5 different strains
  • Antigenic variation due to 11 strands of RNA
  • 1st infection usually severe, but subsequent infections are less severe
  • Symptom; water diarrhoea, abdominal pain, vomiting, loss of electrolytes leading to dehydration
  • Spread same as norovirus, may be respiratory droplets too
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17
Q

Describe adenovirus:

A
  • Double stranded DNA virus
  • 50 serotypes but 40&41 cause gastroenteritis
  • Symptoms: fever and watery diarrhoea
  • Supportive treatment
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18
Q

Describe astrovirus:

A
  • Single stranded, non enveloped RNA virus
  • Causes less severe gastroenteritis than other enteric pathogens
  • Infection usually as sporadic cases but can be outbreaks usually in young children
19
Q

Describe septic arthritis:

A
  • Commonly causesd (G+ve) by staphyloccus aureus or streptococci (S pyogenes or pneumococcus) or (G-ve) e. coli, h. influenzae, n. menigitidis, n. gonorrhoeae
  • Presents with single hot joint, loss of movement and pain
  • Investigations: blood cultures, joint aspirate, FBVC, CRP, imaging
  • Treated with at least 2 weeks of IV abs, often 3 weeks IV and then 3 oral
20
Q

Describe prosthetic joint infection:

A
  • Common aetiology; staph A, CoNS, strep, G-ve bacilli
  • Prosthesis requires fewer bacteria to establish sepsis than soft tissue
  • Avascular surface allows survival of bacteria as they are protected from circulating immune defects and most abs
  • Cement can also inhibit phagocytosis and lymphocyte/complement function
  • Local or haematogenous spread
  • CFs; pain, effusion, warm joint, fever and systemic symptoms
21
Q

Describe treatment of PJIs:

A

Surgical repair options:

  1. DAIR (debride, abx, implant repair (before biofilm forms (acute infection)
  2. Take out infected joint (if infection occurs over 30 days since surgery)
22
Q

What are the typical and atypical causes of CAP?

A 
Typical: 
- streptococcus pneumoniae
- haemophilus influenzae
- mortadella catharralis
Atypical:
- mycoplasma pneumoniae
- legionella pneumoniae
- chlamoydophila pneumoniae/psittaci
23
Q

Describe haemophilius influenzae:

A
  • Often occurs in older people with underlying lung disease
  • Vaccination against type B (causes epiglottitis)
  • CFs: abrupt onset, characteristic of CAP:
    • cough fever, pleuritic chest pain
    • dull percussion, coarse crepitations, increased vocal resonance
  • Tx: amoxicillin, though risk of beta-lactamase so can also use co-amoxiclav
24
Q

Describe streptococcus pneumoniae:

A

RFs: smoking, alcohol, immunosuppression, influenza, airway disease

CFs: characteristic of pneumonia

  • cough, fever, pleuritic chest pain
  • dull percussion, fever, increased vocal resonance

Treatment: with penicillin, if allergic use macrolides (clarithromycin) or tetracycline (doxycycline)

25
Q

Describe atypical CAP:

A

Legionella:

  • found in water and soil, inhaled by humans=
  • diagnosed with history and urinary antigen test
  • CFs flu like illness, develop respiratory symptoms over time
  • Tx: macrolides, quinolones, tetracyclines (intracellular ABX)

Mycoplasma pneumoniae:

  • smallest free living bacterium, and lacks a cell wall so naturally resistant to beta-lactams
  • non specific presentation, spreads person-person,
  • CFs; flu-like illness, headache and fever
  • Systemic effects: haemolysis (cold agglutinins), Guillain-Barre syndrome, erythema multiform (rash), cardiac conduction problems and reactive arthritis
  • Diagnosis by PCR or serology
  • Treated with macrolides, tetracyclines and quinolones
26
Q

What respiratory syndromes are mainly caused by what viruses?

