Infection Flashcards
(620 cards)
1
Q
Q: What is the most common cause of acute pyelonephritis?
A
A: Ascending infection, typically E. coli from the lower urinary tract.
2
Q
Q: How can acute pyelonephritis also occur aside from ascending infection?
A
A: Through bloodstream spread of infection, such as in sepsis.
3
Q
Q: What are the clinical features of acute pyelonephritis?
A
A: Fever, rigors, loin pain, nausea/vomiting, and symptoms of cystitis (dysuria, urinary frequency).
4
Q
Q: What symptoms of cystitis may be present in acute pyelonephritis?
A
A: Dysuria and urinary frequency.
5
Q
Q: What investigation should be done before starting antibiotics in acute pyelonephritis?
A
A: A mid-stream urine (MSU) sample should be sent.
6
Q
Q: When should hospital admission be considered for acute pyelonephritis?
A
A: For patients with signs of acute pyelonephritis.
7
Q
Q: What is the recommended antibiotic treatment for acute pyelonephritis according to the BNF?
A
A: A broad-spectrum cephalosporin or a quinolone (for non-pregnant women) for 7-10 days.
8
Q
Q: What causes amoebiasis?
A
A: Entamoeba histolytica (an amoeboid protozoan).
9
Q
Q: How is amoebiasis spread?
A
A: By the faecal-oral route.
10
Q
Q: What are the possible clinical presentations of amoebiasis?
A
A: Asymptomatic infection, mild diarrhoea, or severe amoebic dysentery.
11
Q
Q: What serious conditions can amoebiasis cause?
A
A: Liver and colonic abscesses.
12
Q
Q: What are the symptoms of amoebic dysentery?
A
A: Profuse, bloody diarrhoea.
13
Q
Q: What can be seen in stool microscopy for amoebic dysentery if examined within 15 minutes or kept warm?
A
A: Trophozoites (known as a ‘hot stool’).
14
Q
Q: What is the treatment for amoebic dysentery?
A
A: Oral metronidazole and a ‘luminal agent’ (e.g., diloxanide furoate).
15
Q
Q: Where is an amoebic liver abscess usually located?
A
A: Usually a single mass in the right lobe, but it may be multiple.
16
Q
Q: How are the contents of an amoebic liver abscess often described?
A
A: As ‘anchovy sauce’.
17
Q
Q: What are the features of an amoebic liver abscess?
A
A: Fever, right upper quadrant pain, systemic symptoms (e.g., malaise), and hepatomegaly.
18
Q
Q: What investigations are used for an amoebic liver abscess?
A
A: Ultrasound and serology (positive in > 95%).
19
Q
Q: What is the management for an amoebic liver abscess?
A
A: Oral metronidazole and a ‘luminal agent’ (e.g., diloxanide furoate).
20
Q
Q: What is the most common organism isolated from animal bites, especially from dogs and cats?
A
A: Pasteurella multocida.
21
Q
Q: How should an animal bite wound be managed?
A
A: Cleanse the wound, and puncture wounds should not be sutured unless cosmesis is at risk.
22
Q
Q: What is the current BNF recommendation for treating animal bites?
A
A: Co-amoxiclav.
23
Q
Q: What should be prescribed if the patient is allergic to penicillin for an animal bite?
A
A: Doxycycline + metronidazole.
24
Q
Q: What type of infection do human bites commonly cause?
A
A: Multimicrobial infection, including both aerobic and anaerobic bacteria.
25
Q: What is the recommended treatment for human bites?
A: Co-amoxiclav, as for animal bites.
26
Q: What viral infections should be considered in human bites?
A: HIV and hepatitis C.
27
Q: What causes anthrax?
A: Bacillus anthracis, a Gram-positive rod.
28
Q: How is anthrax spread?
A: By infected carcasses.
29
Q: What are the features of cutaneous anthrax?
A: Causes painless black eschar (cutaneous 'malignant pustule'), typically painless and non-tender, may cause marked oedema.
30
Q: Can anthrax cause gastrointestinal symptoms?
A: Yes, anthrax can cause gastrointestinal bleeding.
31
Q: What is the current Health Protection Agency advice for the initial management of cutaneous anthrax?
A: Ciprofloxacin.
32
Q: What is the recommended treatment for exacerbations of chronic bronchitis?
A: Amoxicillin or tetracycline or clarithromycin.
33
Q: What is the recommended treatment for uncomplicated community-acquired pneumonia?
A: Amoxicillin (Doxycycline or clarithromycin in penicillin-allergic patients, add flucloxacillin if staphylococci suspected, e.g., in influenza).
34
Q: What is the recommended treatment for pneumonia possibly caused by atypical pathogens?
A: Clarithromycin.
35
Q: What is the recommended treatment for hospital-acquired pneumonia within 5 days of admission?
A: Co-amoxiclav or cefuroxime.
36
Q: What is the recommended treatment for hospital-acquired pneumonia more than 5 days after admission?
A: Piperacillin with tazobactam OR a broad-spectrum cephalosporin (e.g., ceftazidime) OR a quinolone (e.g., ciprofloxacin).
37
Q: What is the recommended treatment for lower urinary tract infection?
A: Trimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporin.
38
Q: What is the recommended treatment for acute pyelonephritis?
A: Broad-spectrum cephalosporin or quinolone.
39
Q: What is the recommended treatment for acute prostatitis?
A: Quinolone or trimethoprim.
40
Q: What is the recommended treatment for impetigo?
A: Topical hydrogen peroxide, oral flucloxacillin or erythromycin if widespread.
41
Q: What is the recommended treatment for cellulitis?
A: Flucloxacillin (clarithromycin, erythromycin, or doxycycline if penicillin-allergic).
42
Q: What is the recommended treatment for cellulitis near the eyes or nose?
A: Co-amoxiclav (clarithromycin + metronidazole if penicillin-allergic).
43
Q: What is the recommended treatment for erysipelas?
A: Flucloxacillin (clarithromycin, erythromycin, or doxycycline if penicillin-allergic).
44
Q: What is the recommended treatment for animal or human bites?
A: Co-amoxiclav (doxycycline + metronidazole if penicillin-allergic).
45
Q: What is the recommended treatment for mastitis during breast-feeding?
A: Flucloxacillin.
46
Q: What is the recommended treatment for throat infections?
A: Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic).
47
Q: What is the recommended treatment for sinusitis?
A: Phenoxymethylpenicillin.
48
Q: What is the recommended treatment for otitis media?
A: Amoxicillin (erythromycin if penicillin-allergic).
49
Q: What is the recommended treatment for otitis externa?
A: Flucloxacillin (erythromycin if penicillin-allergic).
50
Q: What is the recommended treatment for a periapical or periodontal abscess?
A: Amoxicillin.
51
Q: What is the recommended treatment for acute necrotising ulcerative gingivitis?
A: Metronidazole.
52
Q: What is the recommended treatment for gonorrhoea?
A: Intramuscular ceftriaxone.
53
Q: What is the recommended treatment for chlamydia?
A: Doxycycline or azithromycin.
54
Q: What is the recommended treatment for pelvic inflammatory disease?
A: Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole.
55
Q: What is the recommended treatment for syphilis?
A: Benzathine benzylpenicillin or doxycycline or erythromycin.
56
Q: What is the recommended treatment for bacterial vaginosis?
A: Oral or topical metronidazole or topical clindamycin.
57
Q: What is the recommended treatment for the first episode of Clostridioides difficile infection?
A: Oral vancomycin.
58
Q: What is the recommended treatment for the second or subsequent episode of Clostridioides difficile infection?
A: Oral fidaxomicin.
59
Q: What is the recommended treatment for Campylobacter enteritis?
A: Clarithromycin.
60
Q: What is the recommended treatment for Salmonella (non-typhoid)?
A: Ciprofloxacin.
61
Q: What is the recommended treatment for shigellosis?
A: Ciprofloxacin.
62
Q: What is an aspergilloma?
A: A mycetoma (mass-like fungus ball) which often colonises an existing lung cavity (e.g. secondary to tuberculosis, lung cancer, or cystic fibrosis).
63
Q: What are the usual symptoms of an aspergilloma?
A: Usually asymptomatic, but may include cough and haemoptysis (which may be severe).
64
Q: What might be seen on a chest x-ray of a patient with an aspergilloma?
A: A rounded opacity, and a crescent sign may be present.
65
Q: What investigation finding is indicative of aspergilloma?
A: High titres of Aspergillus precipitins.
66
Q: What conditions can lead to the formation of lung cavities that aspergillomas colonise?
A: Tuberculosis, lung cancer, and cystic fibrosis.
67
Q: What type of bacterium is Bacillus cereus?
A: Bacillus cereus is a gram-positive rod, which is highly adaptable to extremes of pH and oxygen levels.
