Microbiology (MedEd) Flashcards

1
Q

A 32-year-old woman presents to the GP with a two-day history of headache and fever. On examination, there is neck stiffness, photophobia and a non-blanching rash. Her temperature is 38.8 degrees. Meningitis is suspected.

Which of the following is the next best management in this patient?
A. 0.9% NaCl 500ml over 15mins
B. Ceftriaxone 2g IV
C. Call the infectious diseases registrar
D. Benzylpenicillin 1.2g IM
E. Dexamethasone 10 mg IV QDS for 4 days

A

Answer: D . Benzylpenicillin 1.2g IM. in the community if meningitis suspected (vs ceftriaxone in hospital)

rash to penicillin is not a contraindication for immediately giving benzylpenicillin to suspected meningococcal meningitis.

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2
Q

A 34-year-old lady presents with a 2 week history of myalgia, arthralgia and recurrent fevers. She has also noticed a loss of appetite, dark urine and pale stools. She admits to being a regular intravenous drug user for many years now. On examination there is notable right upper quadrant tenderness.

A viral screen is performed:

Hepatitis B Surface Antigen - Positive
Hepatitis B Envelope Antigen - Negative
Hepatitis B Surface Antibody - Negative
Hepatitis B Core Antibody (Immunoglobulin G) - Negative
What infection has been confirmed by these results?

A. Acute hepatitis A

B. Recovered from previous hepatitis B

C. Acute hepatitis B

D. Chronic hepatitis B (highly infectious)

E. Acute hepatitis C

A

C. Acute hepatitis B

An elevated hepatitis B surface antigen level is indicative of acute hepatitis B infection. Antigen levels tend to peak at 3-4 months post initial exposure.

Hepatitis B is a double stranded DNA virus which is most often transmitted via exposure to contaminated blood and mucosal surfaces.

Not B: recovered from previous Hep B:

A patient who has recovred from previous hepatitis B infection would test positive for anti-hepatitis B surface and anti-hepatitis B core (IgG) antibodies. They would also test negative for hepatitis B surface antigen.

A patient with highly infectious chronic hepatitis B infection (carrier) would test positive for: hepatitis B surface antigen, hepatitis B envelope antigen, and anti-hepatitis B core antibodies (IgM and IgG).

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3
Q

A 35-year-old woman undergoes routine antenatal screening and is found to be positive for hepatitis B. Her serology is reviewed, and she is identified as high risk for vertical transmission. She is informed her baby will receive intravenous immunoglobulin and a hepatitis B vaccine at birth.

Which of the following has been detected in her serology?

A. HBe antigen

B. Anti-HBc

C. Anti-HBs

D. Anti-HBe

E. HBs antigen

A

A. HBe antigen
90% of mothers who are hepatitis B e antigen-positive will transmit the disease vertically; these patients are the most infectious.

E. HBs antigen is a marker of active infection

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4
Q

A 48-year-old man with a history of chronic injection drug use, presents with sequential foot-drop and then wrist drop associated with pain and occurring over a 3-week period. Nerve conduction studies show evidence of a multifocal axonal neuropathy. He is also noted to have nail fold infarcts in his hands and feet, purpura and hepatomegaly. What is the most likely underlying diagnosis?

A. Hepatitis C related Guillain-Barre syndrome

B. Cytomegalovirus polyradiculopathy

C. Hepatitis C related cryoglobulinaemia

D. Systemic toxoplasmosis

E. Hepatitis B related Guillain-Barre syndrome

A

C. Hepatitis C related cryoglobulinaemia

A sub-acute painful multifocal neuropathy (mononeuritis multiplex) occurring in association with features of systemic inflammation (in this case, seen as nail fold infarcts) raises the possibility of vasculitic neuropathy. Hepatitis C infection may be associated with cryoglobulinaemia (proteins that become insoluble at reduced temperatures), which causes a vasculitic syndrome including neuropathy

Not B:

Hepatitis B related Guillain-Barre syndrome is incorrect. This is not a presentation typical of the Guillain-Barre syndrome (for many reasons, not least the nerve conductions studies which should show evidence of peripheral nerve demyelination – reduced velocities and conduction block)

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5
Q

What does positive anti Hb E Ag indicate?

A

Inactivity of virus & low infectivity

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6
Q

A third-year medical student attends an occupational health appointment before starting her clinical placements. She grew up in Romania and moved to the UK 4 years ago. She reports no symptoms and is eager to begin her placement in infectious diseases. A routine blood test for hepatitis B serology is performed, with the results as follows:

Which of the following is the correct interpretation of her hepatitis B serological testing?

Which of the following is the correct interpretation of her hepatitis B serological testing?

A. Immunity to hepatitis B due to natural infection

B. Chronic hepatitis B infection with low infectivity

C. Immunity to hepatitis due to vaccination

D. Chronic hepatitis B infection with high infectivity

E. Acute hepatitis B infection

A

B. Chronic hepatitis B infection with low infectivity

This patient has serological findings consistent with chronic hepatitis B, namely positive hepatitis B surface antigen (HBsAg) and IgG anti-hepatitis B core (anti-HBc) antibody, and negative anti-HBs and IgM anti-HBc. HBeAg is a measure of viral replication: when this is low or undetectable, as in her case, viral infectivity can also be thought of as low. Similarly, a positive anti-HBe antibody suggests immune suppression of viral replication in chronic infection and low infectivity.

Not D: Chronic hepatitis B infection with high infectivity

Chronic hepatitis B with high infectivity will look similar on serology; however, the difference lies with the HBeAg. HBeAg is a marker of viral replication, with a higher level indicating higher infectivity. Note: HBeAb is also positive, indicating antibody production and suppression of viral replication by the immune system.

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7
Q

what is HBeAg a marker of?

A

viral replication and infectivity. A higher level indicating higher infectivity.

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8
Q

A 35-year-old woman undergoes routine antenatal screening and is found to be positive for hepatitis B. Her serology is reviewed, and she is identified as high risk for vertical transmission. She is informed her baby will receive intravenous immunoglobulin and a hepatitis B vaccine at birth.

Which of the following has been detected in her serology?

A. HBs antigen

B. Anti-HBe

C. Anti-HBs

D. HBe antigen

E. Anti-HBc

A

D. HBe antigen

90% of mothers who are hepatitis B e antigen-positive will transmit the disease vertically; these patients are the most infectious (E antigen indicates infectivity).

Not A. HBs antigen=marker of active infection

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9
Q

A 24-year-old medical student presents with a 1 week history of intermittent fevers, nausea, vomiting, diarrhoea, fatigue, and malaise. He seems quite anxious as this morning he noticed dark coloured urine and pale stools. On further questioning he reports that he returned from his medical elective in India 4 weeks ago. He denies any smoking or illicit substance use. He drinks 10-20 units of alcohol most weeks whilst at university. He was previously fit and well. He reports 2 sexual partners in the past 3 years.

On abdominal examination, there is palpable hepatomegaly extending approximately 2 cm below the right subcostal margin. There is also notable scleral icterus.

What is the most likely cause of his symptoms?

A. Epstein Barr Virus

B. Hepatitis B

C. Alcoholic hepatitis

D. Hepatitis C

E. Hepatitis A

A

E. Hepatitis A infection typically presents with the symptoms described above, and a 2-6 week incubation period following exposure is typical. Poor food hygiene in an endemic country such as India is the likely source of infection in this case. The majority of hepatitis A infections will resolve within 2-3 weeks of symptoms onset.

Not D. Hepatitis C:
Hepatitis C infection is most often asymptomatic. It is strongly associated with specific risk factors, including: intravenous or nasal drug use, HIV infection, history of organ transplant or blood transfusion.

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10
Q

Label Hep B

A
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11
Q

What is the management of TB? how long?

A

Isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months, then Isoniazid and rifampicin for a further 4 months.

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12
Q

When would you extend duration of treatment for TB?

A

Extended duration in TB meningitis, pericarditis, and spinal TB.

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13
Q

A 19-year-old male university student presents to Accident and Emergency with shortness of breath and significant fatigue. He reports a three-week history of fevers and worsening dry cough. On examination, there are inspiratory crepitations in the right lung. The patient also mentions that they have pain in their toes.

A blood test and chest X-ray are requested.

Bloods:

WCC: 11.4x10^9/L (4-11)

CRP: 102mg/L (<5)

Hb: 93g/L (140-180)

Chest radiograph:

Patchy consolidation in the right lower lobe.
What is the most likely causative organism?