A

Common cold:

  • rhinovirus
  • coronavirus
  • also human metapneumovirus (HMPV), adenovirus, RSV, influenza

Pharyngitis:

  • adenovirus
  • also rhinovirus, parainfluenza, RSV

Croup:

  • parainfluenza virus
  • also HMPV, RSV

Acute bronchitis:

  • RSV
  • also HMPV, influenza and adenovirus

Bronchiolitis:

  • RSV
  • also HMPV, parainfluenza, rhinovirus, coronavirus, influenza, human bocavirus

Pneumonia:

  • Influenza
  • RSV
  • also parainfluenza, HMPV, adenovirus and rhinovirus
27
Q

Describe treatment of influenza:

A

Anti-viral agents affecting different parts of virus and viral replication:

  • neuraminidase inhibitors (prevent viral reproduction)
  • M2 inhibitors
  • ribavirin (also used to treat RSV)
28
Q

What are the common and uncommon complications of influenza?

A 
Common
- acute otitis media (children)
- sinusitis
- pneumonia
- exacerbation of underlying diseases
- dehydration (infants)
Uncommon
- encephalopathy
- reye syndrome (children)
- myositis
- myocarditis
- febrile seizures
29
Q

Describe the pathogenesis of disease caused by Neisseria gonorrhoeae:

A
  • G-ve intracellular diplococci
  • Causes urethral discharge, painful urination, inflammation of foreskin
  • Diagnosed with PCR from male urine sample or rectal or vulvovaginal swab
  • Diagnosis confirmed with NAAT with GC culture to show abs resistances
  • Treatment with ceftriaxone and azithromycin
30
Q

Describe the pathogenesis of disease caused by Chlamydia trachomatis:

A
  • G-ve cocci
  • Symptoms: can be asymptomatic, urethral discharge/pain with urination, pain during sex
  • If undiagnosed can lead to tubal damage/infertility
  • Treatment with doxycycline or azithromycin if allergic
31
Q

Describe the pathogenesis of disease caused by Treponema palllidum:

A
  • Multiplication of organism causes distinct stages of illness
    • after incubation period of 10-90 days, multiplication at site of entry produces erythema and chancre (lip and anal)
  • Secondary: highly infectious, but not always present, disseminates around body
  • Gumma (tertiary complication): granuloma/cancer-type lesion
  • Treatment: penicillin IM injection
32
Q

Describe the pathogenesis of disease caused by human papilloma virus:

A
  • Low risk strains of HPV cause genital warts (6+11)
  • Vaccine for strains 6,11,16+18 for school girls and MSM, though soon to be school boys
  • Increased number of partners increases risk of genital warts
  • Can be confused for molluscum contagiosum
  • Treatment for warts: aim for home treatment with condyline (topical cream) or aldara (immune modulator against HPV), can also use liquid nitrogen in clinic
33
Q

Describe the pathogenesis of disease caused by herpes simplex

A

Type 1 and 2 (indicates risk of recurrence)
Type 1 typically cold sores and type 2 is genital, though now 50/50
Treatment is acyclovir

34
Q

What are the routes of transmission of HIV?

A
  • anal or vaginal intercourse
  • injecting drugs + sharing equipment
  • mother to child transmission (before/during birth or through breast milk)
  • transmission in healthcare settings
  • transmission via donated blood/clotting factors
35
Q

Describe HIV lifecycle:

A
  1. Attachement to CD4 receptors on CD4+ T cells
  2. Fusion on HIV envelope with the T cell membrane
  3. Reverse transcription of HIV RNA to HIV DNA by reverse transcriptase
  4. Integration of viral DNA into cellular DNA by enzyme integrase
  5. Replication of HIV using machinery of CD4 T cell
  6. Assembly of the newly created HIV proteins and HIV RNA near the surface of the cell
  7. Budding newly formed HIV pushes itself out of CD4 T cell and releases protease to break up long protein chains that form immature virus
36
Q

What are HIV latency and resistance?

