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MRCP part 1 > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

what antibiotics have anti-anaerobic activity?

A
  • Penicillins
  • Cephalosporins (except ceftazidime)
  • Erythromycin
  • Metronidazole
  • Tetracycline
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2
Q

which 3 antibiotics have no anti-anaerobic activity?

A
  • Gentamicin
  • Ciprofloxacin
  • Ceftazidime
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3
Q

what is the incubation period of:

  • Scarlet fever
  • Influenza
  • Diphtheria
  • Meningococcus
A

1 week

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4
Q 
what is the incubation period of:
• Malaria
• Measles
• Dengue fever
• T yphoid
A

1-2 weeks

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5
Q

what is the incubation period of:
• Mumps
• Rubella
• Chickenpox

A

2-3 weeks

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6
Q 
what is the incubation period of:
• Infectious mononucleosis
• Cytomegalovirus
• Viral hepatitis
• HIV
A

more than 3 weeks

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7
Q 
what type of vaccines are:
• BCG
• measles, mumps, rubella (MMR)
• oral polio
• oral typhoid
• yellow fever
-why is it important to note this?
A

live attenuated

-may pose a risk to immunocompromised patient

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8
Q

what type of vaccines are:
• rabies
• influenza

A

whole killed organism/inactivated

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9
Q

what type of vaccine is tetanus?

A

• tetanus: Detoxified exotoxins

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10
Q 
what type of vaccine are:
• diphtheria
• pertussis ('acellular' vaccine)
• heptitis B
• meningococcus, pneumococcus, hemophilus
A

Fragment/Extracts of the organism or virus (may also be produced using recombinant DNA technology)

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11
Q

what different types of influenza vaccine exist?

A

different types are available, including whole inactivated virus, split virion (virus particles disrupted by detergent treatment) and sub-unit (mainly hemagglutinin and neuraminidase)

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12
Q

what does the vaccine for cholera contain?

A

contains inactivated Inaba and Ogawa strains of Vibrio cholerae together with recombinant B-subunit of the cholera toxin

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13
Q

what does the vaccine for hepatitis B contain?

A

hepatitis B: contains HBsAg adsorbed onto aluminium hydroxide adjuvant and is prepared from yeast cells using recombinant DNA technology

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14
Q

what may be used in hep A post-exposure prophylaxis?

A

• Human Normal Immunoglobulin (HNIG) or hepatitis A vaccine may be used depending on the clinical situation

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15
Q

what is done for hepatitis B post-exposure prophylaxis?

  • if a person is a known responder to HBV vaccine
  • if a person is a non-responder
A
  • HBsAg positive source: if the person exposed is a known responder to HBV vaccine then a booster dose should be given. If they are in the process of being vaccinated or are a non- responder they need to have hepatitis B immune globulin (HBIG) and the vaccine
  • Unknown source: for known responders the green book advises considering a booster dose of HBV vaccine. For known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated you have an accelerated course of HBV vaccine
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16
Q

what to do for post-exposure prophaxis for hepatitis C?

A

• Monthly PCR - if seroconversion then interferon +/- ribavirin

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17
Q

what to do for post-exposure prophylaxis for HIV?

A
  • A combination of oral antiretrovirals (e.g. Tenofovir, emtricitabine, lopinavir and ritonavir) as soon as possible (i.e. Within 1-2 hours, but may be started up to 72 hours following exposure) for 4 weeks
  • Serological testing at 12 weeks following completion of post-exposure prophylaxis
  • ↓ risk of transmission by 80%
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18
Q

what to do for post-exposure prophylaxis for varicella zoster?

A

Varicella zoster

• VZIG for IgG negative pregnant women/immunosuppressed

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19
Q

when is tetanus vaccine given routinely?

A 
Tetanus vaccine is currently given in the UK as part of the routine immunisation schedule at:
• 2 months
• 3 months
• 4 months
• 3-5 years
• 13-18 years
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20
Q

describe what a ‘clean wound’ is?

A

Wounds less than 6 hours old, non-penetrating with negligible tissue damage

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21
Q

describe what a tetanus prone wound is?

A 
puncture-type injuries acquired in a contaminated environment e.g. gardening injuries
    wounds containing foreign bodies
    compound fractures
    wounds or burns with systemic sepsis
    certain animal bites and scratches
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22
Q

describe what a high-risk tetanus prone wound is?

A

heavy contamination with material likely to contain tetanus spores e.g. soil, manure
wounds or burns that show extensive devitalised tissue
wounds or burns that require surgical intervention

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23
Q

what should be done for a patient with a clean/tetanus prone/high risk tetanus prone wound who has had full course of tetanus vaccines <10 years ago?

A

Patient has had a full course of tetanus vaccines, with the last dose < 10 years ago

no vaccine nor tetanus immunoglobulin is required, regardless of the wound severity
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24
Q

what should be done for a patient with a
-tetanus prone wound
-high-risk wound
who have had a full course of tetanus vaccine with the last dose >10 years ago?

A

Patient has had a full course of tetanus vaccines, with the last dose > 10 years ago

if tetanus prone wound: reinforcing dose of vaccine
high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue): reinforcing dose of vaccine + tetanus immunoglobulin
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25
Q

what to do with patients if vaccination history is incomplete or unknown and:

  • clean wound
  • tetanus prone wound
  • high risk wound
A

If vaccination history is incomplete or unknown

reinforcing dose of vaccine, regardless of the wound severity
for tetanus prone and high-risk wounds: reinforcing dose of vaccine + tetanus immunoglobulin
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26
Q

what are the features of tetanus?

A
  • Prodrome fever, lethargy, headache
  • Trismus (lockjaw)
  • Risus sardonicus
  • Opisthotonus (arched back, hyperextended neck)
  • Spasms (e.g. Dysphagia)
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27
Q

what is used in the management of tetanus?

A

• Supportive therapy including ventilatory support and muscle relaxants
• Intramuscular human tetanus immunoglobulin for high-risk wounds (e.g. Compound fractures,
delayed surgical intervention, significant degree of devitalised tissue)
• Metronidazole is now preferred to benzylpenicillin as the antibiotic of choice

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28
Q

HIV seroconversion:

  • how many people is this symptomatic in?
  • how does this present?
  • when does this occur?
  • what conveys poorer long term prognosis?
A

HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever type illness. ↑ symptomatic severity is associated with poorer long term prognosis. It typically occurs
3-12 weeks after infection

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29
Q

Man returns from trip abroad with maculopapular rash and flu-like illness - think ?

A

Man returns from trip abroad with maculopapular rash and flu-like illness - think HIV seroconversion

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30
Q

what are the features of HIV seroconversion?

A
  • Sore throat
  • Lymphadenopathy
  • Malaise, myalgia, arthralgia
  • Diarrhoea
  • Maculopapular rash
  • Mouth ulcers
  • Rarely meningoencephalitis
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31
Q

what is the diagnosis of HIV?

A

• Antibodies to HIV may not be present
• HIV PCR and p24 antigen tests can confirm
diagnosis

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32
Q

what immunological changes are seen in progressive HIV?

A
  • Reduction in CD4 count
  • Increase B2-Microglobulin (IBM)
  • Decrease IL-2 production (DIL=DELL)
  • Polyclonal B-cell activation
  • ↓ NK cell function
  • ↓ delayed hypersensitivity responses
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33
Q

what vaccines can only be used in HIV patients who’s CD4 count is >200?

A

Measles, Mumps, Rubella (MMR) ● V aricella●

Yellow Fever●

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34
Q

what vaccines are contraindicated in HIV patients?

A

Cholera* CVD103-HgR● Influenza-intranasal● Poliomyelitis-oral (OPV) ● Tuberculosis (BCG) ●

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35
Q

what type of virus in HIV and what are the 2 variants?

A

HIV is a RNA retrovirus of the lentivirus genus (lentiviruses are characterized by a long incubation period)
two variants - HIV-1 and HIV-2
HIV-2 is more common in west Africa, has a lower transmission rate and is thought to be less pathogenic with a slower progression to AIDS

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36
Q

describe the basic structure of HIV

A

Basics structure

spherical in shape with two copies of single-stranded RNA enclosed by a capsid of the viral protein p24
a matrix composed of viral protein p17 surrounds the capsid
envelope proteins: gp120 and gp41
pol gene encodes for viral enzymes reverse transcriptase, integrase and HIV protease
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37
Q

how does this HIV virus enter cells?

A

Cell entry
HIV can infect CD4 T cells, macrophages and dendritic cells
gp120 binds to CD4 and CXCR4 on T cells and CD4 and CCR5 on macrophages
mutations in CCR5 can give immunity to HIV

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38
Q

describe how HIV replicates in cells?