A. Streptococcus pnuemoniae

B. Klebsiella species

C. Legionella pneumophila

D. Pseudomonas aeruginosa

E. Mycoplasma pnuemoniae

A

E. Mycoplasma pnuemoniae

This patient has clinical features consistent with mycoplasma pneumonia, including a worsening dry cough and patchy lower lobe consolidation. Mycoplasma infections tend to occur in epidemics and are seen in settings such as hospitals and universities. The pain in the toes and the low haemoglobin a are secondary to a cold autoimmune haemolytic anaemia (a recognised complication of mycoplasma infection)

Not A: streptococcus pneumoniae

This is incorrect. This is a common cause of community acquired pneumonias. However, one would usually expect the cough to be accompanied with sputum production

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14
Q

what’s the incubation period of mycoplasma pneumoniae?

A

2-3 weeks

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15
Q

what is co-adminstered with RIPE TB medication? why?

A

Vitamin B6 (pyridoxine) should be administered to prevent peripheral neuropathy. This is most commonly caused by isoniazid and rarely, ethambutol

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16
Q

A 22 year old Pakistani man has been contacted by his GP as his mother has confirmed pulmonary Tuberculosis. He has no symptoms and reports feeling well.

He was born in Pakistan and was vaccinated against Tuberculosis as a child, then moved to the UK 15 years ago.

What is the next best step in this patients management?

A. BCG vaccination

B. CT chest

C. Acid Fast Bacilli

D. Interferon Gamma Release Assay (IGRA)

E. Chest X-ray

A

D. Interferon Gamma Release Assay (IGRA)

The Interferon gamma release assay (aka quantiferon) is used to identify patients who may have latent TB infection. It can detect latent TB in patients who have already been vaccinated with a BCG (as opposed to a Tuberculin Skin test which can be less accurate in patients who have previously been vaccinated). In practice, both Interferon gamma release assays and the Tuberculin skin test are used in screening, regardless of immunisation status.

Not C: Acid Fast Bacilli

This is used for patients who have evidence of active infection

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17
Q

A 40 year old male presents to A&E with a 1 day history of yellowing of his skin and eyes. He is a known HIV positive patient and has recently been started on medication for tuberculosis. On examination, he is tender in the right upper quadrant of his abdomen.

Liver function tests show bilirubin 108 µmol/L, ALT 260 iU/L, AST 305 iU/L, ALP 58 iU/L, GGT 45 U/L.

Which of the following medications is the most likely cause of his symptoms?

A. Ethambutol

B. Levofloxacin

C. Isoniazid

D. Rifampicin

E. Pyrazinamide

A

E. Pyrazinamide: This is the most likely to cause hepatotoxicity compared to the other anti-TB drugs

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18
Q

What are the components of CURB-65 score and treatment options?

A

Components (1 point for each if present):
1. Confusion +/-
2. Urea >7
3. Respiratory Rate >30
4. Blood pressure: systolic < 90 or diastolic <60
5, More than 65 years old

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19
Q

A 67-year-old woman presents to her GP complaining of a 5-day history of cough productive of yellow sputum. Over the last 2 days, she has developed a sharp pain over the right side of her chest and has been feeling increasingly run down. She describes being unable to sleep because of the pain and ongoing muscle aches, and describes feeling tired and ‘out of sorts’. Her past medical history is significant for hypothyroidism treated with levothyroxine. She has no known drug allergies.

On examination, she is alert and responds appropriately to questioning, but appears visibly short of breath and has frequent but discontinuous coughing fits during the consultation. Air entry is clear on auscultation, with increased vocal resonance on the right side. There is also dullness to percussion over the right side middle zone.

The GP takes some basic observations:

HR 86 bpm
RR 26 breaths per minute
O2 saturation 97% in air
BP 102/68 mmHg
Temperature 38.4 °C
What is the most appropriate management option for this patient?

A. Inpatient treatment with IV co-amoxiclav

B. Reassurance

C. Refer to emergency department for further diagnostic imaging

D. Outpatient treatment with oral amoxicillin

E. ITU referral and treatment with IV co-amoxiclav

A

D. Outpatient treatment with oral amoxicillin

This patient has presented to her GP with features suggestive of community-acquired pneumonia. Her CURB-65 score is 1 (for age over 65 years) and she appears stable during the consultation. Outpatient treatment with oral antibiotics is therefore an appropriate management in this scenario.

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20
Q

A 15 year old boy presents to the GP after being notified through contact tracing that another child at his school has tested positive for active pulmonary Tuberculosis . He has no cough or fever and feels well within himself.

The doctor decides to perform a tuberculin skin test and there is an induration of 1mm size where the tuberculin was injected.

What is the next best step in the management of this patient ?

A. Start quadruple combination tuberculosis antibiotic therapy

B. Organise a CT chest

C. Carry out a lumbar puncture to detect the spread in the central nervous system

D. Send a sputum sample for culture and sensitivity

E. Give BCG vaccination

A

E. According to NICE guidelines, BCG vaccination should be given to tuberculin skin test negative (mantoux negative) contacts of patients with confirmed pulmonary and laryngeal TB, who have not been previously vaccinated and are under the age of 35 or are over the age of 35 and work in healthcare.

This patient had a negative test with only 1mm induration, a positive result would have been 5mm or more (meaning they are previously vaccinated)

Not D. Send a sputum sample for culture and sensitivity

This patient is displaying no signs of TB infection (he has no haemoptysis, fever, weight loss or night sweats). It would not be an appropriate investigation at this point

Not

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21
Q

Which vaccinations can HIV patients receive and which can they not receive?

A

-can receive MMR
-cannot receive BCG or yellow fever

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22
Q

What are some egs of live attenuated vaccine? mnemonic?

A

MMR-VBOYI
-MMR
-VZV
-BCG (heterotypic)
-Oral (polio: sabin, b>l in salk)
-Yellow fever
-Influneza (Fluenz tetra)

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23
Q

what are some examples of inactivated vaccines? mnemonic?

A

RAised ICP

-rabies, hep A
-influenza (quadrivalent)
-Cholera
-Polio (salk), plague (bubonic), pertussis

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24
Q

when is pertussis vaccine given to pregnant women?

A

16 weeks

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25
Q

what are examples of component/subunit vaccines?

A

-Hep B (HbS antigen)
-HPV (capsid)
-Influenza recombinant (quadrivalent)

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26
Q

what are some toxoid vaccines?

A

-diphtheria
-tetanus

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27
Q

what are some examples of conjugate polysaccharide vaccines? mnemonic?

A

NHS (encapsulated bacteria)
-N meningitidis
-H influenzae
-Strep pneumonia

-particularly used in children/splenectomy (hyposplenism)

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28
Q

which virus is usually involved in viral vector vaccines?

A

adenovirus

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29
Q

what is a side effect of adenoviral vector?

A

capillary leak syndrome (eg thrombosis in sinuses)

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30
Q

What can Pfizer vaccine cause as a side effect?

A

myocarditis

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31
Q

what are some egs of viral vector vaccines?

A

-Ebola
-Janssen and AZ COVID vaccines

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32
Q

what are some egs of nucleic acid vaccines?

A

Pfizer and Moderna COVID vaccines

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33
Q

CSF findings in meningitis:

A
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34
Q

which infectious disease typically causes pain behind eyes (retroorbital pain)? Other symptoms?

A

Dengue fever

-headache, joint and bone pain (hence “breakbone fever”), fever and rash

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35
Q

A 4 year old girl is brought into Paediatric Emergency with a 2 day history of high fever and irritability. She has developed red, peeling skin over the past day. Her mother reports that she had a sore throat prior to this, which has since resolved. On examination, she has widespread erythema with several blisters. Her skin is extremely tender to touch and peels easily when rubbed.

What is the most likely diagnosis?

A. Scarlet fever

B. Toxic shock syndrome

C. Staphylococcal scalded skin syndrome

D. Kawasaki disease

E. Cellulitis

A

C. Staphylococcal scalded skin syndrome

This is caused by Staphylococcus aureus. It presents with red tender blistering skin and a positive Nikolsky sign, in which the layers of skin separate on gentle pressure. A prodrome of sore throat or conjunctivitis may occur

Not A: Scarlet fever

This is an exotoxin-mediated disease caused by Streptococcus pyogenes. Patients present with an erythematous rash with a sandpaper texture and desquamation may occur. A strawberry tongue and Pastia’s lines (confluent petechiae in skin creases) are typical of the disease

Not: D: Kawasaki disease

This is a medium sized vasculitis usually presenting with a prolonged fever of more than 5 days. Patients have a widespread polymorphous rash (not usually vesiculo-bullous) and desquamation of the extremities about 2-4 weeks later

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36
Q

clinical features of SSSS (Staphylococcal scalded skin syndrome):

A
  1. It causes superficial fluid-filled blisters and often causes erythroderma (erythema of >90% of the body surface).
  2. There is desquamation (peeling of the epidermis) and Nikolsky sign is positive.
  3. Perioral crusting/fissuring is common and the oral mucosa is usually unaffected, unlike Toxic 4. Epidermal Necrolysis (TEN).
    Due to the infective cause, fever and irritability are common.
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37
Q

what is Nikolsky sign?