68
Q: What are the two main clinical syndromes caused by Bacillus cereus food poisoning?
A: An emetic syndrome and a diarrhoeal syndrome.
69
Q: What causes the emetic syndrome in Bacillus cereus food poisoning?
A: Ingestion of the heat-stable toxin cereulide.
70
Q: How soon do symptoms of the emetic syndrome typically occur after ingestion of Bacillus cereus toxin?
A: Symptoms typically occur between 0.5 and 6 hours of ingestion.
71
Q: What causes the diarrhoeal syndrome in Bacillus cereus food poisoning?
A: Separate exotoxins such as haemolysin BL.
72
Q: How soon do symptoms of the diarrhoeal syndrome typically occur after ingestion of Bacillus cereus?
A: Symptoms typically occur 8-16 hours after ingestion.
73
Q: What are the typical symptoms of the diarrhoeal syndrome caused by Bacillus cereus?
A: Crampy abdominal pain and diarrhoea.
74
Q: Where is Bacillus cereus commonly found in the environment?
A: In soil, fresh water, and salt water. It is also frequently considered a transient commensal organism in the human GI tract and has been found in disinfectant alcohol hand gel.
75
Q: In which patients is Bacillus cereus a significant cause of infection?
A: Immunosuppressed patients, intravenous drug users, and neonates.
76
Q: What types of infections can Bacillus cereus cause in immunosuppressed patients?
A: Bacteraemia, endocarditis, musculoskeletal, and CNS infections.
77
Q: What does bacterial vaginosis (BV) describe?
A: An overgrowth of predominantly anaerobic organisms such as Gardnerella vaginalis, leading to a fall in lactic acid-producing aerobic lactobacilli and a raised vaginal pH.
78
Q: Is bacterial vaginosis considered a sexually transmitted infection?
A: No, but it is seen almost exclusively in sexually active women.
79
Q: What are the features of bacterial vaginosis?
A: Vaginal discharge that is 'fishy' and offensive; asymptomatic in 50% of cases.
80
Q: What is Amsel's criteria for the diagnosis of bacterial vaginosis?
A: Three of the following four points should be present: thin, white homogenous discharge; clue cells on microscopy (stippled vaginal epithelial cells); vaginal pH > 4.5; positive whiff test (fishy odor upon addition of potassium hydroxide).
81
Q: What is the recommended management for asymptomatic bacterial vaginosis?
A: Treatment is not usually required unless the woman is undergoing a termination of pregnancy.
82
Q: What is the recommended treatment for symptomatic bacterial vaginosis?
A: Oral metronidazole for 5-7 days; a single oral dose of metronidazole 2g may be used if adherence is an issue; topical metronidazole or topical clindamycin are alternatives.
83
Q: What are the risks associated with bacterial vaginosis in pregnancy?
A: Increased risk of preterm labor, low birth weight, chorioamnionitis, and late miscarriage.
84
Q: What is the current recommendation for treating bacterial vaginosis during pregnancy?
A: Oral metronidazole is recommended throughout pregnancy; if asymptomatic, discuss treatment with the woman's obstetrician; if symptomatic, use oral metronidazole for 5-7 days or topical treatment. The higher, stat dose of metronidazole is not recommended.
85
Q: What groups require a tuberculin skin test before receiving the BCG vaccine?
A: Infants older than 6 months, tuberculin-negative contacts of TB cases, and new entrants over 6 years old from high-incidence countries.
86
Q: What is the vaccine made of?
A: The BCG vaccine contains live attenuated Mycobacterium bovis.
87
Q: How is the BCG vaccine administered?
A: It is given intradermally, usually to the lateral aspect of the left upper arm.
88
Q: Can the BCG vaccine be given with other vaccines?
A: Yes, it can be given simultaneously with other live vaccines, but if not, there should be a 4-week interval.
89
Q: What are the contraindications for the BCG vaccine?
A: Previous BCG vaccination, a past history of tuberculosis, HIV, pregnancy, and a positive tuberculin test (Heaf or Mantoux).
90
Q: What are the common clinical problems caused by bed bugs?
A: Itchy skin rashes, bites, and allergic symptoms.
91
Q: What is the cause of bed bug infestation?
A: Infestation with Cimex lectularius.
92
Q: Where do bed bugs typically thrive?
A: In mattresses or fabrics.
93
Q: How is itch from bed bug bites managed?
A: Topical hydrocortisone can be used to control itch.
94
Q: What is the definitive management for bed bug infestation?
A: A pest management company and fumigation of the house.
95
Q: How can bed bug numbers be controlled?
A: By hot-washing bed linen and using mattress covers.
96
Q: What type of bacterium causes botulism?
A: Clostridium botulinum, a gram-positive anaerobic bacillus.
97
Q: What does the botulinum toxin do?
A: It irreversibly blocks the release of acetylcholine, leading to paralysis.
98
Q: How can botulism occur?
A: It can result from eating contaminated food (e.g., tinned food) or intravenous drug use.
99
Q: What are the common features of botulism?
A: The patient is usually fully conscious with no sensory disturbance, and may experience flaccid paralysis, diplopia, ataxia, and bulbar palsy.
100
Q: What is the treatment for botulism?
A: Botulism antitoxin and supportive care.
101
Q: What is the most common bacterial cause of infectious intestinal disease in the UK?
A: Campylobacter jejuni.
102
Q: How is Campylobacter infection spread?
A: It is spread by the faecal-oral route.
103
Q: What are the common features of Campylobacter infection?
A: Prodrome with headache and malaise, diarrhoea (often bloody), and abdominal pain (which may mimic appendicitis).
104
Q: How is Campylobacter infection generally managed?
A: It is usually self-limiting, but antibiotics are recommended for severe cases or in immunocompromised patients.
105
Q: What is the first-line antibiotic for severe Campylobacter infection?
A: Clarithromycin.
106
Q: What is an alternative antibiotic to clarithromycin for Campylobacter infection?
A: Ciprofloxacin, although strains with decreased sensitivity to ciprofloxacin are common.
107
Q: What are the possible complications of Campylobacter infection?
A: Guillain-Barré syndrome, reactive arthritis, septicaemia, endocarditis, and arthritis.
108
Q: What is the causative organism of cat scratch disease?
A: Bartonella henselae, a Gram-negative rod.
109
Q: What are the common features of cat scratch disease?
A: Fever, history of a cat scratch, regional lymphadenopathy, headache, and malaise.
110
Q: What is the most common causative organism of cellulitis?
A: Streptococcus pyogenes.
111
Q: What are the common features of cellulitis?
A: Erythema, swelling, systemic upset, fever, malaise, and nausea. It often occurs on the shins and is usually unilateral.
112
Q: How is cellulitis diagnosed?
A: The diagnosis of cellulitis is clinical; no further investigations are required in primary care.
113
Q: When are blood tests or blood cultures requested for cellulitis?
A: Bloods and blood cultures may be requested if the patient is admitted and sepsis is suspected.
114
Q: What is the Eron classification system used for?
A: It is used to guide the management and admission criteria for cellulitis.
115
Q: What are the criteria for Eron Class I cellulitis?
A: No signs of systemic toxicity, no uncontrolled co-morbidities.
116
Q: What are the criteria for Eron Class II cellulitis?
A: The person is systemically unwell or systemically well but has a co-morbidity (e.g., peripheral arterial disease or chronic venous insufficiency).
117
Q: What are the criteria for Eron Class III cellulitis?
A: The person has significant systemic upset (e.g., acute confusion, tachycardia, hypotension) or a limb-threatening infection due to vascular compromise.
118
Q: What are the criteria for Eron Class IV cellulitis?
A: The person has sepsis syndrome or a life-threatening infection (e.g., necrotizing fasciitis).
119
Q: What is the recommended treatment for Eron Class I cellulitis?
A: Oral flucloxacillin as first-line treatment; oral clarithromycin, erythromycin (in pregnancy), or doxycycline if allergic to penicillin.
120
Q: How is Eron Class II cellulitis managed?
A: Admission may not be necessary if intravenous antibiotics and monitoring can be managed in the community; otherwise, oral antibiotics.
121
Q: What is the management for Eron Class III-IV cellulitis?
A: Admission for intravenous antibiotics, with options like co-amoxiclav, clindamycin, cefuroxime, or ceftriaxone.
122
Q: What is the causative organism of chancroid?
A: Haemophilus ducreyi.
123
Q: What are the typical features of chancroid?
A: Painful genital ulcers with sharply defined, ragged, undermined borders and unilateral, painful inguinal lymph node enlargement.
singular ulcer
124
Q: What groups are at increased risk of severe varicella (chickenpox)?
A: Immunosuppressed patients, neonates, and pregnant women.
125
Q: What are the criteria for post-exposure prophylaxis for varicella?
A: 1. Significant exposure to chickenpox or herpes zoster. 2. A clinical condition that increases the risk of severe varicella. 3. No antibodies to the varicella virus.