A

Replication
after entering a cell the enzyme reverse transcriptase creates dsDNA from the RNA for integration into the host cell’s genome

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39
Q

what are the most common causes of diarrhoea in HIV?

A

Diarrhea is common in patients with HIV. This may be due to the effects of the virus itself (HIV enteritis) or opportunistic infections
Possible causes
• Cryptosporidium + other protozoa (most
common)
• Cytomegalovirus
• Mycobacterium avium intracellulare • Giardia

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40
Q

what is the most common cause of diarrhoea in HIV patients?

-what is the incubation period?

A

Cryptosporidium is the most common infective cause of diarrhoea in HIV patients. It is an intracellular protozoon and has an incubation period of 7 days.

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41
Q

describe the presentation and staining used for cryptosporidium in HIV?

A

Presentation is very variable, ranging from mild to severe diarrhoea. A modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium.

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42
Q

what is the management for cryptosporidium diarrhoea in HIV patients?

A

Treatment is difficult, with the mainstay of management being supportive therapy. (nitazoxanide is licensed in the US for immunocompetent patients)

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43
Q

what mycobacterium is seen in HIV patients with a CD4 count below 50?

A

Mycobacterium avium intracellulare is an atypical mycobacteria seen with the CD4 count is below 50.

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44
Q

what are the features of mycobacterium avium intracellulare in HIV patients?

A

Typical features include fever, sweats, abdominal pain and diarrhoea. There may be hepatomegaly and deranged LFTs.

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45
Q

what is the diagnosis and management of mycobacterium avium intracellulare in HIV patients?

A

Diagnosis is made by blood cultures and bone marrow examination.
Management is with rifampicin, ethambutol and clarithromycin

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46
Q

what factores can decrease vertical transmission of HIV?

A 
Factors which ↓ vertical transmission (from 25-30% to 2%)
• Maternal antiretroviral therapy
• Mode of delivery (caesarean section)
• Neonatal antiretroviral therapy
• Infant feeding (bottle feeding)
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47
Q

which pregnant women should be screened for HIV?

A

Screening

• NICE guidelines recommend offering HIV screening to all pregnant women

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48
Q

Pregnant patients with HIV:

  • who should be offered antiretroviral therapy?
  • when should antiretroviral therapy be offered if women are not currently taking it and are pregnant?
A

Antiretroviral therapy
• All pregnant women should be offered antiretroviral therapy regardless of whether they were
taking it previously
• If women are not currently taking antiretroviral therapy it is usually commenced between 28
and 32 weeks of gestation and should be continued intrapartum

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49
Q

what mode of delivery is preferable in HIV positive pregnant ladies?

A

Mode of delivery
• Elective caesarean section
• A zidovudine infusion should be started four hours before beginning the caesarean section

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50
Q

what is usually administered orally to the neonate of a HIV positive mother? how long should this be used for?

A

Neonatal antiretroviral therapy

• Zidovudine is usually administered orally to the neonate for four to six weeks

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51
Q

what is kaposi’s sarcoma caused by?

A

• Caused by HHV-8 (Human Herpes Virus 8)

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52
Q

how can kaposi’s sarcoma present?

A

• Presents as purple papules or plaques on the skin or mucosa (e.g. Gastrointestinal and
respiratory tract)
• Skin lesions may later ulcerate
• Respiratory involvement may cause massive
hemoptysis and pleural effusion

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53
Q

what is the treatment for kaposi sarcoma?

A

• Radiotherapy + resection

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54
Q

Pneumocystis carinii pneumonia - who is this common in? and who should recieve prophylaxis?
(whilst the organism Pneumocystis carinii is now referred to as Pneumocystis jiroveci, the term Pneumocystis carinii pneumonia (PCP) is still in common use)

A
  • Pneumocystis jiroveci is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
  • PCP is the most common opportunistic infection in AIDS
  • All patients with a CD4 count < 200/mm3 should receive PCP prophylaxis
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55
Q

what are the features of PCP pneumonia?

A
  • Dyspnea
  • Dry cough
  • Fever
  • Very few chest sign
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56
Q

what rare Extrapulmonary manifestations for PCP pneumonia exist?

A
  • Hepatosplenomegaly
  • Lymphadenopathy
  • Choroid lesions
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57
Q

what is seen on CXR in PCP pnuemonia?

A

• CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray
findings e.g. lobar consolidation. May be normal

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58
Q

what is a clinical feature of PCP pneumonia?

A

• Exercise-induced desaturation

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59
Q

what investigation can be done for PCP pneumonia?

A

• Sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate
PCP (silver stain)

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60
Q

what is the most common cause of biliary disease in patients with HIV?

A

The most common cause of biliary disease in patients with HIV is sclerosing cholangitis due to
infections such as CMV, Cryptosporidium and Microsporidia

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61
Q

what may pancreatitis in the context of HIV infection be secondary to?

A

Pancreatitis in the context of HIV infection may be secondary to anti-retroviral treatment
(especially didanosine) or by opportunistic infections e.g. CMV

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62
Q 
Describe the CSF findings in bacterial meningitis?
Appearance
Glucose
Protein
White cells
A

Appearance- cloudy
Glucose - low (<1/2 plasma)
Protein - high (>1g/l)
White cells - 10-5000 polymorphs

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63
Q 
Describe the CSF findings in viral meningitis?
Appearance
Glucose
Protein
White cells
A

Appearance - clear/cloudy
Glucose - normal
Protein - normal/raised
White cells - 15-1000 lymphocytes

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64
Q 
Describe the CSF findings in TB meningitis?
Appearance
Glucose
Protein
White cells
A

Appearance - fibrin web
Glucose - low (<1/2 plasma)
Protein - high (>1g/l)
White cells - 10-1000 lymphocytes

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65
Q

what is used in the detection of TB meningitis?

A

The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)

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66
Q

what is the management for meningitis:

Initial empirical therapy aged < 3 months or >50

A

Intravenous cefotaxime + amoxicillin

Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae.

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67
Q

what is the management for meningitis:

Initial empirical therapy aged 3 months - 50 years

A

Intravenous cefotaxime if adult, IV ceftriaxone if child

Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae.

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68
Q

what is the treatment for menigococcal meningitis?

A

Intravenous benzylpenicillin or cefotaxime

Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae.

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69
Q

what is the treatment for penumococcal meningitis or meningitis caused by haemophilus influenzae?

A

Intravenous cefotaxime

Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae.

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70
Q

what is the treatment for meningitis caued by listeria?

A

Intravenous amoxicillin + gentamicin

Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae.

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71
Q

what is used for a patient with meningitis with a history of immediate hypersensitivity to penicillin or to cephalosporin?

A

If the patient has a history of immediate hypersensitivity reaction to penicillin or to cephalosporins the BNF recommends using chloramphenicol.

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72
Q

who should be offered antibiotic prophylaxis for meningitis?

-what is the high risk period?

A

prophylaxis needs to be offered to household and close contacts of patients affected with meningococcal meningitis.
Prophylaxis should also be offered to people who been exposed to respiratory secretion, regardless of the closeness of contact people who have been exposed to a patient with confirmed bacterial meningitis should be given prophylactic antibiotics if they have close contact within the 7 days before onset
the risk is highest in the first 7 days but persists for at least 4 weeks

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73
Q

what is used for meningitis prophylaxis?

A

oral ciprofloxacin or rifampicin or may be used. The Health Protection Agency (HPA) guidelines now state that whilst either may be used ciprofloxacin is the drug of choice as it is widely available and only requires one dose

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74
Q

when should meningococcal vaccination be given to close contacts? what about of pneumococcal meningitis?

A

meningococcal vaccination should be offered to close contacts when serotype results are available, including booster doses to those who had the vaccine in infancy
for pneumococcal meningitis, no prophylaxis is generally needed. There are however exceptions to this. If a cluster of cases of pneumococcal meningitis occur the HPA have a protocol for offering close contacts antibiotic prophylaxis.

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75
Q

what are the investigations for meningococcal septicaemia?

A
  • Blood cultures
  • Blood PCR, if antibiotic was already started.
  • Lumbar puncture is usually contraindicated
  • Full blood count and clotting to assess for disseminated intravascular coagulation
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76
Q

what may streptococci be subdivided into?

A

may be divided into α haemolytic and β hemolytic types

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77
Q

give two α hemolytic Streptococci?

A

The most important α hemolytic Streptococcus is Streptococcus pneumoniae (pneumococcus). Pneumococcus is a common cause of pneumonia, meningitis and otitis media. Another clinical example is Streptococcus viridans

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78
Q

how can you subdivide β hemolytic streptococci?