A

Nikolsky sign is where the superficial epidermis can be dislodged by a slight shearing force. It is positive in SSSS, TEN and pemphigus vulgaris.

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38
Q

Pathophysiology/Diagnosis/Management of SSSS:

A

SSSS is caused by exotoxins released by Staphylococcus aureus, a bacteria that is commonly found in the skin flora of healthy adults. The exotoxins cleave desmoglein-1 resulting in splitting of the stratum granulosum and the formation of superficial blisters.

Diagnosis is usually clinical, although a skin biopsy can be used to differentiate between SSSS and TEN.

Management is with intravenous antibiotics and supportive treatment.

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39
Q

Common causes of meningitis:

A
  1. Bacterial causes
    The most common causative pathogens include:

Streptococcus pneumoniae (pneumococcus)
Neisseria meningitidis (meningococcus)
Haemophilus influenzae
Listeria monocytogenes (often in patients at extremes of age)

  1. Viral causes
    Enteroviruses such as Echoviruses, Coxsackie viruses A and B, poliovirus are the most common causes of viral meningitis.

Other viruses include herpes viruses:

HSV2 (more associated with meningitis)

HSV1 (more associated with meningoencephalitis/encephalitis, particularly affecting the temporal lobes).
Paramyxovirus: can be a complication of mumps infection
Measles and rubella viruses: can cause meningoencephalitis
Varicella Zoster Virus: can be a complication of chicken pox
Arboviruses - arthropod-borne viruses, cause meningoencephalitis
Rabies virus - can cause meningo-encephalitis

  1. Fungal causes
    Fungal (particularly Cryptococcus neoformans) and mycobacterial meningitis are rare, except in the immunosuppressed population.
  2. Parasitic causes
    Amoeba: Acanthamoeba - associated with keratitis and meningitis associated with contact lens fluid contamination.
    Toxoplasma gondii
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40
Q

Causes of non-infective meningitis:

A

-Malignancy (leukaemia, lymphoma and other tumours)
-Chemical meningitis
-Drugs (NSAIDs, trimethoprim)
-Sarcoidosis
-Systemic Lupus Erythematosus
-Behcet’s disease

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41
Q

A 55 year old man presents to his GP with a 6 month history of multiple hypopigmented patches over his torso. He also has multiple burn marks on his hands from accidentally touching hot pans whilst cooking. Nerve conduction studies reveal reduced conduction velocity in the ulnar and median nerves. He is started on dapsone. Which one of the following tests should be performed before starting treatment?

A. Vitamin B12 levels

B. Electrocardiogram (ECG)

C. Glucose-6-phosphate dehydrogenase (G6PD) levels

D. Renal function testing

E. HIV testing

A

C. G6PD levels

Dapsone carries the risk of severe haemolytic anaemia in patients with severe G6PD deficiency

Not A: VitB12 levels

Dapsone inhibits folic acid synthesis and should be given with folate supplementation. It does not affect B12 levels

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42
Q

Differentials for leprosy (other causes of thickened peripheral nerves):

A

Inherited diseases - Charcot Marie Tooth, Refsum’s Disease and Neurofibromatosis

Endocrinological - Acromegaly

Other - AL amyloidosis

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43
Q

Diagnosis of leprosy:

A

Definitive diagnosis is based on clinical assessment and findings of acid-fast bacilli from biopsies/smears (mycobacterium Leprae. symptoms: Skin depigmentation, nodules, trophic ulcers, nerve thickening. Lifelong illness, most disability due to nerve damage)

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44
Q

what type of antibiotic is tazocin?

A

Tazocin EF contains the active ingredients piperacillin and tazobactam. They belong to a group of antibiotics called penicillins that work by killing bacteria.
-broad-spectrum antibiotic eg urinary sepsis

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45
Q

early features of autoimmune encephalitis:

A

Fever, headaches, diarrhoea and upper respiratory-tract infection

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46
Q

investigations for autoimmune encephalitis:

A
  1. Full neurological examination
  2. Blood tests:
    3 a)Low sodium is associated with LG1 encephalitis
    b) Antibodies: LGI1, NMDA receptor, CASPR2
    MRI
  3. Lumbar puncture (will show increased levels of lymphocytes in the cerebrospinal fluid (‘lymphocytic pleocytosis’))
  4. EEG is sensitive but not specific
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47
Q

Treatment/screening for autoimmune encephalitis:

A

The first-line treatment of autoimmune encephalitis includes steroids and intravenous immunoglobulin. Plasma exchange can also be used as an adjunctive treatment in those who are not fully responding to steroids or immunoglobulin; it is rarely used alone.

The most common complications of plasma exchange are infection, hypotension and electrolyte imbalances due to fluid shifts.

Second-line treatment, if patients are not responding within 2 weeks, includes immunosuppressant therapy with agents such as Rituximab and Cyclophosphamide. First line therapy should be continued during this time.

Patients with agitation may be started on second-generation antipsychotics, such as Risperidone. This is due to a reduced side effect profile as compared to the first-generation antipsychotics, such as Haloperidol.

Cancer screening
Encephalitis can occur as a paraneoplastic syndrome where autoimmune disorders are triggered by tumours.

Therefore, it is important to screen for cancer in patients whom you suspect may have an underlying tumour.

Particular associations:

  1. Anti-Hu: Small cell lung cancer
  2. NMDA receptor antibodies: Ovarian teratoma
  3. Anti-Yo: breast and ovarian tumours
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48
Q

What type of vaccine is comprised of a polysaccharide bound to a immunogenic toxin?

A

conjugate

-For encapsulated bacteria.

Consist of bacterial polysaccharides conjugated to an immunogenic toxin (diphtheria toxin).

Used for Haemophilus influenzae, meningococcus and pneumococcus.

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49
Q

The Meningitis C vaccination is an example of what type of vaccination?

A

conjugate

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50
Q

What type of vaccine uses injection of preformed antigenic proteins to induce immunity?

A

subunit vaccine

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51
Q

What is the name given to a substance that increases the effectiveness of an immune response to a vaccination without altering the specificity of the response?

A

Adjuvant

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52
Q

What type of vaccine uses pathogens that are unable to replicate?

A

Inactivated

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53
Q

What is the target of the antibody P-ANCA?

A

Myeloperoxidase

Antineutrophil cytoplasmic antibodies are implicated in pauci-immune conditions such as granulomatosis with polyangiitis or goodpasture’s disease.

Their presence suggests a breakdown in immune tolerance as the immune system has become sensitised to intracellular antigens.

p-ANCA = Myeloperoxidase = UC, Eosinophilic Granulomatosis with Polyangiitis, Primary Sclerosing Cholangitis or Microscopic Polyangiitis

c-ANCA = Proteinase-3 = Granulomatosis with polyangiitis (Wegner’s)

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54
Q

A 21 year old woman reports weight loss, tiredness, diarrhoea and non-bloody offensive smelling stools. She has had three chest infections requiring antibiotics in the last three years. Blood tests are ordered and reveals a hypochromic, microcytic anaemia with low ferritin. Anti-TTG and anti-endomysial antibodies are negative. There are normal levels of IgG, IgM and IgE. No IgA is found.

What is the most likely cause of her gastrointestinal symptoms?

A

Particular caution should be noted in the diagnosis of coeliac disease, as the common autoantibodies that are used for diagnosis are of the type IgA (Anti-Endomysial and Anti-Tissue Transglutaminase).

Hence, in IgA deficiency (1 in 600 people), they may be falsely negative.

IgA levels should always be assessed at the same time when assessing for coeliac disease.

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55
Q

What hematological cells create a “respiratory burst” in order to kill phagocytosed pathogens?

A

neutrophils

Neutrophils kill phagocytosed pathogens by creating a respiratory burst. A respiratory burst involves the release of superoxide species, oxygen free radicals and hydrogen peroxide into the phagolysosome. This process is deficient in chronic granulomatous disease due to the lack or dysfunction of the enzyme NADPH oxidase

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56
Q

most common cause of epididymoorchitis in older males

A

E.coli (which is often associated with urinary tract infections)

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57
Q

A 78 year old man is brought to the Emergency Department from his care home with a 24-hour history of deteriorating mental state, agitation and fever. His past medical history is notable for Alzheimer’s disease, benign prostatic hypertrophy and recurrent episodes of urine retention for which he has a long-term indwelling catheter.