126
Q: What is the recommended post-exposure prophylaxis for at-risk individuals who meet the criteria?
A: Varicella-zoster immunoglobulin (VZIG).
127
Q: When should varicella-zoster immunoglobulin (VZIG) be administered after exposure?
A: Ideally within 7 days of exposure.
128
Q: Why is blood testing for varicella antibodies important in at-risk exposed patients?
A: To confirm the absence of antibodies to varicella before administering post-exposure prophylaxis.
129
Q: What is the most prevalent sexually transmitted infection in the UK?
A: Chlamydia, caused by Chlamydia trachomatis.
130
Q: What are common symptoms of Chlamydia in women?
A: Cervicitis (discharge, bleeding), dysuria.
131
Q: What are common symptoms of Chlamydia in men?
A: Urethral discharge, dysuria.
132
Q: What are potential complications of untreated Chlamydia?
A: Epididymitis, pelvic inflammatory disease, endometritis, ectopic pregnancies, infertility, reactive arthritis, and Fitz-Hugh-Curtis syndrome.
133
Q: What is the investigation of choice for Chlamydia?
A: Nuclear acid amplification tests (NAATs).
134
Q: What is the first-line investigation for men with suspected Chlamydia?
A: First-void urine sample.
135
Q: What is the first-line investigation for women with suspected Chlamydia?
A: Vulvovaginal swab.
136
Q: What is the first-line treatment for Chlamydia?
A: Doxycycline (7-day course).
137
Q: What alternative treatment for Chlamydia is recommended if doxycycline is contraindicated or not tolerated?
A: Azithromycin (1g once, then 500mg daily for 2 days).
138
Q: What is the preferred treatment for pregnant women with Chlamydia?
A: Azithromycin, erythromycin, or amoxicillin.
139
Q: How should Chlamydia contacts be treated?
A: Contacts should be offered treatment before the results of their investigations are known.
140
Q: What bacteria causes Cholera?
A: Vibrio cholerae, a Gram-negative bacteria.
141
Q: What is a characteristic feature of Cholera?
A: Profuse 'rice water' diarrhoea.
142
Q: What are common complications of Cholera?
A: Dehydration and hypoglycaemia.
143
Q: What is the primary management for Cholera?
A: Oral rehydration therapy.
144
Q: What antibiotics can be used to treat Cholera?
A: Doxycycline or ciprofloxacin.
145
Q: What are the Gram-positive cocci?
A: Staphylococci, Streptococci (including Enterococci).
146
Q: What are the Gram-negative cocci?
A: Neisseria meningitidis, Neisseria gonorrhoeae, Moraxella catarrhalis.
147
Q: What is the mnemonic to remember Gram-positive rods?
A: ABCD L - Actinomyces, Bacillus anthracis, Clostridium, Diphtheria (Corynebacterium diphtheriae), Listeria monocytogenes.
148
Q: Which organisms are Gram-negative rods?
A: Escherichia coli, Haemophilus influenzae, Pseudomonas aeruginosa, Salmonella spp., Shigella spp., Campylobacter jejuni.
149
Q: What are Clostridia?
A: Gram-positive, obligate anaerobic bacilli.
150
Q: What does Clostridium perfringens produce, and what does it cause?
A: Produces α-toxin (lecithinase) which causes gas gangrene (myonecrosis) and haemolysis. Features include tender, oedematous skin with haemorrhagic blebs and bullae, and crepitus on palpation.
151
Q: What is the effect of Clostridium botulinum?
A: Prevents acetylcholine release leading to flaccid paralysis. Typically seen in canned foods and honey.
152
Q: What does Clostridium difficile cause and produce?
A: Causes pseudomembranous colitis, typically after broad-spectrum antibiotic use. Produces an exotoxin and a cytotoxin.
153
Q: What does Clostridium tetani produce, and what is its effect?
A: Produces the exotoxin tetanospasmin, which prevents the release of glycine from Renshaw cells in the spinal cord, causing spastic paralysis.
154
Q: What is Cryptosporidiosis, and what species cause it?
A: Cryptosporidiosis is the commonest protozoal cause of diarrhoea in the UK. It is caused by Cryptosporidium hominis and Cryptosporidium parvum.
155
Q: In which patients is Cryptosporidiosis more common?
A: It is more common in immunocompromised patients (e.g., HIV) and young children.
156
Q: What are the features of Cryptosporidiosis?
A: Watery diarrhoea, abdominal cramps, fever. In immunocompromised patients, the entire gastrointestinal tract may be affected, leading to complications like sclerosing cholangitis and pancreatitis.
157
Q: How is Cryptosporidiosis diagnosed?
A: Stool examination using modified Ziehl-Neelsen stain (acid-fast stain) to reveal the characteristic red cysts of Cryptosporidium.
158
Q: What is the management for Cryptosporidiosis?
A: Supportive treatment for immunocompetent patients. For HIV patients, starting antiretroviral therapy often resolves the infection. Nitazoxanide or rifaximin may be used for immunocompromised patients or severe cases.
159
Q: What is Cutaneous Larva Migrans, and what causes it?
A: Cutaneous larva migrans is a dermatological condition caused by the cutaneous penetration and migration of nematode larvae, primarily from the Ancylostoma genus (e.g., Ancylostoma braziliense).
160
Q: How is Cutaneous Larva Migrans transmitted?
A: It is transmitted via faecal-contaminated soil or sand, with significant risk for individuals who have had barefoot beach visits or direct soil contact.
161
Q: What is the clinical presentation of Cutaneous Larva Migrans?
A: An intensely pruritic, 'creeping', serpiginous, erythematous cutaneous eruption that advances over time. It can last for weeks to months and may lead to secondary bacterial infection due to excessive scratching.
162
Q: How is Cutaneous Larva Migrans diagnosed?
A: Diagnosis is typically clinical, based on the patient's exposure history and characteristic skin manifestations.
163
Q: What are the treatment options for Cutaneous Larva Migrans?
A: Anthelmintic agents like ivermectin or albendazole are used. Topical thiabendazole can be effective but is generally less preferred due to lower efficacy and higher side effects.
164
Q: What are the prevention strategies for Cutaneous Larva Migrans?
A: Preventive strategies include avoiding direct skin contact with potentially contaminated soil, patient education on protective measures, and public health measures to control animal defecation.
165
Q: What is Cytomegalovirus (CMV)?
A: CMV is a herpes virus that affects mainly immunocompromised individuals, such as those with HIV or those on immunosuppressants following organ transplantation.
166
Q: What is the characteristic appearance of infected cells in CMV?
A: Infected cells have an 'Owl's eye' appearance due to intranuclear inclusion bodies.
167
Q: What are the features of congenital CMV infection?
A: Features include growth retardation, pinpoint petechial 'blueberry muffin' skin lesions, microcephaly, sensorineural deafness, encephalitis (seizures), and hepatosplenomegaly.
168
Q: What is CMV mononucleosis?
A: A mononucleosis-like illness that may develop in immunocompetent individuals, presenting with symptoms like fever, lymphadenopathy, and fatigue.
169
Q: What is CMV retinitis, and how is it treated?
A: CMV retinitis occurs in HIV patients with a low CD4 count (<50) and presents with blurred vision. Fundoscopy shows retinal haemorrhages and necrosis, often called 'pizza' retina. Treatment is IV ganciclovir.
170
Q: What is CMV encephalopathy?
A: CMV encephalopathy is seen in HIV patients with low CD4 counts and can lead to neurological symptoms, including altered consciousness and seizures.
171
Q: What are the clinical features of Dengue fever?
A: Features include fever, headache (often retro-orbital), myalgia, bone pain, arthralgia ("break-bone fever"), pleuritic pain, facial flushing, maculopapular rash, and haemorrhagic manifestations such as positive tourniquet test, petechiae, purpura/ecchymosis, and epistaxis.
172
Q: What are the "warning signs" in Dengue fever?
A: Warning signs include abdominal pain, hepatomegaly, persistent vomiting, and clinical fluid accumulation (ascites, pleural effusion).
173
Q: What characterizes severe Dengue (dengue haemorrhagic fever)?
A: Severe Dengue involves disseminated intravascular coagulation (DIC) with thrombocytopenia, spontaneous bleeding, and can lead to dengue shock syndrome (DSS) in 20-30% of cases.
174
Q: What are the common investigations for Dengue fever?
A: Common investigations include blood tests showing leukopenia, thrombocytopenia, and raised aminotransferases, along with serology, nucleic acid amplification tests for viral RNA, and NS1 antigen test.
175
Q: What is the treatment for Dengue fever?
A: Treatment is symptomatic, involving fluid resuscitation and blood transfusion as needed. No antiviral treatments are currently available.
176
Q: What causes Diphtheria?