A

Group A and Group B

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79
Q

Group A strep:

  • most important organism
  • what can this cause?
  • what is the antibiotic of choice?
A
  • Most important organism is Streptococcus pyogenes
  • Responsible for erysipelas, impetigo, cellulitis, type 2 necrotizing fasciitis & pharyngitis/tonsillitis • Immunological reactions can cause rheumatic fever or post-streptococcal glomerulonephritis
  • Erythrogenic toxins cause scarlet fever
  • Penicillin is the antibiotic of choice for group A streptococcal infections
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80
Q

Group B strep:

-what organism is under this and what does it cause?

A

• Streptococcus agalactiae may lead to neonatal meningitis and septicemia

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81
Q

what are the most common causes of cellulitis?

A

Streptococcus pyogenes or Staphylcoccus aureus.

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82
Q

what classification is used for cellulitis and describe each class?

A

Eron classification

Class Features
I There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities
II The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
III The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize
IV The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis

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83
Q

what is the criteria for admission for cellulitis?

A

Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.

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84
Q

how is eron class II cellulitis managed?

A

Admission may not be necessary if the facilities and expertise are available in the community to give intravenous antibiotics and monitor the person - check local guidelines.

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85
Q

what is the management of cellulitis:

  • first line
  • if penicillin allergic
  • if pregnant
  • if severe
A

The BNF recommends flucloxacillin as first-line treatment for mild/moderate cellulitis. Clarithromycin, erythromycin (in pregnancy) or doxycyline is recommended in patients allergic to penicillin.
NICE recommend that patients severe cellulitis should be offered co-amoxiclav, cefuroxime, clindamycin or ceftriaxone.

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86
Q

what is the diagnostic criteria for staphylococcal toxic shock syndrome?

A

Centers for Disease Control and Prevention diagnostic criteria
• Fever: temperature > 38.9oc
• Hypotension: systolic blood pressure < 90 mmHg
• Diffuse erythematous rash
• Desquamation of rash, especially of the palms and soles
• Involvement of three or more organ systems: e.g. Gastrointestinal (diarrhoea and vomiting),
mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. Confusion)

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87
Q

what is type 1 and type 2 necrotising fasciitis?

A

It can be classified according to the causative organism:
• Type 1 is caused by mixed anaerobes and aerobes (often
occurs post-surgery in diabetics)
• Type 2 is caused by Streptococcus pyogenes

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88
Q

what are the features of nec fasciitis?

A

Features
• Acute onset
• Painful, erythematous lesion develops (cellulitis like)
• Extremely tender over infected tissue

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89
Q

what is the management for necrotising fasciitis?

A

Management
• Urgent surgical debridement
• IV antibiotics

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90
Q

what type of bacteria is listeria monocytogenes?

  • how is this usually spread?
  • what is the complication in pregnancy?
A

Listeria monocytogenes is a Gram positive bacillus which has the unusual ability to multiply at low temperatures. It is typically spread via contaminated food, typically unpasteurised dairy products. Infection is particularly dangerous to the unborn child where it can lead to miscarriage

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91
Q

how can listeria monocytogenes present?

A

Features - can present in a variety of ways
• Diarrhoea, flu-like illness
• Pneumonia , meningoencephalitis
• Ataxia and seizures

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92
Q

how should suspected listeria infection be investigated?

A

Suspected Listeria infection should be investigated by taking blood cultures. CSF may reveal a
pleocytosis, with ‘tumbling motility’ on wet mounts

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93
Q

what is the management of listeria?

A

Management
• Listeria is sensitive to amoxicillin/ampicillin (cephalosporins usually inadequate)
• Listeria meningitis should be treated with IV amoxicillin/ampicillin and gentamicin

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94
Q

what is anthrax?

  • what type of organism is this?
  • how is this spread?
A

Anthrax is caused by Bacillus anthracis, a Gram positive rod. It is spread by infected carcasses

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95
Q

what are the features of anthrax?

A

Features
• Causes painless black eschar (cutaneous ‘malignant pustule’, but no pus)
• Typically painless and non-tender
• May cause marked edema
• Anthrax can cause gastrointestinal bleeding

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96
Q

what is the management of anthrax?

A

Management
• The current Health Protection Agency advice for the initial management of cutaneous anthrax is ciprofloxacin
• Further treatment is based on microbiological investigations and expert advice

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97
Q

who should be screened for MRSA?

A

• All patients awaiting elective admissions (exceptions include day patients having terminations
of pregnancy and ophthalmic surgery. Patients admitted to mental health trusts are also
excluded)
• From 2011 all emergency admissions will be screened

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98
Q

how is a patient screened for MRSA?

A
  • Nasal swab and skin lesions or wounds
  • The swab should be wiped around the inside rim of a patient’s nose for 5 seconds
  • The microbiology form must be labelled ‘MRSA screen’
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99
Q

what can be used to suppress MRSA in a carrier once identified?

A

• Nose: mupirocin 2% in white soft paraffin, TDS for 5 days
• Skin: chlorhexidine gluconate, OD for 5 days. Apply all over but particularly to the axilla, groin
and perineum

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100
Q

what antibiotics can be used for MRSA infections?

A

The following antibiotics are commonly used in the treatment of MRSA infections:
• Vancomycin
• Teicoplanin

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101
Q

Legionnaire’s disease:

  • what is this caused by?
  • how is this spread?
A

Legionnaire’s disease is caused by the intracellular bacterium Legionella pneumophilia. It is typically colonizes water tanks and hence questions may hint at air-conditioning systems or foreign holidays. Person-to-person transmission is not seen

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102
Q

what are the features of legionnaires disease?

A
  • Flu-like symptoms
  • Dry cough
  • Lymphopenia
  • Hyponatremia
  • Deranged LFTs
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103
Q

what is the diagnosis of legionnaires?

A

Urinary antigen

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104
Q

what is the treatment of legionnaires?

A

• Treat with erythromycin

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105
Q

Leptospirosis is AKA? what demographic of people are affected?

A

leptospirosis is commonly seen in questions referring to sewage workers, farmers, vets or people who work in abattoir.
The term Weil’s disease referrs for the most severe 10% of cases of leptospirosis associated with jaundice

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106
Q

what is leptospirosis caused by? how is this transmitted?

A

It is caused by the spirochaete Leptospira interrogans (serogroup L icterohemorrhagiae), classically being spread by contact with infected rat urine.

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107
Q

when should weil’s disease be considered?

A

Weil’s disease should always be considered in high-risk patients with hepatorenal failure.

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108
Q

what are the features of leptospirosis?

A
  • Fever
  • Flu-like symptoms → WITHOU PRODUCTIVE COUGH
  • Renal failure (seen in 50% of patients)
  • Jaundice
  • Subconjunctival hemorrhage
  • Headache, may herald the onset of meningitis
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109
Q

what is the management of leptospirosis?

A
  • A lumbar puncture should ideally be done first to confirm meningeal involvement, if there are meningeal symptoms.
  • High-dose benzylpenicillin or doxycycline
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110
Q

what is acute epiglottitis caused by?

-who does this occur in?

A

Acute epiglottitis is rare but serious infection caused by Hemophilus influenzae type B. Prompt recognition and treatment is essential as airway obstruction may develop. Epiglottitis generally occurs in children between the ages of 2 and 6 years. The incidence of epiglottitis has ↓ since the introduction of the Hib vaccine

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111
Q

what are the features of acute epiglottitis?

A 
Features
• Rapid onset
• Unwell, toxic child
• Stridor
• Drooling of saliva
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112
Q

what is lyme disease caused by?

A

Lyme Disease: or borreliosis is an emerging infectious disease caused by at least three species of bacteria belonging to the genus Borrelia. Borrelia burgdorferi sensu stricto is the main cause of Lyme disease in the United States, whereas Borrelia afzelii and Borrelia garinii cause most European cases.

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113
Q

describe the early features of lyme disease

A

Early features
• Erythema chronicum migrans (small papule often at site of the tick bite which develops into a larger annular lesion with central clearing, occurs in 70% of patients)
• Systemic symptoms: malaise, fever, arthralgia

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114
Q

what are the later features of lyme disease?

A

Later features
• CVS: heart block, myocarditis
• Neurological: cranial nerve palsies, meningitis
• Polyarthritis

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115
Q

what is used to screen for latent TB?

A

The Mantoux test is the main technique used to screen for latent tuberculosis. In recent years the interferon-gamma blood test has also been introduced. It is used in a number of specific situations such as:

the Mantoux test is positive or equivocal
people where a tuberculin test may be falsely negative (see below)
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116
Q

Describe the mantoux test

A

Mantoux test: 0.1 ml of 1:1,000 purified protein derivative (PPD) injected intradermally result read 2-3 days later
Result is diameter of induration:

< 6mm Negative - no significant hypersensitivity to tuberculin protein Previously unvaccinated individuals may be given the BCG

6 - 15mm Positive - hypersensitive to tuberculin protein Should not be given BCG. May be due to previous TB infection or BCG

> 15mm Strongly positive - strongly hypersensitive to tuberculin protein Suggests tuberculosis infection.