On examination, he is hemodynamically stable, but pyrexial and confused. The catheter is draining foul-smelling, turbid yellow urine, and he displays some suprapubic tenderness. Respiratory and cardiovascular examinations are unremarkable. Urine culture reveals evidence of Pseudomonas growth.

Given the likely diagnosis, which antibiotic is most appropriate?

A. Gentamicin

B. Flucloxacillin

C. Trimethoprim

D. Cefotaxime

E. Nitrofurantoin

A

A. Gentamycin

Aminoglycosides are the agents of choice for pseudomonal urinary tract infections. This is also the only anti-pseudomonal agent listed. Quinolones are alternatives often used in cases such as this

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58
Q

Gram staining of cerebrospinal fluid (CSF) is performed, which shows the presence of Gram-negative diplococci.

What is the most likely causative agent of this patient’s meningitis?

A. Streptococcus pneumoniae

B. Herpes simplex virus 2

C. Klebsiella pneumoniae

D. Haemophilus influenzae

E. Neisseria meningitidis

A

E. Neisseria meningitidis

Not: A; S. pneumoniae appearance on Gram staining would be of a Gram-positive diplococci.

Not C: Klebsiella pneumoniae; It is a Gram-negative rod-shaped bacterium that tends to exhibit variable arrangement on staining.

Not D: Haemophilus influenzae:

its appearance on Gram staining would be of a pleomorphic Gram-negative coccobacilli arranged at random.

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59
Q

primary, secondary, tertiary syphilis features

A

Primary syphilis features
Infection occurs 9-90 days after exposure. Lesions are found at the site of inoculation and are often genital or perianal. Lesions tend to be painless and solitary in nature. They are round with an indurated base, and heal within 3-10 weeks.

Secondary Syphilis features
Occurs 4-8 weeks after primary infection. It presents with a maculopapular symmetrical rash on the palms, legs, soles and face. There is also lymphadenopathy and ulcers present on the mucous membranes. Other less common features include malaise and fever

Tertiary Syphilis features
It is rare due to the advent of penicillin, but if found it must be treated with urgently. Tertiary features include syphilitic aortitis, tabes dorsalis, ocular manifestations such as Argyll-Robertson pupil and the presence of granulomatous-type lesions on the skin. If Tertiary Syphilis is confirmed, a CSF examination is indicated in order to test for CNS involvement.

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60
Q

A 50-year-old male presents to the emergency department with fever and lethargy. He has also complained of backache and weight loss over the last 2-3 months. He works as a farmer. On examination, he has a new heart murmur and palpable hepatosplenomegaly. An echocardiogram is performed, which reveals vegetations on the aortic valve, and initial blood cultures are negative.

What is the likely organism responsible?

A

Brucella (Brucella melitensis is the most pathogenic; B abortus is associated with less frequent infection and a greater proportion of subclinical cases).

Brucellosis is a zoonotic infection, and high-risk occupations include farmers and vets. The symptoms are often vague, and complications include subacute and infective endocarditis, which is likely in this case. This form of infective endocarditis is often culture-negative.

Staphylococcus/pseudomonas associated with IV drug users

Clostridium species are often found in the bowels, and endocarditis caused by this should warrant suspicion of colon cancer.

Candida: Fungal endocarditis is seen primarily in patients who are immunocompromised or in those who have prosthetic valves.

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61
Q

what are pandemic features of

A
  1. novel antigenicity (antigenic shift: involves sudden “mixing” of genes from influenza viruses from different species. & antigenic drift: acculumulation of mutations over time; gives rise to influenza vaccine)
  2. efficient replication in airways
  3. efficient transmission between people
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62
Q

2 most important genes in influenza virus:

A
  1. neuraminidase (cleaves sialic acid, facilitates viral release, more prone to antigenic shift, s for shift)
  2. haemagluttinin (binds to sialic acid, facilitates viral entry. especially prone to antigenic drift)
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63
Q

what invesigation determines influenza virus?

A

PCR

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64
Q

what are some influenza antiretrovirals:

A

Neuraminidase inhibitors:
1. oral oseltamivir
2. inhaled zanamivir (can’t give in asthmatics or COPD as it can cause bronchospasm)
3. IV peramivir (if can’t tolerate oral medications)

Endonuclease inhibitor:
-oral baloxavir

M2 antagonist:
-oral amantidine

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65
Q

what feature of influenza viruses causes antigenic shift to occur?

A

multi-segmented viral genome

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66
Q

what presentation of herpes virus indicates potentially uncontrolled HIV:

A

herpes oesophagitis

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67
Q

JC virus is responsible for which clinical entity?

A

PML (progressive multifocal Leukoencephalopathy)

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68
Q

CMV is a member of which viral family

A

herpesvirus (HHV-5)

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69
Q

EMV is a member of which vital family?

A

herpes virus family.
(also known as HHV4)

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70
Q

what is HSV1 associated with?

A

herpes labialis, HSV encephalitis (one; has an e in it–> encephalitis)

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71
Q

what is HSV2 associated with?

A

genital herpes, HSV meningitis

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72
Q

rarer presentations of herpes simplex virus:

A
  1. HSV oesophagitis (AIDS-defining illness)/colitis /herpes gingivostomatitis
  2. Eczema herpeticum
  3. Herpetic whitlow (painful infection of the finger caused by the herpes virus: most common presentation of herpes in HCPs)
  4. Disseminated cutaneous herpes
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73
Q

what is varicella zoster also known as?

A

HHV3

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74
Q

how does chickenpox present?

A

Chickenpox is characterised by widespread, erythematous, raised, vesicular (fluid filled), blistering lesions (first macule then papule then vesicles) .

The rash usually starts on the trunk or face and spreads outwards affecting the whole body over 2 – 5 days. Eventually the lesions scab over, at which point they stop being contagious.

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75
Q

what can opthalmic herpes zoster cause vs Ramsay Hunt syndrome?

A

hutchinson’s sign: vesicles on the tip of the nose (v1 of trigeminal nerve affected–> send to opthalmologist)

RHS: vesicles on ear (affecting facial nerve)
Weakness on one side of the face that causes difficulty closing one eye, eating (food falls out of the weak corner of the mouth), making expressions, and making fine movements of the face, as well as facial droop and paralysis on one side of the face.

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76
Q

what should be avoided in children with chichenpox:

A

Ibuprofen (increased risk of necrotising fascitis)

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77
Q

sequela of Herpes virus?

A

post-herpetic neuralgia

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78
Q

EBV in children

A

posterior cervical chain (symmetrical lymphadenitis) (vs tonsilitis: anterior cervical chain)

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79
Q

EBV presentation:

A

fever, pharyngitis & lymphadenopathy (posterior cervical chain (symmetrical lymphadenitis)),
-also: hepatitis +/- splenomegaly

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80
Q

Diagnosis of EBV suggested by:

A
  1. atypical lymphocytes on blood film
  2. heterophile antibody (monospot test)
  3. EBV serology
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81
Q

avoid of EBV:

A

-avoid alcohol (due to hepatitis)
-avoid high contact sports (splenic rupture risk)

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82
Q

EBV associations:

A
  1. Burkitt’s lymphoma
  2. Post-transplant lymphoproliferative disease
  3. nasopharyngeal carcinoma

(EBV lives dormant in B cells)

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83
Q

CMV presentation:

A

-owl’s eye inclusion bodies
-typically asymptomatic or infectious mononuclosis symptoms
-Can reactivate in immunosuppressive patients /look out for HIV patients(PRCE):
-pneumonitis
-retinitis
-colitis
-encephalitis

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84
Q

HOwl eye mnemonic -

A

Hodgkin (reed-sternberg cells), Owl eye

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85
Q

HHV6 & HHV8:

A

-HHV6–> roseola–> febrile convulsions
-can very rarely cause encephalitis

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86
Q

HHV8 complications:

A
  1. kaposi’s sarcoma esp in HIV patients (purple lesions on skin and GI tract–> can haemorrhage–> treat the immunosuppresion vs treating the cancer)
  2. castleman disease: are disorder that involves an overgrowth of cells in your body’s lymph nodes. The most common form of the disorder affects a single lymph node, usually in the chest or abdomen. This form is called unicentric Castleman disease.
  3. primary effusion lymphoma (B cell)
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87
Q

what does adenovirus cause in immunocompromised patients:

A

(especially transplant): 1. Encephalitis
2. Pneumonitis/pneumonia
3. Colitis
4. haemorrhagic cystitis

88
Q

what does BK virus cause?