A: Diphtheria is caused by the Gram-positive bacterium Corynebacterium diphtheriae.
177
Q: What is the typical presentation of Diphtheria?
A: Features include sore throat with a grey, pseudomembrane on the posterior pharyngeal wall (diphtheric membrane), bulky cervical lymphadenopathy, a "bull neck" appearance, neuritis (e.g. cranial nerves), and heart block. Recent visitors to Eastern Europe/Russia/Asia may be at higher risk.
178
Q: What are the possible complications of Diphtheria?
A: Complications include necrosis of myocardial, neural, and renal tissue due to the systemic distribution of the diphtheria toxin.
179
Q: How is Diphtheria diagnosed?
A: Diagnosis is made through culture of a throat swab using tellurite agar or Loeffler's media.
180
Q: What is the management for Diphtheria?
A: Treatment involves intramuscular penicillin and diphtheria antitoxin.
181
Q: How is Ebola virus transmitted?
A: Ebola spreads through human-to-human transmission via direct contact with blood, secretions, organs, or other bodily fluids of infected people, and with contaminated surfaces and materials.
182
Q: What are the early symptoms of Ebola?
A: Early symptoms include sudden onset of fever, fatigue, muscle pain, headache, and sore throat.
183
Q: What are some later symptoms of Ebola?
A: Later symptoms include vomiting, diarrhoea, rash, impaired kidney and liver function, and both internal and external bleeding.
184
Q: Who should be considered for Ebola virus in primary care?
A: Ebola should be suspected in patients with a fever of 37.5°C or a history of fever in the past 24 hours who have recently visited affected areas or have had contact with the body fluids of an infected person or laboratory animal.
185
Q: How should a patient suspected of having Ebola be managed in primary care?
A: The patient should be isolated in a single room, and physical contact should be avoided. Public Health England (PHE) should be contacted for further advice.
186
Q: What causes enteric fever (typhoid and paratyphoid)?
A: Enteric fever is caused by Salmonella typhi (typhoid) and Salmonella paratyphi (paratyphoid).
187
Q: How is typhoid fever transmitted?
A: Typhoid fever is transmitted via the faecal-oral route, often through contaminated food and water.
188
Q: What are the common symptoms of typhoid fever?
A: Symptoms include headache, fever, arthralgia, abdominal pain, distension, and constipation.
189
Q: What is relative bradycardia and when is it seen?
A: Relative bradycardia is a slower-than-expected heart rate for the degree of fever and is seen in typhoid fever.
190
Q: What are rose spots and in which type of fever are they more common?
A: Rose spots are small, blanching, pink macules that appear on the trunk in 40% of patients with enteric fever, and are more common in paratyphoid.
191
Q: What are the potential complications of typhoid fever?
A: Potential complications include osteomyelitis (especially in sickle cell disease), GI bleeding/perforation, meningitis, cholecystitis, and chronic carriage (especially in adult females).
192
Q: Which pathogen is a common cause of osteomyelitis in sickle cell disease?
A: Salmonella is a common cause of osteomyelitis in sickle cell disease.
193
Q: What type of viruses are enteroviruses?
A: Enteroviruses are positive-sense, single-stranded RNA viruses.
194
Q: Which viruses are included in the enterovirus family?
A: The enterovirus family includes Coxsackievirus, echovirus, and rhinovirus, among others.
195
Q: What is the most common cause of viral meningitis in the adult population?
A: Enteroviruses are the most common cause of viral meningitis in adults.
196
Q: What diseases are caused by enteroviruses?
A: Enteroviruses can cause a wide range of diseases, including Hand, Foot and Mouth disease, herpangina, and pericarditis.
197
Q: What is Hand, Foot and Mouth disease and which virus causes it?
A: Hand, Foot and Mouth disease is a viral infection characterized by rash and sores on the hands, feet, and mouth, commonly caused by enteroviruses, particularly Coxsackievirus.
198
Q: What malignancies are associated with Epstein-Barr virus (EBV) infection?
A: The malignancies associated with EBV infection include Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma, and HIV-associated central nervous system lymphomas.
199
Q: What non-malignant condition is associated with Epstein-Barr virus (EBV) infection?
A: The non-malignant condition associated with EBV infection is hairy leukoplakia.
200
Q: What type of Burkitt's lymphoma is associated with Epstein-Barr virus (EBV)?
A: EBV is associated with both African and sporadic Burkitt's lymphoma.
201
Q: What type of bacteria is Escherichia coli (E. coli)?
A: Escherichia coli is a facultative anaerobic, lactose-fermenting, Gram-negative rod.
202
Q: What diseases can Escherichia coli infections cause in humans?
A: E. coli infections can lead to diarrhoeal illnesses, urinary tract infections (UTIs), and neonatal meningitis.
203
Q: What is E. coli O157:H7 known for?
A: E. coli O157:H7 is associated with severe, haemorrhagic, watery diarrhoea, high mortality, and complications such as haemolytic uraemic syndrome. It is often spread by contaminated ground beef.
204
Q: What defines travellers' diarrhoea?
A: Travellers' diarrhoea is defined as at least 3 loose to watery stools in 24 hours with or without abdominal cramps, fever, nausea, vomiting, or blood in the stool.
205
Q: What is the most common cause of travellers' diarrhoea?
A: The most common cause of travellers' diarrhoea is Escherichia coli.
206
Q: What causes acute food poisoning?
A: Acute food poisoning is typically caused by Staphylococcus aureus, Bacillus cereus, or Clostridium perfringens.
207
Q: What are the typical presentations for different gastroenteritis infections?
Escherichia coli: Common amongst travellers, watery stools, abdominal cramps, nausea
Giardiasis: Prolonged, non-bloody diarrhoea
Cholera: Profuse, watery diarrhoea, severe dehydration, weight loss
Shigella: Bloody diarrhoea, vomiting, abdominal pain
Staphylococcus aureus: Severe vomiting, short incubation period
Campylobacter: Flu-like prodrome, crampy abdominal pains, fever, bloody diarrhoea, complications like Guillain-Barre syndrome
Bacillus cereus: Vomiting within 6 hours (due to rice) or diarrhoeal illness after 6 hours
Amoebiasis: Gradual onset bloody diarrhoea, abdominal pain, tenderness lasting several weeks
208
Q: What are the typical features of genital herpes?
A: Painful genital ulceration, dysuria, pruritus, more severe primary infection, systemic features like headache, fever, malaise, tender inguinal lymphadenopathy, urinary retention.
209
Q: How does the severity of primary genital herpes compare to recurrent episodes?
A: The primary infection is often more severe than recurrent episodes.
210
Q: What are the investigations of choice for genital herpes?
A: Nucleic acid amplification tests (NAAT), considered superior to viral culture. HSV serology may be useful for recurrent genital ulceration of unknown cause.
211
Q: What are the general management measures for genital herpes?
A: Saline bathing, analgesia, topical anaesthetic agents like lidocaine, oral aciclovir, and long-term aciclovir for frequent exacerbations.
212
Q: What is the recommended management for genital herpes during pregnancy?
A: Elective caesarean section is advised if a primary attack occurs after 28 weeks gestation. Women with recurrent herpes should receive suppressive therapy, as the risk of transmission to the baby is low.
213
Q: What causes genital warts?
A: Genital warts are caused by human papillomavirus (HPV), especially types 6 and 11.
214
Q: Which HPV types are associated with an increased risk of cervical cancer?
A: HPV types 16, 18, and 33.
215
Q: What are the typical features of genital warts?
A: Small (2-5 mm) fleshy protuberances, slightly pigmented, may bleed or itch.
216
Q: What are the first-line treatments for genital warts?
A: Topical podophyllum or cryotherapy, depending on the location and type of lesion.
217
Q: How are multiple, non-keratinised genital warts treated?
A: They are generally best treated with topical agents.
218
Q: How are solitary, keratinised genital warts treated?
A: They respond better to cryotherapy.
219
Q: What is the second-line treatment for genital warts?
A: Imiquimod, a topical cream.
220
Q: What causes giardiasis?
A: Giardiasis is caused by the flagellate protozoan Giardia lamblia.
221
Q: How is giardiasis spread?
A: Giardiasis is spread by the faeco-oral route.
222
Q: What are the risk factors for giardiasis?
A: Foreign travel, swimming or drinking water from a river or lake, and male-male sexual contact.
223
Q: What are the common features of giardiasis?
A: Often asymptomatic, non-bloody diarrhoea, steatorrhoea, bloating, abdominal pain, lethargy, flatulence, weight loss, malabsorption, and lactose intolerance.
224
Q: How is giardiasis diagnosed?
A: Stool microscopy for trophozoite and cysts (sensitivity around 65%), stool antigen detection assay (greater sensitivity and faster turn-around time), and PCR assays.
225
Q: What is the treatment for giardiasis?