117
Q

what may cause false negative mantoux tests?

A

False negative tests may be caused by:

    miliary TB
    sarcoidosis
    HIV
    lymphoma
    very young age (e.g. < 6 months)
118
Q

what investigations are used to diagnose TB?

A

Chest x-ray: upper lobe cavitation is the classical finding of reactivated TB, bilateral hilar lymphadenopathy

Sputum smear: 3 specimens are needed, rapid and inexpensive test, stained for the presence of acid-fast bacilli (Ziehl-Neelsen stain), all mycobacteria will stain positive (i.e. nontuberculous mycobacteria)

  • the sensitivity is between 50-80%
  • this is decreased in individuals with HIV to around 20-30%

Sputum culture: the gold standard investigation

  • more sensitive than a sputum smear and nucleic acid amplification tests
  • can assess drug sensitivities
  • can take 1-3 weeks (if using liquid media, longer if solid media)

Nucleic acid amplification tests (NAAT)

  • allows rapid diagnosis (within 24-48 hours)
  • more sensitive than smear but less sensitive than culture
119
Q

what is the management for treating active TB?

A

RIPE:2 months then lose PE for next 4 months
• Rifampicin
• Isoniazid
• Pyrazinamide
• Ethambutol (in 2006 NICE recommend giving a ‘fourth drug’ such as ethambutol routinely -
previously this was only added if drug-resistant tuberculosis was suspected)

120
Q

what is used to treat latent TB?

A

isoniazid alone for 6 months

121
Q

how long is the management for TB meningitis and what is used in addition to abx?

A

prolonged period (at least 12 months) with the addition of steroids

122
Q

which patients are given directly observed therapy for TB (3 per week dosing regimen)

A
  • Homeless people with active tuberculosis
  • Patients who are likely to have poor concordance
  • All prisoners with active or latent tuberculosis
123
Q

what is used for resistant TB?

A

Streptomycin: (aminogycoside) used in resistant TB

124
Q

what are the side effects of rifampicin?

A
  • Potent liver enzyme inducer
  • Hepatitis
  • Orange secretions
  • Flu-like symptoms
125
Q

what are the side effects of isoniazid?

A
  • Peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
  • May also cause optic neuritis but it is not as common a cause as ethambutol.
  • Hepatitis, agranulocytosis
  • Liver enzyme inhibitor
126
Q

what are the side effects of Pyrazinamide?

A
  • Hyperuricemia causing gout

* Hepatitis

127
Q

what are the side effects of ethambutol?

A
  • Optic neuritis: check visual acuity before and during treatment
  • Dose needs adjusting in patients with renal impairment
128
Q

what are the side effect of streptomycin?

A
  • Vestibular damage → Vertigo and Vomiting
  • Cochlear damage → deafness
    • Angioedema or angioneuritic edema
  • Nephrotoxicosis
129
Q

what is leprosy caused by?

A

Leprosy: Hansen’s disease (HD) is a chronic disease caused by Mycobacterium leprae and Mycobacterium lepromatosis.

130
Q

what are the features of leprosy?

A

Features:
• Nodular skin lesions
• Erythremaous raised plaque like lesions in arms and legs

Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs, and eyes.

131
Q

what is the management of leprosy?

A

Management:
• Skin biopsy and needle test in cold area (ear lobuleand elbow)
• Pauci-bacillary leprosy (<5 lesions) Treat with rifampicin and dapsone for 6 months
• Multi-bacillary leprosy (>5 lesions) → rifampicin, clofazimine and dapsone for 12 months

132
Q

what are the features of severe malaria?

A
  • Schizonts on a blood film
  • Parasitemia > 2%
  • Hypoglycemia
  • Temperature > 39 °c
  • Severe anemia
  • Complications
133
Q

what are the complications of malaria?

A

• Cerebral malaria: seizures, coma
• ARF: blackwater fever, secondary to intravascular
hemolysis, mechanism unknown
• Acute respiratory distress syndrome (ARDS)
• Hypoglycemia
• Disseminated intravascular coagulation (DIC)

134
Q

what is the treatment of uncomplicated falciparum malaria?

A

strains resistant to chloroquine are prevalent in certain areas of Asia and Africa
the 2010 WHO guidelines recommend artemisinin-based combination therapies (ACTs) as first-line therapy
examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine, artesunate plus sulfadoxine-pyrimethamine, dihydroartemisinin plus piperaquine

135
Q

what is the treatment for severe falciparum malaria?

A

Severe falciparum malaria

a parasite counts of more than 2% will usually need parenteral treatment irrespective of clinical state
intravenous artesunate is now recommended by WHO in preference to intravenous quinine
if parasite count > 10% then exchange transfusion should be considered
shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic collapse
136
Q

what is the most common cause of non-flaciparum malaria?

A

The most common cause of non-falciparum malaria is Plasmodium vivax, with Plasmodium ovale and Plasmodium malariae accounting for the other cases. Plasmodium vivax is often found in Central America and the Indian Subcontinent whilst Plasmodium ovale typically comes from Africa.

Plasmodium knowlesi is another non-falciparum species which causes clinical pathology, found predominantly in South East Asia.

137
Q

what are the features of non-falciparum malaria?

A

general features of malaria: fever, headache, splenomegaly
Plasmodium vivax/ovale: cyclical fever every 48 hours. Plasmodium malariae: cyclical fever every 72 hours
Plasmodium malariae: is associated with nephrotic syndrome.

138
Q

what is the treatment of non-falciparum malaria?

A

in areas which are known to be chloroquine-sensitive then WHO recommend either an artemisinin-based combination therapy (ACT) or chloroquine
in areas which are known to be chloroquine-resistant an ACT should be used
ACTs should be avoided in pregnant women
patients with ovale or vivax malaria should be given primaquine following acute treatment with chloroquine to destroy liver hypnozoites and prevent relapse

139
Q

which malaria may relapse?

A

Ovale and vivax malaria have a hypnozoite stage and may therefore relapse following treatment.

140
Q

what is leishmaniasis caused by?

  • how is this spread
  • what is the incubation period?
A

Leishmaniasis is caused by the intracellular protozoa Leishmania, usually being spread by sand flies. The organism multiply in monocytes and macrophages, its incubation period may extend upto 10 years.

141
Q

what are 3 forms of leishmaniasis?

A
  • Cutaneous leishmaniasis
  • Mucocutaneous leishmaniasis
  • Visceral leishmaniasis (kala-azar)
142
Q

Cutaneous leishmaniasis:

  • what is this caused by?
  • what does the lesion look like?
A
  • Caused by Leishmania tropica or Leishmania mexicana
  • Crusted lesion at site of bite
  • May be underlying ulcer
143
Q

Mucocutaneous leishmaniasis:

  • what is this caused by?
  • where may skin lesions involve?
A
  • Caused by Leishmania brasiliensis

* Skin lesions may spread to involve mucosae of nose, pharynx

144
Q

Visceral leishmaniasis (kala-azar):

  • what is this caused by?
  • where does this occur?
  • what are the features?
A
  • Mostly caused by Leishmania donovani
  • Occurs in Mediterranean, Asia, South America, Africa
  • Fever (typically ↑ twice in 24hours), sweats, rigors
  • Massive splenomegaly, hepatomegaly
  • Pancytopenia secondary to hypersplenism
  • Poor appetite*, weight loss
  • Grey skin - ‘kala-azar’ means black sickness or black fever
145
Q

Trypanosomiasis: what forms of this disease are recognised?

A

Trypanosomiasis: Two main form of this protozoal disease are recognised - African
trypanosomiasis (sleeping sickness) and American trypanosomiasis (Chagas’ disease)

146
Q

what two forms of sleeping sickness are found?

-how are these spread?

A

Two forms of African trypanosomiasis, or sleeping sickness, are seen - Trypanosoma gambiense in
West Africa and Trypanosoma rhodesiense in East Africa. Both types are spread by the tsetse fly.

147
Q

Trypanosoma rhodesiense:

-clinical features?

A

tends to follow a more acute course.
Clinical features include:
• Trypanosoma chancre - tender subcutaneous nodule at site of infection
• Enlargement of posterior cervical lymph nodes
• Later: central nervous system involvement e.g. Meningoencephalitis

148
Q

Trypanosoma rhodesiense:

-management

A

Management
• Early disease: IV pentamidine or suramin
• Later disease or central nervous system involvement: IV melarsoprol

149
Q

what is American trypanosomiasis/ chagas disease caused by?

A

American trypanosomiasis, or Chagas’ disease, is caused by the protozoan Trypanosoma cruzi.