A

(worry in transplants: 1. kidney–> BK nephropathy, 2. bone marrow transpalnts–>
BK haemorrhagic cystitis: A condition in which the lining of the bladder becomes inflamed and starts to bleed.)
-difficult to treat as you need to taper down the immunosuppression which may cause transplant to be rejected

89
Q

hep a and e features:

A
  1. present in travellers/faecal-oral transmission/can function as STDs in MSM communities
  2. both acute infections
  3. presentation: incubation period (classically 4-6 weeks)
    -prodromal malaise
    -jaundice, hepatitis, cholestasis
    -resolution 2 months later
90
Q

which group worried about hep A fulminant hepatitis:

A

Elderly population

91
Q

which group worried about hep E fulminant hepatitis:

A

pregnant women

92
Q

what type of hepatitis will hep B cause?

A

acute (>chronic). 5-10% fail to clear acute hep B–> chronic infection (cirrhosis & HCC) younger you are–> more chance being chronic (eg via vertical infection in children)

93
Q

what does hep B surface antibody mean?

A

neutralising antibodies- by definition makes you immune to hep B

94
Q

what do core antibodies in hep B mean?

A

you’ve had the virus in your body (IgM-acute response, IgG-chronic response)
-no core antibodies (never had the virus in you–> have been vaccinated)

95
Q

Hep B serology summary

A
96
Q

HEP C infection sequelae:

A

glomerulonephritis

97
Q

main marker for Hep C infection:

A

viral load (vs serology)

98
Q

how is treatment judged in Hep C:

A

at 12 weeks–> do you have a detectable viral load?
-judged by sustained virologic response (SVR)
-no vaccine

99
Q

classic 1st presentation of HSV1?

A

herpetic gingivostomatitis

100
Q

PUO definition (pyrexia of unknown origin):

A

a persistent fever above 38.3°C (100°F) that evades diagnosis for at least 3 weeks, including 1 week of investigation in hospital.

101
Q

nosocomial meaning:

A

originating in a hospital.

102
Q

what is still’s disease?

A

a rare type of arthritis that is thought to be autoummune or autoinflammatory. It has similar symptoms to systemic-onset juvenile idiopathic arthritis – fever, rash and joint pain. It begins in adulthood, so it’s compared to rheumatoid arthritis

103
Q

treating a weird infection, most likely antibotic:

A

doxycycline

104
Q

presentation of typhoid fever:

A

fever, malaise, headache, epistaxis, constipation
-Faget’s sign (bradycardia with fever, typically expect fever to cause tachycardia in other infections, rose spots (chest/abdomen), hepatomegaly, cytopenias

-lives in peyer’s patches (complication: massive GI haemorrhage/intestinal perforation)

105
Q

presentation of typhoid fever:

A

fever, malaise, headache, epistaxis, constipation
-Faget’s sign (bradycardia with fever, typically expect fever to cause tachycardia in other infections, rose spots, hepatomegaly, cytopenias

106
Q

diagnosis of typhoid fever:

A

Blood/bone marrow culture
-serology (Widal test) or cultures

107
Q

2 buzzwords for dengue:

A

retro-orbital headache
-sunburnt rash

-SE asia (thailand, cambodia)

108
Q

antibiotic for typhoid:

A

IV ceftriaxone then PO azithromycin

109
Q

Bad sequelae of malaria:

A

Shock, ARDS, cerebral malaria, blackwater fever (pronounced dark black urine–>haemolysis, leak haemoglobin into urine–> damages kidney), DIC

110
Q

thick vs thin blood film malaria:

A

thick: malaria, thin: which species (5 species)

111
Q

species of malaria:

A

Falciparum Vs Non-Falciparum
oP. falciparum: most common and most severe (over 48 hours: spikes every 2 days)
o Non-falciparum: P. vivax, P. ovale, P. malariae, P. knowlesi
a) Symptoms as for falciparum but less severe
b) 48hr (tertian) fever (apart from P. malariae – 72hrs)
c) Schüffner’s dots on blood film
d) Rx: chloroquine then primaquine

112
Q

which malaria types cause hypnozoites?

A

P. vivax (as well as P. ovale): lay dormant; can be reactivated later (hypnozoites aren’t treated by antivirals)

113
Q

falciparum malaria treatment:

A

Mild: artemesin combination therapy (Riamet – artemether + lumefantrine)
- Severe (eg clinically severe illness, parasitaemia >2%, hypoglycaemia, metabolic/lactic acidosis, severe anaemia): IV artesunate

114
Q

features of severe or complicated malaria in adults vs children:

A

Features of severe or complicated malaria in adults include:

  1. Shock
  2. Cerebral malaria — impaired conscious level (Glasgow coma score less than 11) or seizures
  3. Renal failure
  4. Haemoglobinuria — P. falciparum can cause severe haemolysis with dark red urine (‘blackwater fever’)
  5. Hypoglycaemia (< 2.2 mmol/L)
  6. Acidosis
  7. Sepsis — more common in pregnant women
  8. DIC
  9. Respiratory distress which may be due to pulmonary oedema or acute respiratory distress syndrome (ARDS) — common in pregnant women
  10. Parasitaemia > 10%
  11. Severe anaemia

Features of severe or complicated malaria in children include:

  1. Respiratory distress or acidosis (may present with acidotic breathing)
  2. Hypoglycaemia (< 2.2 mmol/L).
  3. Severe anaemia
  4. Cerebral malaria (as above)
  5. Parasitaemia > 2% red blood cells parasitized.
  6. Inability to stand or sit
115
Q

Brucellosis buzzwords:

A

contracted from raw dairy & farm animals
-aka “undulant fever”=evening fever
-epidural abscess & epididimo-orchitis

116
Q

how does rabies present/management:

A

excess salivation, hydrophobia, affects CNS: furious & dumb rabies

-contracted from animals; dogs & bats

-Negri body pathognomic (inclusion body in neurones)

-If infected: vaccine & immunoglobulins

117
Q

rabies treatment:

A

-only treat it before they’re symptomatic

118
Q

what transmits plague?

A

rat fleas (yersinia pestis)

119
Q

how does plague present?

A

o Bubonic plague–fleabites human–Swollen LN( Bubo: big axillary/inguinal lymph nodes that are filled with dense black fluid when you aspirate)–dry gangrene

o Pneumonic plague–Usually seen during epidemics, person-persons pread

120
Q

plague diagnosis/treatment :

A

PCR (p for plague)
-doxycycline

121
Q

how is infection caused in leptospirosis?

A

rat urine (eg swimming in lake/rivers/exposure to stagnant water)

122
Q

buzzwords for leptospirosis:

A

jaundice, conjunctival suffusion eg inflamed eye with hepatomegaly (dry conjunctivitis without exudate)
-Mx: doxycycline

123
Q

bartonella aka:

A

cat scratch fever (caused by bartonella henselae)

124
Q

presentation of bartonella:

A

painless erythematous crusted papule at scratch site
-parinaud oculoglandular syndrome (big lymph nodes & conjunctivitis)

125
Q

lyme disease transmission:

A

Ixodes tick (Borrelia spp)

126
Q

lyme disease presentation:

A

erythema migrans (bullseye rash; diagnosed clinically) , arthralgias, Cardiac problems

127
Q

Leishmaniasis presentation:

A

-transmitted by sandflies

Microscopy; protozoa
-liposomal amphoteracin B (treatment for visceral; easier to treat vs cutaneous form; hard to treat)

128
Q

Anthrax transmission/presentation:

A

wild animals
Anthrax - Bacillus anthracis
* Cutaneous: Painless round black lesions + rim of oedema
* Pulmonary: Massive lymphadenopathy + mediastinal haemorrhage

-eschar: incoluted through skin (painless, necrotic skin lesion)
-widened mediastinum (pulmonary problems)

129
Q

organism causing tinea infections/dermatophytoses:

A

Trichophyton rubrum

130
Q

organism causing pityriasis versicolor:

A

Malassezia furfur

131
Q

treatment of severe candida:

A

Treat with amphoteracin B/echinocandins if severe infection

132
Q

treatment of tinea capitis/unguium:

A

oral antifungals (systemic vs topical): (oral azole antifungal but azoles are more prone to cause hepatic injury, terbinafine)

133
Q

diagnosis with cultures of candida (vs aspergillosis):

A

positive beta-D glucan (D for candida) and negative galactomannan

Vs

aspergillus (g and L in aspergillus and beta-D GLucan, P in Aspergillus; both positive); galactomannan & positive beta-D glucan
-A negative galactomannan test result suggests the absence of Aspergillus infection (double letters: aspergiLLus and galactomaNNan)

134
Q

how is sporotrichosis contracted:

A

rose thorns
-necrotic rash
-abscesses in bones, joints & CNS

135
Q

what does murcomyosis cause:

A

rhinocerebral infection, necrotic faces
-vascular invasion (high mortality)

136
Q

causes of Prion disease:

A
  1. Sporadic (80%): Creutzfeld-Jakob disease [BUZZWORDs = rapid <1yr decline]
  2. Genetic (15%):
    ● Gerstmann-Straussler-Scheinkler syndrome (GSS)
    ● Fatal familial insomnia (insomnia, paranoia, hallucinations)
  3. Acquired (<5%):
    ● Kuru [BUZZWORD = cannibalism, Papa new guinea]
    ● Variant CJD (linked to bovine spongiform encephalopathy a.k.a. mad cow disease: eating cows affected, prion protein found in tonsils: tonsilar biopsy is specific for variant CJD)
    ● Iatrogenic CJD (following flood transfusions of surgical procedures)
137
Q

A 25 year old female presents to A&E with a 3 day history of fever and bilateral painless parotid swelling. She also complains of right sided hearing loss. She has no other past medical history. There are no other abnormalities on physical examination.