A: Treatment is with metronidazole.
226
Q: What causes gonorrhoea?
A: Gonorrhoea is caused by the Gram-negative diplococcus Neisseria gonorrhoeae.
227
Q: What are the common features of gonorrhoea in males?
A: Urethral discharge and dysuria.
228
Q: What are the common features of gonorrhoea in females?
A: Cervicitis, leading to vaginal discharge.
229
Q: What are the common features of rectal and pharyngeal gonorrhoea?
A: Rectal and pharyngeal infections are usually asymptomatic.
230
Q: What are the local complications of gonorrhoea?
A: Urethral strictures, epididymitis, and salpingitis, which can lead to infertility.
231
Q: What is the treatment for gonorrhoea?
A: The current first-line treatment is a single dose of IM ceftriaxone 1g. If sensitivities are known, a single dose of oral ciprofloxacin 500mg can be used.
232
Q: What are the key features of disseminated gonococcal infection (DGI)?
A: Tenosynovitis, migratory polyarthritis, and dermatitis (maculopapular or vesicular lesions).
233
Q: What complications can arise from disseminated gonococcal infection?
A: Septic arthritis, endocarditis, and perihepatitis (Fitz-Hugh-Curtis syndrome).
234
Q: What is the incubation period for hepatitis A?
A: The incubation period for hepatitis A is 2-4 weeks.
235
Q: How is hepatitis A transmitted?
A: Hepatitis A is transmitted via faecal-oral spread, often in institutions.
236
Q: Does hepatitis A cause chronic disease?
A: No, hepatitis A does not cause chronic disease.
237
Q: What are the common features of hepatitis A?
A: Flu-like prodrome, right upper quadrant abdominal pain, tender hepatomegaly, jaundice, and deranged liver function tests.
238
Q: Is there a vaccine for hepatitis A?
A: Yes, there is an effective vaccine for hepatitis A.
239
Q: Who should be vaccinated against hepatitis A?
A: Those travelling to or residing in areas of high or intermediate prevalence, people with chronic liver disease, patients with haemophilia, men who have sex with men, injecting drug users, individuals at occupational risk (e.g. lab workers, sewage workers, and those working with primates).
240
Q: How is hepatitis B transmitted?
A: Hepatitis B is spread through exposure to infected blood or body fluids, including vertical transmission from mother to child.
241
Q: What is the incubation period for hepatitis B?
A: The incubation period for hepatitis B is 6-20 weeks.
242
Q: What are the common features of hepatitis B infection?
A: Fever, jaundice, and elevated liver transaminases.
243
Q: What are the complications of hepatitis B infection?
A: Chronic hepatitis (5-10%), fulminant liver failure (1%), hepatocellular carcinoma, glomerulonephritis, polyarteritis nodosa, and cryoglobulinaemia.
244
Q: What is the routine vaccination schedule for hepatitis B in the UK?
A: Children born in the UK are vaccinated at 2, 3, and 4 months of age.
245
Q: Who should be vaccinated against hepatitis B?
A: Healthcare workers, intravenous drug users, sex workers, close family contacts of an individual with hepatitis B, individuals receiving regular blood transfusions, chronic kidney disease patients, prisoners, and chronic liver disease patients.
246
Q: When should anti-HBs levels be tested?
A: Testing for anti-HBs is recommended for healthcare workers and patients with chronic kidney disease, 1-4 months after primary immunisation.
247
Q: What treatments are available for hepatitis B?
A: Pegylated interferon-alpha, tenofovir, entecavir, and telbivudine (a synthetic thymidine nucleoside analogue).
248
Q: What are the at-risk groups for hepatitis C infection?
A: Intravenous drug users, patients who received a blood transfusion prior to 1991 (e.g., haemophiliacs).
249
Q: What is the incubation period for hepatitis C?
A: The incubation period for hepatitis C is 6-9 weeks.
250
Q: Can mothers with hepatitis C breastfeed?
A: Yes, breastfeeding is not contraindicated in mothers with hepatitis C.
251
Q: What are the features of acute hepatitis C infection?
A: Transient rise in serum aminotransferases, jaundice, fatigue, and arthralgia.
252
Q: What is the investigation of choice to diagnose acute hepatitis C infection?
A: HCV RNA is the investigation of choice.
253
Q: How is chronic hepatitis C defined?
A: Chronic hepatitis C is defined as the persistence of HCV RNA in the blood for 6 months.
254
Q: What are the potential complications of chronic hepatitis C?
A: Rheumatological problems (arthralgia, arthritis), eye problems (Sjogren's syndrome), cirrhosis, hepatocellular cancer, cryoglobulinaemia, porphyria cutanea tarda, and membranoproliferative glomerulonephritis.
255
Q: What are the current treatments for chronic hepatitis C?
A: Combination of protease inhibitors (e.g., daclatasvir + sofosbuvir, sofosbuvir + simeprevir) with or without ribavirin.
256
Q: What are the complications of ribavirin treatment?
A: Haemolytic anaemia, cough, and it is teratogenic (women should not become pregnant within 6 months of stopping ribavirin).
257
Q: What are the side effects of interferon alpha treatment for hepatitis C?
A: Flu-like symptoms, depression, fatigue, leukopenia, and thrombocytopenia.
258
Q: How is hepatitis D transmitted?
A: Hepatitis D is transmitted parenterally, similar to hepatitis B (through exchange of bodily fluids).
259
Q: What does hepatitis D require to complete its replication and transmission cycle?
A: Hepatitis D requires hepatitis B surface antigen to complete its replication and transmission cycle.
260
Q: What is co-infection in the context of hepatitis B and D?
A: Co-infection is when a person is infected with both hepatitis B and hepatitis D at the same time.
261
Q: What is superinfection in the context of hepatitis B and D?
A: Superinfection occurs when a person who is already hepatitis B surface antigen positive subsequently develops a hepatitis D infection.
262
Q: How is hepatitis D diagnosed?
A: Hepatitis D is diagnosed via reverse polymerase chain reaction (PCR) of hepatitis D RNA.
263
Q: What is the treatment for hepatitis D?
A: Interferon is used as treatment, but with a poor evidence base.
264
Q: How is hepatitis E transmitted?
A: Hepatitis E is spread by the faecal-oral route.
265
Q: What is the incubation period for hepatitis E?
A: The incubation period for hepatitis E is 3-8 weeks.
266
Q: How does hepatitis E compare to hepatitis A?
A: Hepatitis E causes a similar disease to hepatitis A, but carries a significantly higher mortality (about 20%) during pregnancy.
267
Q: What conditions are associated with HSV-1 and HSV-2?
A: HSV-1 typically causes oral lesions (cold sores), and HSV-2 typically causes genital herpes, though there is considerable overlap.
268
Q: What is the primary infection of HSV?
A: The primary infection may present with severe gingivostomatitis.
269
Q: What is the typical management for gingivostomatitis caused by HSV?
A: Treatment includes oral aciclovir and chlorhexidine mouthwash.
270
Q: How are cold sores treated?
A: Cold sores are typically treated with topical aciclovir, although the evidence base for this treatment is modest.
271
Q: How is genital herpes treated?
A: Genital herpes is treated with oral aciclovir. Some patients with frequent exacerbations may benefit from long-term aciclovir.
272
Q: What advice is given to pregnant women with a primary herpes attack at greater than 28 weeks gestation?
A: Elective caesarean section at term is advised.
273
Q: How should pregnant women with recurrent herpes be managed?
A: They should be treated with suppressive therapy, and the risk of transmission to the baby is low.
274
Q: What are the characteristic features of herpes simplex virus infection on a Pap smear?
A: Multinucleated giant cells, with features including multinucleation, margination of chromatin, and molding of nuclei.
275
Q: What is the most common cause of diarrhoea in HIV patients?
A: Cryptosporidium, an intracellular protozoa, is the most common infective cause of diarrhoea in HIV patients.
276
Q: How is Cryptosporidium identified in stool samples?
A: Cryptosporidium can be identified using a modified Ziehl-Neelsen (acid-fast) stain, which reveals the characteristic red cysts.
277
Q: What is the primary treatment for Cryptosporidium diarrhoea in HIV patients?
A: The primary treatment for Cryptosporidium diarrhoea is supportive therapy.
278
Q: What are the typical features of Mycobacterium avium intracellulare infection in HIV patients?
A: Typical features include fever, sweats, abdominal pain, diarrhoea, hepatomegaly, and deranged liver function tests (LFTs).
279
Q: When does Mycobacterium avium intracellulare typically occur in HIV patients?
A: Mycobacterium avium intracellulare is seen in HIV patients with a CD4 count below 50.
280
Q: How is Mycobacterium avium intracellulare diagnosed?
A: Diagnosis is made by blood cultures and bone marrow examination.
281
Q: What is the treatment regimen for Mycobacterium avium intracellulare?