150
Q

what are the clinical features of American trypanosomiasis / chagas disease?

A

(95%) of patients are asymptomatic in the acute phase although a chagoma (an erythematous nodule at site of infection) and periorbital edema are sometimes seen. Chronic Chagas’ disease mainly affects the heart and gastrointestinal tract

151
Q

what are the complications of American trypanosomiasis/ chagas disease?

A

• Myocarditis may lead to heart failure and arrhythmias. (leading cause of death)
• Gastrointestinal features includes megaesophagus and megacolon causing dysphagia and
constipation

152
Q

what is the management of American trypanosomiasis /chagas disease?

A
  • Treatment is most effective in the acute phase using azole or nitroderivatives such as benznidazole or nifurtimox
  • Chronic disease management involves treating the complications e.g. heart failure
153
Q

what type of infection is schistosomiasis?

-what types are recognised?

A

Schistosomiasis, or Bilharzia, is a parasitic flatworm infection. The following types of schistosomiasis are recognised:
• Schistosoma mansoni and Schistosoma intercalatum: intestinal schistosomiasis
• Schistosoma Hematobium: urinary schistosomiasis

154
Q

how does schistosoma hematobium present? what is this a risk factor for?

A

Schistosoma Hematobium
This typically presents as a ‘swimmer’s itch’ in patients who have recently returned from Africa. Schistosoma Hematobium is a risk factor for squamous cell bladder cancer

155
Q

what are the features of schistosoma hematobium?

A

Features
• Frequency
• Hematuria
• Bladder calcification

156
Q

what is the management of schistosoma hematobium?

A

Single oral dose of praziquante

157
Q

what are the features of rabies?

A
  • Prodrome: headache, fever, agitation
  • Hydrophobia: water-provoking muscle spasms
  • Hypersalivation
158
Q

what should be done following an animal bite in at risk countries for rabies?

A

Following an animal bite in at risk countries:
• If an individual is already immunised then 2 further doses of vaccine should be given
• If not previously immunised then human rabies immunoglobulin (HRIG) should be given along
with a full course of vaccination

159
Q

what is the management of animal bites in the UK?

A

Management
• Cleanse wound
• Current BNF recommendation is co-amoxiclav
• If penicillin-allergic then doxycycline + metronidazole is recommended

160
Q

what is cat scratch disease caused by?

A

Cat scratch disease is generally caused by the Gram negative rod Bartonella henselae

161
Q

what are the features of cat scratch disease?

A 
Features
• fever
• history of a cat scratch
• regional lymphadenopathy
• headache, malaise
162
Q

what is chicken pox caused by?

A

Chickenpox is caused by primary infection with varicella zoster virus. Shingles is reactivation of dormant virus in dorsal root ganglion. Varicella zoster virus is the MOST CONTAGIOUS ORGANISM

163
Q

how is varicella-zoster spread?

  • describe the infectivity of varicella zoster
  • what is the incubation period?
A

• Spread via the respiratory route
• Can be caught from someone with shingles
• Infectivity = 4 days before rash, until 5 days after the rash first
appeared (traditionally taught patients were infective until all lesions had scabbed over)
• Incubation period = 11-21 days

164
Q

what are the clinical features of varicella zoster?

A

• Fever initially
• Itchy, rash starting on head/trunk before spreading. Initially
macular then papular then vesicular
• Systemic upset is usually mild

165
Q

describe the management of varicella zoster

-how does this change for immunocompromised patients and newborns with peripartum exposure?

A
  • Keep cool, trim nails
  • Calamine lotion
  • Immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops then IV aciclovir should be considered
166
Q

describe school exclusion due to varicella zoster

A

• School exclusion: current HPA advice is 5 days from
start of skin eruption. They also state ‘Traditionally children have been excluded until all lesions are crusted. However, transmission has never been reported beyond the fifth day of the rash.’

167
Q

what are complications of varicella zoster?

  • common
  • rare
A

A common complication is secondary bacterial infection of the lesions.

Rare complications include:
• Pneumonia: varicella pneumonia is the most common and serious complication of chickenpox
infection in adults. Auscultation of the chest is often unremarkable → IV acyclovir
• Encephalitis (cerebellar involvement may be seen)
• Disseminated hemorrhagic chickenpox
• Arthritis, nephritis and pancreatitis may very rarely be seen

168
Q

Chickenpox exposure in pregnancy - first step is to check ?

A

Chickenpox exposure in pregnancy - first step is to check antibodies

169
Q

what is fetal varicella syndrome?

  • what is the risk?
  • when does this occur?
  • what are the features?
A
  • Risk of FVS following maternal varicella exposure is around 1% if occurs before 20 weeks gestation
  • Studies have shown a very small number of cases occurring between 20-28 weeks gestation and none following 28 weeks
  • Features of FVS include skin scarring, eye defects (microphthalmia), limb hypoplasia, microcephaly and learning disabilities
170
Q

what is the management of pregnant women with suspected varicella zoster?

A
  • If there is any doubt about the mother previously having chickenpox maternal blood should be checked for varicella antibodies
  • If the pregnant woman is not immune to varicella she should be given varicella zoster immunoglobulin (VZIG) as soon as possible. RCOG and Greenbook guidelines suggest VZIG is effective up to 10 days post exposure
  • Consensus guidelines suggest oral aciclovir should be given if pregnant women with chickenpox present within 24 hours of onset of the rash
171
Q

what type of virus is measles?

  • how is this spread?
  • when is this infective?
  • what is the incubation period?
A 
Overview
• RNA paramyxovirus
• Spread by droplets
• Infective from prodrome until 5 days after rash starts
• Incubation period = 10-14 days
172
Q

what are the features of measles?

A

• Prodrome: irritable, conjunctivitis, fever
• Koplik spots (before rash): white spots (‘grain of salt’) on buccal mucosa
• Rash: starts behind ears then to whole body, discrete maculopapular rash becoming blotchy &
confluent

173
Q

what are the complications of measles (long list, name a few)

A

• Encephalitis: typically occurs 1-2 weeks after the onset of the illness.
• Subacute sclerosing panencephalitis: very rare, may present 5-10 years
following the illness
• Febrile convulsions
• Pneumonia, tracheitis
• Keratoconjunctivitis, corneal ulceration
• Diarrhoea
• ↑ incidence of appendicitis
• Myocarditis

174
Q

how are contacts of measles patients managed?

A

Management of contacts
• If a child not immunized against measles comes into contact with measles then MMR should be offered (vaccine-induced measles antibody develops more rapidly than that following natural infection)
• This should be given within 72 hours

175
Q

what is gonorrhoea caused by? what type of organism is this?

-what is the incubation period?

A

Gonorrhoea is caused by the Gram negative diplococcus Neisseria gonorrhoea. Acute infection can occur on any mucous membrane surface, typically genitourinary but also rectum and pharynx. The incubation period of gonorrhoea is 2-5 days

176
Q

what are the clinical features of gonorrhoea?

A
  • ♂s: urethral discharge, dysuria
  • ♀s: cervicitis e.g. Leading to vaginal discharge
  • Rectal and pharyngeal infection is usually asymptomatic, but may present as rectal bleeding

Local complications that may develop include urethral strictures, epididymitis and salpingitis (hence may lead to infertility). Disseminated infection may occur.

177
Q

what is the treatment of gonorrhoea?

A

• Ciprofloxacin 500mg PO used to be the treatment of choice
Previously the first-line treatment was IM ceftriaxone + oral azithromycin. The new first-line treatment is a single dose of IM ceftriaxone 1g (i.e. no longer add azithromycin). If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given
if ceftriaxone is refused (e.g. needle-phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used

178
Q

what is the most common cause of septic arthritis in young adults?

A

Disseminated gonococcal infection (DGI) and gonococcal arthritis may also occur, with gonococcal infection being the most common cause of septic arthritis in young adults.

179
Q

what is the pathophysiology of disseminated gonococcal infection?

A

The pathophysiology of DGI is not fully understood but is thought to be due to Hematogenous spread from mucosal infection (e.g. asymptomatic genital infection).

180
Q

what are the clinical features of disseminated gonococcal infection?

A

Initially there may be a classic triad of symptoms: tenosynovitis, migratory polyarthritis and dermatitis. Later complications include septic arthritis, endocarditis and perihepatitis (Fitz-Hugh-Curtis syndrome)

  • Tenosynovitis
  • Migratory polyarthritis
  • Dermatitis (lesions can be maculopapular or vesicular)
181
Q

what are genital warts caused by?

-what else can this virus predispose to?

A

Genital warts (also known as condylomata accuminata) are a common cause of attendance at genitourinary clinics. They are caused by the many varieties of the human papilloma virus HPV, especially types 6 & 11. It is now well established that HPV (primarily types 16, 18 & 33) predisposes to cervical cancer.