Which is the next best investigation to confirm the diagnosis?

A

Salivary IgM testing

This is the diagnostic test for mumps, which detects mumps IgM antibodies. Mumps causes parotid swelling and occasionally sensorineural hearing loss. Reverse transcriptase PCR on an oral swab may also be performed

Not: Serum angiotensin converting enzyme (ACE) levels: This is a test for sarcoidosis, which may cause parotid swelling and hearing loss due to cranial nerve involvement. However, extrapulmonary sarcoidosis affecting only the parotids is rare; this should be considered after infective causes such as mumps have been ruled out

Not: Sialogram;
This is involves injection of contrast into a salivary duct and visualisation on X-ray. This may be used to investigate obstructions (unlikely as it is painless), neoplasms, and to rule out other salivary gland pathology in the absence of acute infection

Not: Antinuclear antibodies, anti-Ro, anti-La and rheumatoid factor; This would be useful in diagnosing Sjogren’s syndrome. However, this is unlikely given the fever and acute onset suggesting an infective aetiology

138
Q

E.coli gram stain:

A

gram negative rod

139
Q

listeria monocytogenes/treatment::

A

gram-positive rod, amoxicillin

140
Q

HSV or varicella treatment vs
EBV or CMV:

A

HSV or varicella –> aciclovir
EBV or CMV–> ganciclovir

141
Q

Hep A features:

A

travel history (eg India/south america), no history of IVDU, not sexually active, presents with flu-like symptoms, RUQ pain, tender hepatomegaly and deranged LFTs

142
Q

who should be vaccinated with Hep A vaccine?

A

an effective vaccine is available
-after the initial dose a booster dose should be given 6-12 months later

Who should be vaccinated? (Based on the Green book guidelines)
1. people travelling to or going to reside in areas of high or intermediate prevalence, if aged > 1 year old
2. people with chronic liver disease
patients with 3. haemophilia
4. men who have sex with men (MSM)
5. injecting drug users
6. individuals at occupational risk: laboratory worker; staff of large residential institutions; sewage workers; people who work with primates

143
Q

Men who have sex with men should be offered immunisation against:

A

Hepatitis A (no Hep C vaccination)

144
Q

which antibiotics cause C difficile? Treatment: complication:

A

4Cs: ciprofloxacin, cephalosporins, co-amoxiclav, clindamycin

-vancomycins or metronidazole

-pseudomembranous colitis

145
Q

4 mechanisms of antibiotic resistance (mnemonic):

A

BEAT
1.BYPASS antibiotic-sensitive step in pathway
2. ENZYME-mediated drug inactivation eg betalactamases
3. Impairment of ACCUMULATION of the drug eg tetracycline resistance
4. modification of the drug’s TARGET eg quinolone resistance

146
Q

strep strains and endocarditis:

A
147
Q

antibiotic classes

A

protein synthesis inhibitors: MALT (macrolides, aminoglycosides, lincosamides, tetracyclines) or TAMCO:

Tetracyclines (e.g. Doxycycline)

Aminoglycosides (e.g. Gentamicin)

Macrolides (e.g. Erythromycin)

Chloramphenicol

Oxazilidinediones

(TA): Aminoglycosides and Tetracyclines work by binding to the 30S subunit of ribosomes.

(MC): Macrolides and Chloramphenicol work by binding to the 50S subunit of ribosomes.

Oxazilidinediones works by binding to the 23S component of the 50S subunit of ribosomes.

148
Q

Which class of antibiotics has concentration dependent killing (i.e. the goal of therapy is to maximise peak > MIC)

A

Class 1 (concentration dependent): Aminoglycosides: act on 30s subunit

149
Q

Man has recently returned from trip to India, has high fever and abdominal pain but no diarrhoea. His blood cultures - gram-ve bacilli. Malaria rapid diagnostic test is -ve. What is the most appropriate antibiotic therapy?

A

IV ceftriaxone then PO azithromycin

Typhoid assumed: not diarrhoea (usually it causes constipation), gram negative bacilli (salmonella typhi), India=endemic for typhoid.

150
Q

what gram stain is TB?

A

tuberculosis is an acid-fast bacterium (AFB), and is therefore, undetectable when stained using a Gram stain technique
(is considered a gram-positive bacterium rod , although it does not strictly follow the gram-positive or gram-negative classification due to its unique cell wall structure.)

151
Q

Elderly woman has 24 hour history of headache, confusion, photophobia, fever. Gram stain of CSF shows gram+ve rods. What is the causative organism?

A

Listeria monocytogenes (affects extremes of age: neonates & elderly)

152
Q
A

Yersinia pestis (causes plague. black aspirate)

153
Q

Which human herpes virus is associated with post transplant lymphoproliferative disorder?

A

EBV (HHV4)

154
Q

which microorganism gram +ve cocci “grape-bunch clusters”

A

staphylococcus aureus

155
Q

Moraxella catarrhalis gram stain & shape:

A

gram negative cocci

156
Q

Klebsiella pneumoniae gram stain & shape:

A

Gram-negative rod-shaped bacterium that tends to exhibit variable arrangement on staining.

157
Q

what ab is given for cellulitis if patient is penicillin allergic:

A

clindamycin (macrolide)

158
Q

Patient receiving chemotherapy for leukaemia. She has prolonged neutropenia and ongoing fever, raised inflammatory markers despite broad antibacterial therapy with meropenem and amikacin. CT scan shows multiple nodules with surrounding hypo-attenuation (halo sign). What is the most likely organism?

A

Aspergillus fumigatus

The presence of multiple nodules with surrounding hypo-attenuation (halo sign) on CT scan in a patient with prolonged neutropenia and ongoing fever, despite broad-spectrum antibacterial therapy, is highly suggestive of invasive fungal infection. The halo sign indicates that there is an area of ground-glass attenuation around a nodule, which is caused by the presence of edema and inflammation. In this case, the most likely organism is an invasive mold, such as Aspergillus. Therefore, antifungal therapy, such as voriconazole or liposomal amphotericin B, should be started as soon as possible.

159
Q

Young woman has severe headache, neck stiffness, fever. She is HIV+ve but is poorly compliant with medication, does not attend her appointments. She has yeasts in her CSF. What is the causative organism?

A

Cryptococcus neoformans,

Cryptococcal meningitis is a fungal infection caused by the encapsulated yeast Cryptococcus neoformans, which commonly affects immunocompromised individuals, including those with HIV/AIDS. Noncompliance with antiretroviral therapy and poor immune status can increase the risk of developing cryptococcal meningitis. Treatment typically involves a combination of antifungal medications, including amphotericin B and flucytosine, followed by long-term maintenance therapy with fluconazole.

160
Q

Aid worker returns from camp in Yemen. He has profuse watery diarrhoea, which looks like water rice has been cooked in. He is very dehydrated. What is the likely cause of his diarrhoea?

A

Vibrio cholera

161
Q

Poorly controlled person with T2DM has headache, sinus pain, periorbital oedema and orbital cellulitis. His symptoms have progressed rapidly. He has purulent discharge from his nose. ENT surgeons bring him to theatre as an emergency. What antifungal therapy should be started ASAP?

A

voriconazole

The patient’s symptoms suggest a fungal infection, specifically invasive fungal sinusitis. The most common cause of invasive fungal sinusitis is Aspergillus species. Voriconazole is the drug of choice for invasive aspergillosis. Therefore, the antifungal therapy that should be started ASAP for this patient is voriconazole.

162
Q

What is Praziquantel used to treat?

A
  1. Schistosoma ((bilharzia): infection with a type of worm that lives in the bloodstream)
  2. Liver fluke (infection with a type of worm that lives in or near the liver)
163
Q

What is the most common imported non-GI helminth?