A: The treatment regimen includes rifabutin, ethambutol, and clarithromycin.
282
Q: What virus causes Kaposi's sarcoma?
A: Kaposi's sarcoma is caused by Human Herpesvirus 8 (HHV-8).
283
Q: What is the typical presentation of Kaposi's sarcoma?
A: Kaposi's sarcoma presents as purple papules or plaques on the skin or mucosa (e.g., gastrointestinal and respiratory tract).
284
Q: What complications can arise if Kaposi's sarcoma involves the respiratory system?
A: Respiratory involvement in Kaposi's sarcoma may cause massive haemoptysis and pleural effusion.
285
Q: What are the treatments for Kaposi's sarcoma?
A: Treatments for Kaposi's sarcoma include radiotherapy and resection.
286
Q: What is the general approach to antiretroviral therapy (ART) for HIV?
A: ART involves a combination of at least three drugs, typically two nucleoside reverse transcriptase inhibitors (NRTI) and either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI), to decrease viral replication and reduce the risk of viral resistance.
287
Q: According to the 2015 BHIVA guidelines, when should antiretroviral therapy (ART) be initiated in HIV patients?
A: ART should be started as soon as a patient is diagnosed with HIV, rather than waiting for a particular CD4 count.
288
Q: What are some examples of nucleoside analogue reverse transcriptase inhibitors (NRTIs)?
A: Examples of NRTIs include zidovudine (AZT), abacavir, emtricitabine, didanosine, lamivudine, stavudine, zalcitabine, and tenofovir.
289
Q: What are the common side effects of NRTIs?
A: Common side effects of NRTIs include peripheral neuropathy. Specific side effects of individual drugs include renal impairment and osteoporosis with tenofovir, anaemia and myopathy with zidovudine, and pancreatitis with didanosine.
290
Q: What are examples of non-nucleoside reverse transcriptase inhibitors (NNRTIs)?
A: Examples of NNRTIs include nevirapine and efavirenz.
291
Q: What side effects are associated with non-nucleoside reverse transcriptase inhibitors (NNRTIs)?
A: Side effects of NNRTIs include P450 enzyme interaction (nevirapine induces) and rashes.
292
Q: What are examples of protease inhibitors (PIs) used in HIV treatment?
A: Examples of PIs include indinavir, nelfinavir, ritonavir, and saquinavir.
293
Q: What are the side effects of protease inhibitors (PIs)?
A: Side effects of PIs include diabetes, hyperlipidaemia, buffalo hump, central obesity, and P450 enzyme inhibition. Specific side effects include renal stones and asymptomatic hyperbilirubinaemia with indinavir, and potent P450 system inhibition with ritonavir.
294
Q: What is the most common cause of cerebral lesions in HIV patients?
A: Toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV.
295
Q: What are the typical symptoms and CT findings for toxoplasmosis in HIV patients?
A: Symptoms include constitutional symptoms, headache, confusion, and drowsiness. CT typically shows single or multiple ring-enhancing lesions with mass effect.
296
Q: What is the treatment for toxoplasmosis in HIV patients?
A: The treatment for toxoplasmosis includes sulfadiazine and pyrimethamine.
297
Q: What is the second most common cause of cerebral lesions in HIV patients?
A: Primary CNS lymphoma accounts for around 30% of cerebral lesions in HIV patients.
298
Q: What are the typical CT findings and treatment for primary CNS lymphoma in HIV patients?
A: CT shows single or multiple homogenous enhancing lesions. Treatment generally includes steroids, chemotherapy (e.g., methotrexate), and possibly whole brain irradiation. Surgical resection may be considered for lower-grade tumors.
299
Q: How can toxoplasmosis and primary CNS lymphoma be differentiated?
Toxoplasmosis: Multiple lesions, ring or nodular enhancement, Thallium SPECT negative.
Lymphoma: Single lesion, solid (homogenous) enhancement, Thallium SPECT positive.
300
Q: What is the typical CT finding for tuberculosis in HIV patients?
A: Tuberculosis in HIV patients presents as a single enhancing lesion on CT.
301
Q: What are the potential causes of encephalitis in HIV patients?
A: Encephalitis in HIV patients may be due to CMV, HIV itself, or less commonly HSV.
302
Q: What is the most common fungal infection of the CNS in HIV patients?
A: Cryptococcus is the most common fungal infection of the CNS in HIV patients.
303
Q: What are the symptoms and CSF findings for Cryptococcus infection in HIV patients?
A: Symptoms include headache, fever, malaise, nausea/vomiting, seizures, and focal neurological deficit. CSF shows high opening pressure, elevated protein, reduced glucose, and normally a lymphocyte predominance (but may have normal white cell count in HIV).
304
Q: What are the typical CT findings for Cryptococcus infection in HIV patients?
A: CT may show meningeal enhancement and cerebral oedema. Meningitis is the typical presentation but can occasionally cause a space-occupying lesion.
305
Q: What is Progressive Multifocal Leukoencephalopathy (PML) in HIV patients?
A: PML is widespread demyelination caused by infection of oligodendrocytes by JC virus, resulting in symptoms like behavioral changes, motor impairment, and visual impairment.
306
Q: What are the typical CT and MRI findings for Progressive Multifocal Leukoencephalopathy (PML)?
A: CT shows single or multiple lesions without mass effect and no enhancement. MRI shows high-signal demyelinating white matter lesions.
307
Q: What is AIDS dementia complex and how does it present?
A: AIDS dementia complex is caused by HIV itself and presents with behavioral changes and motor impairment. CT shows cortical and subcortical atrophy.
308
Q: What is the most common cause of oesophagitis in patients with HIV?
A: Oesophageal candidiasis is the most common cause of oesophagitis in patients with HIV.
309
Q: In which patients is oesophageal candidiasis typically seen in HIV?
A: Oesophageal candidiasis is generally seen in patients with a CD4 count of less than 100.
310
Q: What are the typical symptoms of oesophageal candidiasis in HIV patients?
A: Typical symptoms include dysphagia (difficulty swallowing) and odynophagia (painful swallowing).
311
Q: What are the first-line treatments for oesophageal candidiasis in HIV patients?
A: First-line treatments for oesophageal candidiasis include fluconazole and itraconazole.
312
Q: What opportunistic infections or disorders are associated with a CD4 count of 200-500 cells/mm³ in HIV patients?
A: Oral thrush (Candida albicans), shingles (herpes zoster), hairy leukoplakia (EBV), and Kaposi sarcoma (HHV-8).
313
Q: What opportunistic infections or disorders are associated with a CD4 count of 100-200 cells/mm³ in HIV patients?
A: Cryptosporidiosis, cerebral toxoplasmosis, progressive multifocal leukoencephalopathy (JC virus), Pneumocystis jirovecii pneumonia, and HIV dementia.
314
Q: What opportunistic infections or disorders are associated with a CD4 count of 50-100 cells/mm³ in HIV patients?
A: Aspergillosis (Aspergillus fumigatus), oesophageal candidiasis (Candida albicans), cryptococcal meningitis, and primary CNS lymphoma (EBV).
315
Q: What opportunistic infections or disorders are associated with a CD4 count of <50 cells/mm³ in HIV patients?
A: Cytomegalovirus retinitis, mycobacterium avium-intracellulare infection.
316
Q: What is Pneumocystis jiroveci pneumonia (PCP) in HIV patients?
A: PCP is the most common opportunistic infection in AIDS, caused by Pneumocystis jiroveci, a unicellular eukaryote classified as a fungus or protozoa.
317
Q: What CD4 count should prompt Pneumocystis jiroveci pneumonia (PCP) prophylaxis in HIV patients?
A: All patients with a CD4 count < 200/mm³ should receive PCP prophylaxis.
318
Q: What are the common features of Pneumocystis jiroveci pneumonia (PCP)?
A: Dyspnoea, dry cough, fever, and very few chest signs.
319
Q: What is a common complication of Pneumocystis jiroveci pneumonia (PCP)?
A: Pneumothorax.
320
Q: What investigations are used to diagnose Pneumocystis jiroveci pneumonia (PCP)?
A: CXR (bilateral interstitial pulmonary infiltrates), exercise-induced desaturation, sputum analysis (often fails to show PCP), and bronchoalveolar lavage (BAL) (silver stain shows cysts).
321
Q: What is the first-line treatment for Pneumocystis jiroveci pneumonia (PCP)?
A: Co-trimoxazole.
322
Q: What is the management for severe Pneumocystis jiroveci pneumonia (PCP)?
A: IV pentamidine or aerosolized pentamidine (less effective, with a risk of pneumothorax).
323
Q: When does HIV seroconversion typically occur after infection?
A: HIV seroconversion typically occurs 3-12 weeks after infection.
324
Q: What are the common symptoms of HIV seroconversion?