182
Q

what are the features of genital warts?

A

Features
• Small (2 - 5 mm) fleshy protuberances which are slightly pigmented
• May bleed or itch

183
Q

what is the treatment for genital warts?

A

• Topical podophyllum or cryotherapy are commonly used as first-line treatments depending on the location and type of lesion. Multiple, non-keratinised warts are generally best treated with topical agents whereas solitary, keratinised warts respond better to cryotherapy
• Imiquimod is a topical cream which is generally used second line
• Genital warts are often resistant to treatment and recurrence is common although the majority of
anogenital infections with HPV clear without intervention within 1-2 years

184
Q

Genital herpes is caused by what?

-what is the difference between primary and secondary attacked?

A

Genital Ulcers: genital herpes is most often caused by the herpes simplex virus (HSV) type 2 (cold sores are usually due to HSV type 1). Primary attacks are often severe and associated with fever whilst subsequent attacks are generally less severe and localised to one site

185
Q

Genital ulcers
• Painful: ?
• Painless: ?

A

Genital ulcers
• Painful: herpes&raquo_space; chancroid
• Painless: syphilis > lymphogranuloma venereum + granuloma inguinale

186
Q

what is syphillis caused by?

  • what are the stages of syphillis infection?
  • what is the incubation period?
A

Syphilis is a sexually transmitted infection caused by the spirochaete Treponema pallidum. Infection is characterized by primary, secondary and tertiary stages.
The incubation period= 9-90 days

187
Q

describe the primary features of syphilis?

A

Primary features
• Chancre - painless ulcer at the site of sexual contact
• Often not seen in women

188
Q

what are the secondary features of syphilis?

A

Secondary features - occurs 4-10 weeks after primary infection
• Systemic symptoms: fevers, lymphadenopathy
• Rash on trunk, palms and soles
• Buccal ‘snail track’ ulcers (30%)
• Condylomata lata

189
Q

what are the tertiary features of syphilis?

A

Latent period
Tertiary features
• Gummas
• Aortic aneurysms
• General paralysis of the insane
• Tabes dorsalis (slow degeneration of the sensory neurons. The degenerating nerves are in the
dorsal column; proprioception, vibration, and fine touch).

190
Q

how is syphilis diagnosed?

A

Treponema pallidum is a very sensitive organism and cannot be grown on artificial media. The diagnosis is therefore usually based on clinical features; serology and microscopic examination of infected tissue

191
Q

describe the serological tests for syphilis

A

Serological tests can be divided into
• Cardiolipin tests (not treponeme specific)
• Treponemal specific antibody tests

Cardiolipin tests
• Syphilis infection leads to the production of non-specific antibodies that react to cardiolipin
• Examples include VDRL (venereal disease research laboratory) & RPR (rapid plasma reagin)
• Insensitive in late syphilis
• Becomes negative after treatment

Treponemal specific antibody tests
• Example: TPHA (Treponema pallidum hemagglutination test)
• Remains positive after treatment

Therefore, following treatment for syphilis:

VDRL becomes negative
TPHA remains positive
192
Q

what are causes for false positive cardiolipin tests?

A
  • Pregnancy
  • SLE, anti-phospholipid syndrome
  • TB
  • Leprosy
  • Malaria
  • HIV
193
Q

what is Lymphogranuloma venereum caused by?

A

Lymphogranuloma venereum is caused by Chlamydia trachomatis.

194
Q

what are the three stages of lymphogranuloma venereum?

A
  • Stage 1: small painless pustule which later forms an ulcer
  • Stage 2: painful inguinal lymphadenopathy
  • Stage 3: proctocolitis
195
Q

what is the management for HSV:

  • cold sores
  • gingivostomatitis
  • genital herpes
A

Management:
• Gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
• Cold sores: topical aciclovir although the evidence base for this is modest
• Genital herpes: oral aciclovir. Some patients with frequent exacerbations may benefit from
longer term aciclovir

196
Q

what are 4 other causes of genital ulcers?

A

Other causes of genital ulcers
• Behcet’s disease
• Carcinoma
• Granuloma inguinale: Klebsiella granulomatis (previously called Calymmatobacterium granulomatis)

Chancroid is a tropical disease caused by Hemophilus ducreyi. It causes painful genital ulcers associated with inguinal lymph node enlargement.

197
Q

Describe a chancre:

  • caused by
  • features
  • course of disease
  • occurs
A

Treponema pallidum
Painless, non-exudative, hard indurated edge
Heal spontaneously within 3 - 6 weeks, even in the absence of treatment
Can occur in the pharynx as well as on the genitals

198
Q

Describe a chancroid:

  • caused by
  • features
A

Haemophilus ducreyi

Painful, grey/yellow purulent exudate, soft edge

199
Q

describe Trichomonas vaginalis:

  • what discharge
  • what does the cervix appear like
A

Offensive, yellow/green, frothy discharge Vulvovaginitis

Strawberry cervix

200
Q

what is BV?

A

Bacterial vaginosis (BV) describes an overgrowth of predominately anaerobic organisms such as Gardnerella vaginalis. This leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH. Whilst it’s not a sexually transmitted infection it is seen almost exclusively in sexually active women.

201
Q

what criteria is used for BV?

A

Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present:
• Thin, white homogenous discharge
• Clue cells on microscopy
• Vaginal pH > 4.5
• Positive whiff test (addition of potassium hydroxide results in fishy odour)

202
Q

what are the complications of BV in pregnancy?

-what is the treatment?

A
  • Results in an increased risk of preterm labour, low birth weight and chorioamnionitis, late miscarriage
  • It was previously taught that oral metronidazole should be avoided in the 1st trimester and topical clindamycin used instead. Recent guidelines however recommend: oral metronidazole is used throughout pregnancy. BNF is against the use of high dose metronidazole regimes
203
Q

what is the management of BV?

A

Management
• Oral metronidazole for 5-7 days
• 70-80% initial cure rate
• Relapse rate > 50% within 3 months

204
Q

Chlamydia:

  • is this common
  • what is the organism
  • what is the incubation period?
A

Chlamydia is the most prevalent sexually transmitted infection in the UK
Chlamydia trachomatis, an obligate intracellular pathogen. Approximately 1 in 10 young women in the UK have Chlamydia. The incubation period is around 7-21 days, although it should be remembered a large percentage of cases are asymptomatic

205
Q

what are the features of chlamydia?

A

Features
• Asymptomatic in around 70% of women and 50% of ♂s
• Women: cervicitis (discharge, bleeding), dysuria
• Men: urethral discharge, dysuria

206
Q

what are the complications of chlamydia?

A
  • Epididymitis
  • Pelvic inflammatory disease
  • Endometritis
  • ↑ incidence of ectopic pregnancies
  • Infertility
  • Reactive arthritis
  • Perihepatitis (Fitz-Hugh-Curtis syndrome)
207
Q

what are the investigations for chlamydia?

A

traditional cell culture is no longer widely used
nuclear acid amplification tests (NAATs) are now the investigation of choice
urine (first void urine sample), vulvovaginal swab or cervical swab may be tested using the NAAT technique
for women: the vulvovaginal swab is first-line
for men: the urine test is first-line
Chlamydiatesting should be carried out two weeks after a possible exposure

208
Q

what is seen on swab in gonorrhoea vs chlamydia?

A

Gonorrhoea would be demonstrated by the presence of Gram negative diplococci on the swab. If
the swab showed non-specific urethritis a diagnosis of Chlamydia is most likely. Both many times
infect together

209
Q

what is the screening programme for chlamydia in UK?

A
  • In England the National Chlamydia Screening Programme is open to all men and women aged 15-24 years
  • The 2009 SIGN guidelines support this approach, suggesting screening all sexually active patients aged 15-24 years
  • Relies heavily on opportunistic testing
210
Q

what is used in the management of chlamydia?

-how does this change in pregnancy?

A

• Doxycycline (7 day course) or azithromycin (single dose). The 2009 SIGN guidelines suggest azithromycin should be used first-line due to potentially poor compliance with a 7 day course of doxycycline
-a test of cure should be carried out post-treatment

If pregnant then erythromycin or amoxicillin may be used. The SIGN guidelines suggest considering azithromycin ‘following discussion of the balance of benefits and risks with the patient’

211
Q

what is the contact tracing involved with chlamydia?

A

Patients diagnosed with Chlamydia should be offered a choice of provider for initial partner notification - either trained practice nurses with support from GUM, or referral to GUM
• For men with symptomatic infection all partners from 4 weeks prior to the onset of symptoms should be contacted
• For women and asymptomatic men all partners from the last 6 months or the most recent sexual partner should be contacted
• Contacts of confirmed Chlamydia cases should be offered treatment prior to the results of their investigations being known (treat then test)

212
Q

what is chlamydia psittaci?