A

Schistosomiasis

164
Q

Describe the life cycle of schistosomiasis

A

Parasitic disease

(Cercariae invade human skin when in contact with contaminated water. Worms develop in venous plexus. Eggs excreted in faeces/ urine which then hatch and deposit)

  1. Eggs: The life cycle begins when Schistosoma eggs are passed in the feces or urine of an infected person into freshwater sources such as lakes, rivers, and streams.
  2. Miracidia: In freshwater, the eggs hatch and release miracidia, which are free-swimming larvae that must infect a specific freshwater snail species in order to develop further.
  3. Sporocysts: Once inside the snail, the miracidia transform into sporocysts, which then produce thousands of cercariae, the infective stage for humans.
  4. Cercariae: Cercariae are released from the snail into freshwater and can penetrate the skin of humans who come into contact with contaminated water while swimming, bathing, or working.
  5. Schistosomula: Once inside the human host, the cercariae shed their tails and transform into schistosomula, which migrate through the bloodstream and tissues to reach their final destination in the veins surrounding the bladder, intestines, or liver.
  6. Adult worms: The schistosomula mature into adult male and female worms that mate and produce eggs. The female worms deposit eggs in the walls of the host’s blood vessels, which then pass out of the body through faeces or urine, completing the life cycle.
165
Q

Who are the definitive hosts in schistosomiasis?

A

Humans

166
Q

Where is schistosomiasis mostly found?

A

Central-Southern Africa (also Lake Malawi: East African Rift system and Egypt: AbdelHalim Hafiz swimming in river Nile)

167
Q

symptoms of schistosomiasis:

A

The symptoms of schistosomiasis can range from mild to severe and can include itching, rash, fever, abdominal pain, and blood in the urine or stool.

Long-term infection can lead to chronic illness, such as liver and bladder damage, and an increased risk of bladder cancer.

168
Q

What is the name of the bacteria we find in urine microscopy in schistosomiasis?

A

Schistosoma haematobium

169
Q

What is the treatment for schistosomiasis?

A

Praziquantel

170
Q

How is hookworm transferred?

A
  1. Infected feces: An infected person or animal passes hookworm eggs in their feces, which then contaminate the soil in areas where sanitation and hygiene are poor.
  2. Larvae in soil: In warm and moist conditions, hookworm eggs hatch into larvae that can survive in the soil for weeks to months.
  3. Penetration of skin *(transdermal): When a person or animal comes into contact with contaminated soil, the hookworm larvae can penetrate the skin of the feet or legs and enter the bloodstream.
  4. Migration to lungs: The larvae migrate through the bloodstream to the lungs, where they can cause respiratory symptoms such as coughing and wheezing.
  5. Swallowing: The larvae are then coughed up and swallowed, where they pass through the digestive system to reach the small intestine.
  6. Adult worms: Once in the small intestine, the larvae develop into adult worms that attach to the intestinal wall and feed on blood, causing anemia.
171
Q

Which parasite is transferred through food?

A

Ascaris

172
Q

What is the location of the ascaris worm in the host?

A

Human blood vessel

-Ascaris lumbricoides is a parasitic roundworm that can infect humans. After a person ingests the eggs of Ascaris, they hatch in the small intestine and release larvae, which then penetrate the intestinal wall and enter the bloodstream. The larvae are carried to the lungs, where they break out of the bloodstream and migrate up the airways to the throat. The infected person then swallows the larvae, which are carried back to the small intestine, where they mature into adult worms.

173
Q

What is myiasis?

A

Parasitisation of human flesh by fly larvae (maggots)

174
Q

Which is the most common human worm infection?

A

The most common human worm infection is caused by the roundworm species called Ascaris lumbricoides

175
Q

Which is the worm that ‘comes out of your leg?’

A

Guinea worm (also known as dracunculiasis)

176
Q

Someone stands in sand with contaminated dog poo. What is the likely helminth?

A

Hookworm (transdermal infection)
- Toxocara canis is a common parasite found in the intestines of dogs, particularly puppies.

177
Q

What would an average parasite screen include?

A
  1. Stool examination - This is a microscopic examination of a patient’s stool sample to detect the presence of parasite eggs, larvae, or adult forms. Various techniques such as direct wet mount, concentration methods, and staining may be used to improve the sensitivity of the test.
  2. *Serology - This is a blood test that detects antibodies against specific parasites, indicating the presence of a current or past infection. Serology can be particularly useful in detecting parasitic infections that may not be detected by stool examination.
    Serology: Strongyloides, schistosoma, filaria
  3. Imaging studies - Imaging tests such as X-rays, CT scans, or ultrasound may be used to detect the presence of parasites in specific organs or tissues, such as the liver, spleen, or lungs.
  4. Biopsy - In some cases, a tissue biopsy may be necessary to confirm the presence of parasites in organs or tissues.
178
Q

Which are the three types of helminths? (mnemonic)

A

Cestode, nematode, trematode (CeNT)

179
Q

Fluke is which form of helminth?

A

Trematode

180
Q

Pork, beef and fish tape worms are which kind of worms?

A

Cestodes, which are a group of parasitic flatworms that include tapeworms.
beef=Taenia saginata

181
Q

Which are the three roundworms? (mnemonic)

A

ASH:
-ascarid
-strongyloides
-hookworm

182
Q

Humans eating undercooked pork are most likely to ingest which helminth?

A

Humans eating undercooked pork are most likely to ingest the larvae of Taenia solium, also known as the pork tapeworm

183
Q

What is the scientific name of the pork tapeworm?

A

Taenia solium

184
Q

What is a hydatid?

A

A dog tapeworm

185
Q

What is the typical host for filariasis?

A

Filariasis is a parasitic disease caused by thread-like filarial nematodes (roundworms) that are transmitted to humans through the bites of infected mosquitoes.

Therefore, while humans are the definitive host for filarial nematodes, mosquitoes are the intermediate hosts that carry and transmit the parasites from one human to another.

186
Q

What condition is a fetus at risk of if its mother is infected by Parvovirus B19?

A

Hydrops Fetalis

187
Q

what is the regimen for RIPE medication for TB (& side effects):

A

The standard first-line treatment regime for Mycobacterium tuberculosis lung infection is RIPE:

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
All four antibiotics are given for 2 months. Rifampicin and Isoniazid are continued for a further 4 months.

Side effects of TB medication include:

Rifampicin: Hepatotoxicity (deranged LFTs), Drug interactions (induces cytochrome P450), Orange secretions

Isoniazid: Hepatotoxicity, Peripheral neuropathy

Pyrazinamide: Hepatotoxicity, Hyperuricaemia

(RIP: hepatotoxicity)

Ethambutol: Optic neuritis

188
Q

Aminoglycosides act on which part of the bacterial ribosome?

A

30s subunit

189
Q

what groups of antibiotics work by inhibiting protein synthesis (mnemonic)?

A

TAMCO:

Tetracyclines (e.g. Doxycycline)

Aminoglycosides (e.g. Gentamicin)

Macrolides (e.g. Erythromycin)

Chloramphenicol

Oxazilidinediones

190
Q

A patient with suspected meningitis is asked by their consultant to lie supine, with a flexed hip and knee.

The consultant passively extends both knees slowly. However, the patient stops the doctor and refuses to extend the knee past 120 degrees of flexion due to pain.

What sign has the consultant elicited?

A

Kernig’s Sign

191
Q

In what cell in the human body do Leishmania parasites multiply?

A

macrophages

Leishmaniasis is a protozoan disease spread by sandflies. Leishmania parasites multiply inside macrophages in the human body.

It is endemic in Africa, India and South/Central America. The areas of highest prevalence include Brazil, East Africa and India.

There are three main forms of the disease:

  1. Cutaneous Leishmaniasis

This is a skin infection classically presenting with an open sore where the patient was bitten. It is classically poorly healing, taking up to a year to resolve and often scars.

They are typically ulcerative, plaque or verruca like affecting readily exposed skin, such as forearms or shins.

This is generally managed conservatively unless the patient is at high risk. In

  1. Mucocutaneous Leishmaniasis

This form of leishmaniasis causes skin and mucosal ulcers of the nose and mouth.

This is generally treated. Examples of therapies include sodium stibogluconate, liposomal amphotericin B or meglumine antimonate.

  1. Visceral leishmaniasis (“black fever”: kala azar)

Here, the parasite migrates to the liver, spleen and bone marrow.

Signs and symptoms include (massive) splenomegaly, hepatomegaly. Otherwise, symptoms are nonspecific and include fever, weight loss, lethargy and anaemia. Rarely, hyperpigmentation of skin may occur - leading to the name “black fever”.

High mortality is associated with this condition due to concomitant bacterial infections due to the progressive destruction of the reticulo endothelial system (tissue resident macrophages in the liver and spleen).

It is diagnosed with microscopy of splenic or bone marrow aspirate.

This is generally treated with amphotericin B and a combination of other anti-leishmanial drugs.