A: Sore throat, lymphadenopathy, malaise, myalgia, arthralgia, diarrhoea, maculopapular rash, mouth ulcers.
325
Q: What are the standard tests for diagnosing HIV?
A: ELISA (screening) and Western Blot Assay (confirmatory).
326
Q: What is the recommended test for diagnosing HIV in asymptomatic patients?
A: Combination tests (HIV p24 antigen and HIV antibody) are standard for diagnosing HIV.
327
Q: When should testing for HIV be repeated in asymptomatic patients after an initial negative result?
A: After an initial negative result, HIV testing should be repeated at 12 weeks.
328
Q: What test is commonly used now for confirmation of HIV?
A: HIV-1/HIV-2 differentiation assays are now more commonly used for confirmation, replacing the Western blot.
329
Q: How long after exposure do most people develop antibodies to HIV?
A: Most people develop antibodies to HIV at 4-6 weeks after exposure, but 99% do by 3 months.
330
Q: What is the current first-line test for HIV screening in asymptomatic individuals or patients with chronic infection?
A: The fourth-generation HIV test (HIV antibody and p24 antigen) is the first-line test for HIV screening.
331
Q: Which strains of HPV are most important in terms of cancer risk?
A: HPV strains 16 and 18 are linked to a variety of cancers, most notably cervical cancer.
332
Q: What cancers are linked to HPV infection?
A: HPV infection is linked to over 99.7% of cervical cancers, around 85% of anal cancers, around 50% of vulval and vaginal cancers, and around 20-30% of mouth and throat cancers.
333
Q: What other risk factors contribute to the development of cervical cancer?
A: Smoking, combined oral contraceptive pill use, and high parity are other important risk factors for cervical cancer.
334
Q: What is the color of gram-positive bacteria after gram staining?
A: Gram-positive bacteria turn purple/blue after gram staining.
335
Q: Which bacteria are classified as gram-positive rods (bacilli)?
A: Gram-positive rods include Actinomyces, Bacillus anthracis, Clostridium, Corynebacterium diphtheriae, and Listeria monocytogenes.
336
Q: How do Staphylococci differ from Streptococci in terms of catalase production?
A: Staphylococci produce catalase, while Streptococci do not.
337
Q: What are the two types of Staphylococci based on coagulase production?
A: S. aureus produces coagulase, while S. epidermidis and S. saprophyticus do not.
338
Q: How can you differentiate between S. epidermidis and S. saprophyticus?
A: S. epidermidis is novobiocin sensitive, while S. saprophyticus is novobiocin resistant.
339
Q: What are the different types of Streptococci based on hemolysis patterns?
A: Streptococci can be α-haemolytic (partial hemolysis), β-haemolytic (complete hemolysis), or γ-haemolytic (no hemolysis).
340
Q: What is the most common cause of infectious mononucleosis (glandular fever)?
A: Infectious mononucleosis is most commonly caused by the Epstein-Barr virus (EBV), also known as human herpesvirus 4 (HHV-4).
341
Q: What is the classic triad of symptoms seen in infectious mononucleosis?
A: The classic triad consists of sore throat, pyrexia (fever), and lymphadenopathy.
342
Q: How does the lymphadenopathy in infectious mononucleosis differ from tonsillitis?
A: In infectious mononucleosis, lymphadenopathy is often present in both the anterior and posterior triangles of the neck, while tonsillitis typically causes enlargement in the upper anterior cervical chain only.
343
Q: What are some other common features of infectious mononucleosis?
A: Other features include malaise, anorexia, headache, palatal petechiae, splenomegaly (in 50% of patients), transient rise in ALT (hepatitis), lymphocytosis, and haemolytic anaemia due to cold agglutinins (IgM).
344
Q: What is a common rash seen in infectious mononucleosis?
A: A maculopapular, pruritic rash can develop in around 99% of patients who take ampicillin or amoxicillin while they have infectious mononucleosis.
345
Q: How is infectious mononucleosis diagnosed?
A: The diagnosis is confirmed with a heterophil antibody test (Monospot) and by blood tests such as FBC, typically performed in the second week of illness.
346
Q: What is the typical management for infectious mononucleosis?
A: Management is supportive, including rest, hydration, avoidance of alcohol, and simple analgesia for pain. Contact sports should be avoided for 4 weeks to reduce the risk of splenic rupture.
347
Q: What is the key difference in the flu vaccine given to children and at-risk groups compared to the elderly?
A: Children receive a live intranasal vaccine, while the elderly and at-risk groups receive an inactivated vaccine.
348
Q: What are the key points about the children's influenza vaccine?
A: It is given intranasally, the first dose is given at ages 2-3 years and then annually, and it is a live vaccine.
349
Q: What are the contraindications for the intranasal flu vaccine in children?
A: Contraindications include immunocompromised status, age <2 years, current febrile illness or blocked nose, current wheeze, history of severe asthma, egg allergy, pregnancy/breastfeeding, and use of aspirin.
350
Q: What are common side effects of the intranasal flu vaccine in children?
A: Side effects include blocked nose, headache, and anorexia.
351
Q: How long does it take for the influenza vaccine to reach protective levels?
A: It takes around 10-14 days after immunisation for antibody levels to reach protective levels.
352
Q: What is invasive aspergillosis, and which species of Aspergillus are commonly involved?
A: Invasive aspergillosis is a systemic Aspergillus infection, typically caused by Aspergillus fumigatus, Aspergillus flavus, and Aspergillus terreus. It is a leading cause of death in immunocompromised patients.
353
Q: What are the main risk factors for developing invasive aspergillosis?
A: Risk factors include HIV, leukaemia, and following broad-spectrum antibiotics.
354
Q: What causes Legionnaire's disease and where does it typically colonize?
A: Legionnaire's disease is caused by Legionella pneumophilia, which typically colonizes water tanks and is often associated with air-conditioning systems or foreign holidays. Person-to-person transmission is not seen.
355
Q: What are the main symptoms of Legionnaire's disease?
A: Symptoms include flu-like features such as fever, dry cough, relative bradycardia, confusion, lymphopaenia, hyponatraemia, deranged liver function tests, and pleural effusion (seen in around 30% of patients).
356
Q: What is the diagnostic test of choice for Legionnaire's disease?
A: The diagnostic test of choice is a urinary antigen test.
357
Q: How is Legionnaire's disease treated?
A: Treatment includes erythromycin or clarithromycin.
358
Q: What is a key difference between Legionella and Mycoplasma pneumonia in terms of chest x-ray findings?
A: Legionella pneumonia often shows a mid-to-lower zone predominance of patchy consolidation and pleural effusions, whereas Mycoplasma pneumonia typically presents with more diffuse infiltrates without prominent pleural effusion.
359
Q: What is Lemierre's syndrome?
A: Lemierre's syndrome is an infectious thrombophlebitis of the internal jugular vein, often secondary to a bacterial sore throat caused by Fusobacterium necrophorum.
360
Q: What is the typical cause of Lemierre's syndrome?
A: It is most often caused by Fusobacterium necrophorum, which leads to a peritonsillar abscess and subsequent thrombosis of the internal jugular vein.
361
Q: What are the common symptoms of Lemierre's syndrome?
A: Symptoms include a history of bacterial sore throat, followed by neck pain, stiffness, tenderness (which may be mistaken for meningitis), fever, rigors, and potential septic pulmonary emboli.
362
Q: What causes leprosy?
A: Leprosy is caused by Mycobacterium leprae, a granulomatous bacterium that primarily affects the peripheral nerves and skin.
363
Q: What are the common features of leprosy?
A: Features include patches of hypopigmented skin, typically on the buttocks, face, and extensor surfaces of limbs, along with sensory loss.
364
Q: What is the WHO-recommended treatment for leprosy?
A: The WHO-recommended treatment for leprosy is a triple therapy regimen: rifampicin, dapsone, and clofazimine.
365
Q: What causes leptospirosis?
A: Leptospirosis is caused by the spirochaete Leptospira interrogans, particularly the serogroup L. icterohaemorrhagiae, and is typically spread by contact with infected rat urine.
366
Q: What are the features of leptospirosis?
A: Features include fever, flu-like symptoms, subconjunctival suffusion, haemorrhage, acute kidney injury, hepatitis (jaundice, hepatomegaly), and aseptic meningitis.
367
Q: How is leptospirosis diagnosed?
A: Diagnosis is typically through serology (antibodies to Leptospira), PCR, culture (though it takes several weeks for growth), and urine cultures (positive after the second week of illness).
368
Q: What is the management for leptospirosis?
A: For mild to moderate disease, doxycycline or azithromycin is used. Severe disease requires IV benzylpenicillin.
369
Q: What causes Lyme disease?
A: Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks.
370
Q: What are the early features of Lyme disease?