  • what are the clinical features?
  • what is pathognomonic?
  • what are the drugs of choice?
A

Chlamydia psittaci (psittacosis) also known as parrot disease, parrot fever, it is characterized by malaise, fever, myalgias and pneumonia. Exposure to an ill bird and a rash (Horder’s spots) are pathognomonic. Erythromycin or tetracyclines are the drugs of choice.

213
Q

what is the management of UTI in non pregnant women?

A

Non-pregnant women

local antibiotic guidelines should be followed if available
CKS/2012 SIGN guidelines recommend trimethoprim or nitrofurantoin for 3 days
send a urine culture if:
    aged > 65 years
    visible or non-visible haematuria
214
Q

what is the management of symptomatic UTI in pregnant women?

A

Pregnant women

if the pregnant woman is symptomatic:
    a urine culture should be sent in all cases
    should be treated with an antibiotic for
    first-line: nitrofurantoin (should be avoided near term)
    second-line: amoxicillin or cefalexin
215
Q

how is asymptomatic bacteruria treated in pregnant women?

A

asymptomatic bacteriuria in pregnant women:

a urine culture should be performed routinely at the first antenatal visit
Clinical Knowledge Summaries recommend an immediate antibiotic prescription of either nitrofurantoin (should be avoided near term), amoxicillin or cefalexin. This should be a 7-day course
the rationale of treating asymptomatic bacteriuria is the significant risk of progression to acute pyelonephritis
a further urine culture should be sent following completion of treatment as a test of cure
216
Q

what is the most common congenital infection?

A

Cytomegalovirus is the most common congenital infection in the UK. Maternal infection is usually asymptomatic

217
Q

Congenital infections: Rubella

  • characteristic features
  • other features
A

Characteristic:
Sensorineural deafness
Congenital cataracts
Congenital heart disease (e.g. patent ductus arteriosus) Glaucoma

Other:
Growth retardation
Hepatosplenomegaly
Purpuric skin lesions
'Salt and pepper' chorioretinitis 
Microphthalmia
Cerebral palsy
218
Q

Congenital infections: Toxoplasmosis

  • characteristic features
  • other features
A

Characteristic features:
Cerebral calcification
Chorioretinitis
Hydrocephalus

other features:
Anemia
Hepatosplenomegaly Cerebral palsy

219
Q

Congenital infections: cytomegalovirus

  • characteristic features
  • other features
A

Characteristic features:
Growth retardation
Purpuric skin lesions

Other features:
Sensorineural deafness
Encephalitiis Pneumonitis Hepatosplenomegaly Anemia
Jaundice
Cerebral palsy
220
Q

Toxoplasma gondii: what type of organism

  • entry point
  • pathophysiology
  • what is the usual animal reservoir?
A

Toxoplasma Gondii is a protozoa which infects the body via the GI tract, lung or broken skin. Its oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.

221
Q

what are clinical features of toxoplasmosis?

A

Most infections are asymptomatic. Symptomatic patients usually have a self-limiting infection, often having clinical features resembling infectious mononucleosis (fever, malaise, and lymphadenopathy). Other less common manifestations include meningioencephalitis and myocarditis.

222
Q

what is the investigation for toxoplasmosis?

A

Investigation for Toxoplasmosis
• Antibody test
• Sabin-Feldman dye test

223
Q

what is the treatment of toxoplasmosis?

A

Treatment is usually reserved for those with severe infections or patients who are immunosuppressed
• Pyrimethamine + Sulphadiazine for at least 6 weeks.

224
Q

what is cholera caused by?

A

is caused by Vibro cholerae - Gram negative bacteria

225
Q

what are the features of cholera?

A
  • Profuse ‘rice water’ diarrhoea
  • Dehydration
  • Hypoglycemia
226
Q

what is the management of cholera?

A
  • Oral rehydration therapy

* Antibiotics: doxycycline, ciprofloxacin

227
Q

what is giardiasis caused by?

A

Giardiasis is caused by the flagellate protozoan Giardia lamblia. It is spread by the faeco-oral route

228
Q

what are the features of giardiasis?

A
  • Often asymptomatic
  • Lethargy, bloating, abdominal pain
  • Non-bloody diarrhoea
  • Chronic/prolonged diarrhoea, malabsorption and lactose intolerance can occur
229
Q

what are th investigations of giardiasis?

A

• Stool microscopy for trophozoite and cysts are classically negative, therefore duodenal fluid
aspirates or ‘string tests’ (fluid absorbed onto swallowed string) are sometimes needed

230
Q

what is the treatment of giardiasis?

A

Treatment is with metronidazole

231
Q

what type of organism is e coli?

A

Escherichia coli: a facultative anaerobic, lactose-fermenting, Gram negative rod which is a normal gut commensal.

232
Q

E coli 0157: what is this assoc with? what can complicate this?

A

E coli O157:H7 is a particular strain associated with severe, hemorrhagic, watery diarrhoea. It has a high mortality rate and can be complicated by hemolytic uremic syndrome.

233
Q

how is e coli 0157 transmitted?

A

It is often spread by contaminated ground beef.

234
Q

what are the clinical features of ecoli 0157?

A
  • Diarrhoea
  • Renal Failure or Impairment
  • Thrombocytopenia
  • ↓ Hb due to hemorrhage
235
Q

what type of organism is salmonella?

A

salmonella group contains many members, most of which cause diarrhoeal diseases. They are aerobic, Gram negative rods which are not normally present as commensals in the gut.

236
Q

what is typhoid and paratyphoid caused by?

A

Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are often termed enteric fevers, producing systemic symptoms such as headache, fever, and arthralgia.

237
Q

what can body lice spread?

A

Body louse is a vector (transmitter) of diseases. Body lice can spread epidemic typhus, trench fever, and louse-borne relapsing fever.

238
Q

when can louse-born typhyus occur?

A

Although louse-borne (epidemic) typhus is no longer widespread, outbreaks of this disease still occur during times of war, civil unrest, natural or man-made disasters, and in prisons where people live together in unsanitary conditions. Louse-borne typhus still exists in places where climate, chronic poverty, and social customs or war and social upheaval prevent regular changes and laundering of clothing

239
Q

what are the features of typhoid/paratyphoid?

A

• Initially systemic upset as above
• Relative bradycardia
• Abdominal pain, distension
• Constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more
common in typhoid
• Rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid

240
Q

what are possible complications of typhoid/paratyphoid?

A
  • Osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
  • GI bleed/perforation
  • Meningitis
  • Cholecystitis
  • Chronic carriage (1%, more likely if adult ♀s)
241
Q

what does shigella cause?

-what is the treatment?

A

• Causes bloody diarrhoea, abdo pain
• Severity depends on type: S sonnei (e.g. from UK) may be mild, S flexneri or S dysenteriae
from abroad may cause severe disease
• Treat with ciprofloxacin

242
Q

how is pyrexia of unknown origin defined?

A

Pyrexia of Unkown Origin: defined as a prolonged fever of > 3 weeks which resists diagnosis after a week in hospital

243
Q

what neoplasia can cause pyrexia of unknown origin?

A
  • Lymphoma
  • Hypernephroma
  • Preleukemia
  • Atrial myxoma
244
Q

what kind of infections could caused pyrexia of unknown origin?

A
  • Abscess

* TB

245
Q

what is african tick typhus caused by?

A

African Tick Typhus: caused by Rickettsiae.

246
Q

what are the clinical features of african tick typhus?

A 
Diagnosis:
• Black sopits on thigh
• Hx of tick bites
• Low grade fever
• Faint macular rash
247
Q

what is rocky mountain spotted fever?

A

Rocky Mountain Spotted Fever: is the most lethal and most frequently reported rickettsial infection, spreads by ticks, common in USA

248
Q

what is the presentation of rocky mountain spotted fever?

A

Presentation:
• Fever
• Rash on hands, feet which later → desequamte (peel)
• Tachycardia with no hypotension (unlike Staphylococcal Toxic Shock Syndrome)

249
Q

what is the management of rocky mountain spotted fever?

A

Management: Doxycycline

250
Q

what is mediterranean spotted fever caused by? how is this transmitted?

A

Mediterranean Spotted Fever: (Boutonneuse fever) is a fever caused by the Rickettsia
conorii and transmitted by the dog tick Rhipicephalus sanguineus.

251
Q

what is the incubation period of mediterranean spotted fever?

A

Incubation period: 7 days.

252
Q

what are the clinical features of mediterranean spotted fever?

A

• The disease manifests abruptly with chills, high fevers, myalgia and joints pain, severe
headache, photophobia and diarrhea.
• The location of the bite forms a black spots or ulcerous crust (tache noire). Around the fourth
day of the illness an exanthem (widespread rash) appears, first macular and then
maculopapular and sometimes petechial.