A

Latency:

  • a state of reversibly non-productive infection of individual cell
  • used to describe the long asymptomatic period between initial infection and advanced AIDs in HIV

Resistance:

  • HIV can mutate while under treatment to become resistant to HIV treatment
  • Can develop or be infected with resistant strains of HIV
  • Drug resistance testing is possible
  • Chances of resistance developing much lower with adherence to medication
37
Q

What are the clinical manifestations of HIV?

A

Acute (2-6 weeks after infection):

  • fever
  • pharyngitis
  • rash
  • lymphadenopathy
  • myalgia
  • headache/neuropathy

AIDs defining illnesses (late stage, opportunistic infections)

  • cancer (Karposi’s sarcoma, cervical cancer, lymphoma)
  • TB (mycoplasma)
  • pneumonia (recurrent)
  • fungal infections (PCP)
38
Q

Describe HIV therapy:

A
  • Highly active ARV treatment
  • Uses 2 nucleoside/nucleotide reverse transcriptase inhibitors and 1 other drug from another class
  • Aim to suppress viral load to undetectable
  • SEs: rash, hypersensitivity, CNS, GI, renal, hepatic
  • Long term causes lipoatrophy or lipodystrophy and renal, hepatic and bone changes
  • Interacts with other drugs, mediated by CYP450: PPIs, statins, antipsychotics
39
Q

How does the immune system develop through childhood?

A

Immune system functionally immunodeficient at birth, move from sterile envoment to pathogenic

Balance of Th1 and Th2 cytokines- initial prevalence of Th2 moving to Th1 late in gestation

Increased susceptibility to pathogens and reduced response to vaccines in neonates

Transfer of protection from mum to baby: IgG transfer predom in 3rd trimester and by B feeding

Acquire resistances from having disease or vaccination and developing antibody mediated immunity

40
Q

What pathogens affects children at what stages?

A

Lower Respiratory Tract Infections:

  • Neonates
    • Group B strep, E coli, resp viruses, enteroviruses
  • Young infants
    • respiratory viruses, enteroviruses, chylamydia
  • Infants and young children
    • strep pneumonia, resp viruses
  • Older children
    • mycoplasma pneumonia, strep pneumonia, resp viruses

Meningitis:

  • Neonates
    • group B strep, E coli, HiB, meningococcus, strep pneumonia, listeria
  • 1-3 months
    • meningococcus, strep pneumonia, HiB, listeria
  • 3 months-5 years
    • meningococcus, strep pneumonia, HiB (rare)
  • > 6 years
    • meningococcus, strep pneumonia
41
Q

Describe the microbiology of mycobacterium tuberculosis:

A

Acid fast bacilli

Covered in mycolic acid so impossible to gram stain, therefore Ziehl-Neelsen stain or fluorescent stains such as auramine (not as specific) staining used to identify MTB

MTB takes a long time to grow

Aerobic and requires high levels of oxygen

Diagnosed with tuberculin (Mantoux) skin test (for latent TB), acid-fast stain, culture and PCR

42
Q

Describe the treatment of MTB:

A

Long duration of treatment

Combination of drugs to reduce resistance

Rifampicin, isoniazid, ethambutol (covers resistance), pyrazinamide (effective against quick growing strains)
6-month treatment on rifampicin and isoniazid (most effective against slow growing), other two for 2 months

Rifampicin is CYP450 inducer, alters hepatic metabolism of drugs

SE of all TB drugs can cause hepatitis
Isoniazid can cause encephalopathy

43
Q

Describe the pathogenesis of MTB:

A

Pathogenesis: enters lungs, spread by air droplets from infected, and is phagocytosed by macrophage which cannot lyse MTB.

MTB grows within granuloma: hallmark of TB

  • many macrophages come to site of TB
  • centre becomes necrosed causing a site where MTB can multiply
  • area liquifies in reactivation

Only 5-10% of infected will develop TB. Most disease comes from reactivation of TB, in HIV, smoking or immunosuppression

Phase 3 (14 decks)

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