192
Q

There is an outbreak of diarrhoea and vomiting on a cruise ship.

The onset of symptoms in affected individuals is sudden and lasts for a few days. Spread of the virus has not been abated despite the rigorous use of alcohol gel by patrons aboard.

Affected individuals have eaten different food prepared in different kitchens.

What is the likely pathogen responsible?

A

Norovirus (secretory diarrhoea, adult outbreaks, self-limiting)

193
Q

What is the recommended antibiotic prophylaxis for bites by either cat, dog or human in a patient with no known allergies?

A

Co-amoxiclav

194
Q

A 26 year old IV drug user is diagnosed with infective endocarditis. He described a short history, with symptoms appearing over a period of three weeks, culminating in admission to the hyperacute stroke unit following a stroke.

A transthoracic echocardiogram reveals a vegetation on the tricuspid valve.

What organism is most likely responsible?

A

Staphylococcus Aureus is the best answer here. It is the most commonly implicated organism in IVDU associated infective endocarditis.

195
Q

criteria for endocarditis (mnemonic):

A
196
Q

endocarditis mnemonic:

A

FROM JANE
F: fever.
R: Roth’s spots.
O: Osler’s nodes ( on the tip of the finger or toes and painful)
M: murmur of heart.
J: Janeway lesions ( occur on palm and soles and are non-painful): n for non-painful
A: anaemia.
N: nail haemorrhage.
E: embolism.

197
Q

Acute vs subacute endocarditis differences/causes:

A
  • Acute: fulminant illness, pt is very unwell
  • Subacute: over weeks-months, pt less unwell, more signs O/E (see below)

Pathogens:

  • Acute (high-virulence bacteria): Strep pyogenes (Group A Strep), Staph aureus
    (most common in IVDU), CoNS (most common in prosthetic valve)
    -acute usually from IVDU
    -subacute usually from dental procedures
  • Subacute (low-virulence bacteria): Staph epidermidis, Strep viridans,
    HACEK (uncommon causes and do not grow cultures)
    consider if high suspicion but culture -ve
    H-Haemophilus
    A-Acinetobacter
    C-Cardiobacterium
    E- Eikinella
    K- Kingella
198
Q

A patient is suspected to have a community acquired pneumonia. Their CRB 65 is 3 and they have no known allergies.

In addition to clarithromycin, what is the other first line antibiotic that should be prescribed for this patient?

A

Co-amoxiclav

199
Q

spectrum of antibiotics summary

A
200
Q

What class of antibiotics does ceftriaxone belong to?

A

Third generation cephalosporin (broader group: beta lactams which inhibit cell wall synthesis including 1. penicillins, 2. cephalosporins, 3. carbapenems

201
Q

Cancer of what organ is commonly associated with schistosomiasis infection?

A

Bladder cancer

202
Q

What growth medium is used to differentiate Streptoccoci in the laboratory setting?

A

Blood agar

Classifying Streptococci

All streptococci can be split into two groups - alpha haemolytic (incubated on blood agar, the agar will turn green [partial haemolysis]) and beta haemolytic (incubated on blood agar, the agar goes clear [full haemolysis]).

Note that alpha haemolytic is not the same as Group A and similarly for group B/beta haemolytic - they are different things

Beta Haemolytic (pale blood agar) -> Lancefield Grouping

Most other streptococci can be further classified by their Lancefield grouping. It has largely fallen out of use in the scientific world, except in medicine for some reason.

There are Lancefield groups A - L

Here are the main pathogens in each lancefield group:

(PAE ABD)
Group A - Streptococcus pyogenes (skin infections, nec fasc)
Group B - Streptococcus agalactiae (neonatal infection)
Group D - Enterococci
Alpha haemolytic (green blood agar)

2 main pathogens - Streptococcus pneumoniae and Streptococcus viridans.

These pathogens do not have any Lancefield antigens.

203
Q

intrapartum antibiotics for chorioamnionitis (mnemonic):

A

GBM
-IV gentamicin, benzylpenicillin and metronidazole

204
Q

What fungal antigen may be detected in blood samples in a patient with invasive aspergillosis?

A

Galactomannan (double N GalactomaNNan: and double L: AspergiLLus)

205
Q

ways of diagnosing fungal infections:

A

Diagnosing Fungal Infection

  1. The gold standard for diagnosing fungal infection is culture - however, this takes ages and a large number of fungi do not culture well. Hence, we use proxy measures for identifying fungal infection.
  2. Chemical Reaction

Potassium hydroxide mixed with nail/skin clippings is a decent diagnostic test for the presence of tinea or trycophyton (skin fungal infections)

  1. Microscopy

This may be used for diagnosis of:
1. Cryptococcus (india ink staining)
2. Pneumocystis (Silver staining or Periodic acid-Schiff stain)
3. Candida (Periodic Acid-Schiff or methenamine silver stain)
4. Aspergillus (Methenamine Silver Stain or PAS stain)

  1. Fungal serology

Used in histoplasmosis

  1. Antigenic tests

Significant false positive rate (may be falsely positive due to beta-lactam antibiotic [fungal product] administration)

  1. Cryptococcus Glucuronoxylomannan (GXM)
  2. Aspergillus Galactomannan
  3. Candida/Asperg/PCP Beta-D-Glucan

The future will be PCR testing but for now this is what we’re left with

206
Q

PCP tests:

A
  1. PCR
  2. Microscopy
    a) Silver staining with Gomori’s methenamine-silver stain of Pneumocystis cysts in lung tissue Cysts contain one to eight sporozoites within
    b) Periodic acid-Schiff stain: PAS)
  3. Antigenic tests with Beta-D-Glucan
207
Q

To the nearest 10%, what is the lifetime risk of latent TB reactivation in an immunocompetent individual?

A

10%

208
Q

blood diarrhoea (dysentery) causes (mnemonic):

A

: (SEECSY sounds like SEXY)

Escherichia coli O157:H7 =EHEC

209
Q

How is Q fever typically diagnosed?

A

Serology

Q Fever (Coxiella Burnetii) is a disease characterised by abrupt onset of flu-like symptoms, fever, headache, muscle pain, chills which may progress (for exam purposes) to an atypical pneumonia and ARDS or endocarditis. However, most patients are asymptomatic.

Diagnosis is via serology and it is treated effectively with doxycycline or ciprofloxacin. Only one bacterium is required to cause infection.

Typically Q fever is transmitted via contaminated dust or contact with the bodily fluids of infected animals (milk, urine, feces of cows, sheep, goats)

Typically only found in people at high risk of infection e.g. vets, farmers

210
Q

what microorganism causes Q fever?

A

Coxiella Burnetii

211
Q

What specific histological stain is used for Mycobacterium tuberculosis?

A

Ziehl Neelsen stain

212
Q

what culture medium is used for TB?

A

Lowenstein-Jensen medium

213
Q

difference between Ziehl Neelsen and Lowenstein-Jensen

A

Ziehl Neelsen is a stain for Mycobacterium vs Lowenstein-Jensen is a medium to culture it

acid fast rods seen in Ziehl Neelsen stain

Buff and rough (brown coffee coloured and breadcrumb shaped & tough) appearance on Lowenstein-Jensen culture

214
Q

What viral protein is responsible for the virulence and tropism of SARS-CoV-2?

A

Spike protein

SARS-CoV-2 is a member of the Coronaviridae family.

It is a small, single stranded RNA virus with the ability to cause Coronavirus Disease 19 (COVID-19) in humans.

Its main proteins include the S protein (required for binding to ACE2 on human cells) and the N protein - the nucleocapsid.

215
Q

A pregnant woman at term (38+3) has her urine dipped which shows the presence of nitrites and leukocytes.

However, she denies any dysuria or other symptoms.

If indicated, what is the first line antibiotic for the treatment of this patient?

(If you do not feel an antibiotic is indicated, type “N/A”)

A

Cefalexin (or amoxicillin)

Nitrofurantoin is not recommended in late pregnancy due to the risk of neonatal hemolytic anemia.

216
Q

A fine art student travels to New York, where he eats scrambled eggs.

12 hours later, he becomes unwell with profuse diarrhoea. There is no blood. He has diffuse abdominal pain with pain that comes and goes in waves.

What organism is likely responsible for his symptoms?

A

Salmonella enterica

Salmonella enterica is commonly associated with foodborne illness and can cause symptoms such as vomiting, diarrhea, and abdominal pain.

The consumption of undercooked eggs is a known risk factor for Salmonella enterica infection.

A possible differential is campylobacter, but this is typically associated with undercooked chicken and often produces bloody diarrhoea.

Staphylococcus aureus typically has a more rapid onset (1-2 hours). Viral gastroenteritis often isn’t preceded by a foodborne trigger, as the incubation period is days.