253
Q

what is the treatment of mediterranean spotted fever?

A

• Treated by Doxycycline.

254
Q

what is dengue fever?

A

Dengue fever is a type of viral hemorrhagic fever (also yellow fever, Lassa fever, Ebola)

255
Q

Low platelet count and raised transaminase level is typical of ?

A

Low platelet count and raised transaminase level is typical of dengue fever

256
Q

Dengue fever:
how is this transmitted?
what is the incubation period?
what complication may develop?

A

• Transmitted by the Aedes aegyti mosquito
• Incubation period of 7 days
• A form of disseminated intravascular coagulation (DIC) known as dengue hemorrhagic fever
(DHF) may develop. Around 20-30% of these patients go on to develop dengue shock syndrome (DSS)

257
Q

what are the featues of dengue fever?

A
  • Causes headache (often retro-orbital)
  • Myalgia
  • Pleuritic pain
  • Facial flushing (dengue)
  • Maculopapular rash
  • Pyrexia
258
Q

what is the treatment of dengue fever?

A

Treatment is entirely symptomatic e.g. fluid resuscitation, blood transfusion etc

259
Q

what is infectious mononucleosis caused by? who is this most common in?

A

Infectious mononucleosis (glandular fever) is caused by the Epstein-Barr virus (also known as human herpesvirus 4, HHV-4). It is most common in adolescents and young adults.

260
Q

what are the features of infectious mononucleosis?

A
  • Sore throat
  • Lymphadenopathy
  • Pyrexia
  • Malaise, anorexia, headache
  • Palatal petechiae
  • Splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
  • Hepatitis
  • Presence of 50% lymphocytes with at least 10% atypical lymphocytes
  • Hemolytic anaemia
261
Q

what is the management of infectious mononucleosis?

A

• Rest during the early stages, drink plenty of fluid, avoid alcohol
• Simple analgesia for any aches or pains
• Consensus guidance in the UK is to avoid playing contact sports for 8 weeks after having
glandular fever to reduce the risk of splenic rupture

262
Q

what malignancies are assoc. with EBV?

A

• Burkitt’s lymphoma*
• Hodgkin’s lymphoma
• Nasopharyngeal carcinoma
• HIV-associated central nervous system lymphomas
The non-malignant condition hairy leukoplakia is also associated with EBV infection. *EBV is currently thought to be associated with both African and sporadic Burkitt’s

263
Q

what type of virus is hep E? how is this spread? where is this commonly found?

A
  • RNA virus
  • Spread by the faecal-oral route, incubation period = 3-8 weeks
  • Common in Central and South-East Asia, North and West Africa, and in Mexico
264
Q

what are the features of hep E?

A

• Causes a similar disease to hepatitis A, but carries a significant mortality (about 20%) during
pregnancy
• Does not cause chronic disease
• A vaccine is currently in development, but is not yet in widespread use

265
Q

H1N1 - what causes this?

A 
H1N1 influenza (Swine Flu): outbreak was first observed in Mexico in early 2009. In June 2009, the WHO declared the outbreak to be a pandemic.
H1N1 virus is a subtype of the influenza A virus and the most common cause of flu in humans. The 2009 pandemic was caused by a new strain of the H1N1 virus.
266
Q

which groups are most commonly at risk of H1N1?

A
  • Patients with chronic illnesses and those on immunosuppressants
  • Pregnant women
  • Young children under 5 years old
267
Q

what are the clinical features of H1N1?

A 
the majority of symptoms are typical of those seen in a flu-like illness:
• Fever greater than 38oC • Myalgia
• Lethargy
• Headache
• Rhinitis
• Sore throat
• Cough
• Diarrhoea and vomiting
• A minority of patients may go on to
develop an acute respiratory distress syndrome which may require ventilatory support
268
Q

what is the treatment for H1N1?

A
  1. Oseltamivir (Tamiflu)
    “ Oral medication
    “ A neuraminidase inhibitor which prevents new viral particles from being
    released by infected cells
    “ Common side-effects include nausea, vomiting, diarrhoea and headaches
2. Zanamivir (Relenza)
" Inhaled medication
" Also a neuraminidase inhibitor
" May induce bronchospasm in asthmatics
intravenous preparations are available for patients who are acutely unwell
269
Q

what kind of virus is parvovirus B19?

A

Parvovirus B19 is a DNA virus which causes a variety of clinical presentations. It was identified in the 1980’s as the cause of erythema infectiosum

270
Q

what is erythema infectiosum?

-what are the clinical features?

A

Erythema infectiosum (also known as fifth disease or ‘slapped-cheek syndrome’) caused by parvovirus B19
• Most common presenting illness
• Systemic symptoms: lethargy, fever, headache
• ‘slapped-cheek’ rash spreading to proximal arms and extensor surfaces

271
Q

aside from erythema infectiosum - what other presentations of parvovirus B19 exist?

A

• Asymptomatic
• Pancytopenia in immunosuppressed patients
• Aplastic crises e.g. in sickle-cell disease (parvovirus B19 suppresses erythropoiesis for about a
week so aplastic anemia is rare unless there is a chronic hemolytic anemia)

272
Q

what is orf? what is this caused by?

A

Orf is generally a condition found in sheep and goats although it can be transmitted to humans. It is caused by the parapox virus.

273
Q

what are the features of orf in animals? what are the features in humans?

A

In animals
• ‘scabby’ lesions around the mouth and nose

In humans
• Generally affects the hands and arms
• Initially small, raised, red-blue papules
• Later may ↑ in size to 2-3 cm and become
flat-topped and hemorrhagic

274
Q

Nematodes:

what is ancylostoma braziliense?

A

Ancylostoma braziliense
• Most common cause of cutaneous larva migrans
• Common in Central and Southern America

275
Q

Nematodes

-how is strongyloides stercoralis aquired?

A

Strongyloides stercoralis

• Acquired percutaneously (e.g. Walking barefoot)

276
Q

what are the clinical features of strongyloides stercoralis?

A

• Causes pruritus and larva currens - this has a similar appearance to cutaneous larva migrans but
moves through the skin at a far greater rate
• Abdo pain, diarrhoea, pneumonitis
• May cause gram negative septicemia due to carrying of bacteria into bloodstream
• Eosinophilia sometimes seen

277
Q

what is the management of strongyloides stercoralis?

A

• Management: thiabendazole, albendazole. Ivermectin also used, particularly in chronic
infections

278
Q

nematodes:

-what is toxocara canis?

A

Toxocara canis

• Commonly acquired by ingesting eggs from soil contaminated by dog faeces

279
Q

what are the clinical features of toxocara canis?

A
  • Commonest cause of visceral larva migrans

* Other features: eye granulomas, liver/lung involvement

280
Q

what are tape worms made up of?

A

Tape worms are made up of repeated segments called proglottids. These are often present in faeces and are useful diagnostically

281
Q

what is Cysticercosis caused by?

A
  • Caused by Taenia solium (from pork) and Taenia saginata (from beef)
  • Management: niclosamide
282
Q

what is hydatid disease?

-what is the lifecycle?

A
  • Caused by the dog tapeworm Echinococcus granulosus

* Life-cycle involves dogs ingesting hydatid cysts from sheep liver

283
Q

what are the clinical features of hydatid disease?

A
  • Often seen in farmers

* May cause liver cysts

284
Q

what is the management of hyatid disease?

A

• Management: albendazole

285
Q

what are three causes of otitis externa?

A

Causes of otitis externa include:
• Infection: bacterial (Staphylococcus aureus, Pseudomonas aeruginosa) or fungal
• Seborrhoeic dermatitis
• Contact dermatitis (allergic and irritant)

Pseudomonas aeruginosa causes malignant otitis externa

286
Q

what are the features of otitis externa?

A

Features
• Ear pain, itch, discharge
• Otoscopy: red, swollen, or eczematous canal

287
Q

what is the recommended initial management of otitis externa?

A

The recommend initial management of otitis externa is:
• Topical antibiotic or a combined topical antibiotic with steroid
• If the tympanic membrane is perforated aminoglycosides should not be used
• If there is canal debris then consider removal
• If the canal is extensively swollen then an ear wick is sometimes inserted

288
Q

what are second line options for treatment of otitis externa?

A

Second line options include
• Consider contact dermatitis secondary to neomycin
• Oral antibiotics if the infection is spreading
• Taking a swab inside the ear canal
• Empirical use of an antifungal agent

289
Q

what is malignant otitis externa?

A

Malignant otitis externa is more common in elderly diabetics. In this condition there is extension of infection into the bony ear canal and the soft tissues deep to the bony canal. Intravenous antibiotics may be required.

MRCP part 1 (17 decks)

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