A: Early features within 30 days include erythema migrans (bulls-eye rash), headache, lethargy, fever, and arthralgia. The rash typically develops 1-4 weeks after the tick bite, is usually painless, and increases in size.
371
Q: What are the later features of Lyme disease?
A: Later features include cardiovascular symptoms such as heart block and peri/myocarditis, as well as neurological symptoms like facial nerve palsy, radicular pain, and meningitis.
372
Q: How is Lyme disease diagnosed?
A: Lyme disease can often be diagnosed clinically if erythema migrans is present. If needed, the first-line test is ELISA for antibodies to Borrelia burgdorferi. If the test is negative or unclear, it can be repeated or followed by an immunoblot test.
373
Q: What is the management for asymptomatic tick bites?
A: Tick bites do not require routine antibiotic treatment according to NICE guidelines. If the tick is still present, it should be removed using fine-tipped tweezers and the area should be washed.
374
Q: What is the management for suspected or confirmed Lyme disease?
A: For early disease, doxycycline is used. Amoxicillin is an alternative in cases such as pregnancy. If the disease is disseminated, ceftriaxone is used. People with erythema migrans should start antibiotics without further tests. A Jarisch-Herxheimer reaction may occur after the first dose of antibiotics.
375
Q: What causes malaria?
A: Malaria is caused by Plasmodium protozoa, which is spread by the female Anopheles mosquito.
376
Q: What are the four species of Plasmodium that cause malaria in humans?
A: The four species are Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae.
377
Q: Which Plasmodium species causes nearly all episodes of severe malaria?
A: Plasmodium falciparum causes nearly all episodes of severe malaria.
378
Q: Which Plasmodium species is most commonly responsible for benign malaria?
A: Plasmodium vivax is the most common species that causes benign malaria.
379
Q: What genetic factors provide protection against malaria?
A: Protective factors include sickle-cell trait, G6PD deficiency, HLA-B53, and absence of Duffy antigens.
380
Q: What is the most common and severe type of malaria?
A: Plasmodium falciparum malaria is the most common and severe type of malaria.
381
Q: What are the classical symptoms of falciparum malaria?
A: The classical triad includes paroxysms of fever, chills, and sweating, which may occur every 48 hours, corresponding to the erythrocytic cycle of the parasite.
382
Q: What are some common gastrointestinal symptoms of falciparum malaria?
A: Anorexia, nausea, vomiting, abdominal pain, and occasionally diarrhoea, particularly in children.
383
Q: What is the hallmark symptom of malaria?
A: Fever, typically cyclical, often accompanied by sweating and sometimes rigors.
384
Q: What are some neurological symptoms in falciparum malaria?
A: Headache (often severe), dizziness, and sleep disturbances.
385
Q: What are features of severe falciparum malaria?
A: Schizonts on a blood film, parasitaemia > 2%, hypoglycaemia, acidosis, temperature > 39°C, and severe anaemia.
386
Q: What are some complications of severe falciparum malaria?
A: Cerebral malaria (seizures, coma), acute renal failure (blackwater fever), ARDS, hypoglycaemia, and disseminated intravascular coagulation (DIC).
387
Q: What is the recommended first-line treatment for uncomplicated falciparum malaria?
A: Artemisinin-based combination therapies (ACTs) such as artemether plus lumefantrine or artesunate plus amodiaquine.
388
Q: What is the treatment for severe falciparum malaria?
A: Intravenous artesunate is recommended by WHO in preference to intravenous quinine. Exchange transfusion should be considered if parasitaemia > 10%.
389
Q: What parasite count requires parenteral treatment in severe falciparum malaria?
A: A parasite count of more than 2% usually requires parenteral treatment regardless of the clinical state.
390
Q: What is the most common cause of non-falciparum malaria?
A: Plasmodium vivax is the most common cause of non-falciparum malaria.
391
Q: What are the general features of malaria?
A: Fever, headache, and splenomegaly.
392
Q: How often does fever occur in Plasmodium vivax and Plasmodium ovale malaria?
A: Cyclical fever every 48 hours.
393
Q: How often does fever occur in Plasmodium malariae malaria?
A: Cyclical fever every 72 hours.
394
Q: What condition is Plasmodium malariae associated with?
A: Nephrotic syndrome.
395
Q: What is the treatment for malaria in areas where chloroquine is sensitive?
A: WHO recommends either an artemisinin-based combination therapy (ACT) or chloroquine.
396
Q: What is the treatment for malaria in areas where chloroquine is resistant?
A: An ACT should be used.
397
Q: What should be given to patients with Plasmodium ovale or Plasmodium vivax malaria following acute treatment with chloroquine?
A: Primaquine should be given to destroy liver hypnozoites and prevent relapse.
398
Q: What is the Mantoux test used for?
A: The Mantoux test is used to detect previous exposure to Mycobacterium tuberculosis, indicating possible tuberculosis (TB) infection.
399
Q: What indicates a positive Mantoux test result?
A: Erythema and induration greater than 10mm indicates a positive result, implying previous exposure, including from BCG vaccination.
400
Q: What is the most common cause of meningitis in neonates (0-3 months)?
A: The most common causes of meningitis in neonates are Group B Streptococcus, E. coli, and Listeria monocytogenes.
401
Q: What are the common causes of meningitis in children aged 3 months to 6 years?
A: The common causes in this age group are Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae.
402
Q: What are the common causes of meningitis in individuals aged 6 years to 60 years?
A: The common causes of meningitis in this age group are Neisseria meningitidis and Streptococcus pneumoniae.
403
Q: What are the most common causes of meningitis in individuals over 60 years?
A: The most common causes are Streptococcus pneumoniae, Neisseria meningitidis, and Listeria monocytogenes.
404
Q: What are the common causes of meningitis in immunosuppressed individuals?
A: The most common cause in immunosuppressed individuals is Listeria monocytogenes.
405
Q: What are the CSF findings in bacterial meningitis?
A: In bacterial meningitis, the CSF is cloudy, glucose is low (< 1/2 plasma), protein is high (> 1 g/l), and white cells are between 10 - 5,000 polymorphs/mm³.
406
Q: What are the CSF findings in viral meningitis?
A: In viral meningitis, the CSF is clear/cloudy, glucose is 60-80% of plasma glucose, protein is normal or raised, and white cells are between 15 - 1,000 lymphocytes/mm³.
407
Q: What are the CSF findings in tuberculous meningitis?
A: In tuberculous meningitis, the CSF is slightly cloudy with a fibrin web, glucose is low (< 1/2 plasma), protein is high (> 1 g/l), and white cells are between 30 - 300 lymphocytes/mm³.
408
Q: What are the CSF findings in fungal meningitis?
A: In fungal meningitis, the CSF is cloudy, glucose is low, protein is high, and white cells are between 20 - 200 lymphocytes/mm³.
409
Q: What is the first step in managing suspected bacterial meningitis?
A: The first step is to urgently transfer the patient to the hospital. In pre-hospital settings, such as a GP surgery, intramuscular benzylpenicillin may be given if meningococcal disease is suspected, but it should not delay transport.
410
Q: When should a lumbar puncture (LP) be delayed in suspected bacterial meningitis?
A: LP should be delayed in cases of severe sepsis, rapidly evolving rash, severe respiratory/cardiac compromise, significant bleeding risk, raised intracranial pressure, focal neurological signs, papilloedema, continuous seizures, or a GCS ≤ 12.
411
Q: What is the recommended IV antibiotic treatment for suspected bacterial meningitis in patients aged 3 months - 50 years?
A: IV cefotaxime (or ceftriaxone) is recommended for patients aged 3 months - 50 years.
412
Q: What is the recommended adjunctive treatment for bacterial meningitis, especially if pneumococcal meningitis is suspected?
A: IV dexamethasone should be considered as adjunctive treatment, preferably starting before or with the first dose of antibiotics, but no later than 12 hours after starting antibacterial treatment.
413
Q: What are the key investigations in suspected bacterial meningitis?
A: Blood tests should include full blood count, renal function, glucose, lactate, clotting profile, and CRP. CSF analysis should include glucose, protein, microscopy, culture, lactate, meningococcal and pneumococcal PCR, and enteroviral, herpes simplex, and varicella-zoster PCR.
414
Q: What is the recommended antibiotic treatment for meningococcal meningitis?
A: IV benzylpenicillin or cefotaxime (or ceftriaxone) is recommended for meningococcal meningitis.
415
Q: What antibiotic should be given as prophylaxis to close contacts of a meningococcal meningitis patient?
A: Close contacts should be given oral ciprofloxacin or rifampicin, with ciprofloxacin being the drug of choice.
416
Q: What is a major adverse effect of metronidazole when combined with alcohol?
A: Metronidazole can cause a disulfiram-like reaction with alcohol, leading to symptoms like nausea, vomiting, and flushing.
417
Q: How does metronidazole interact with warfarin?
A: Metronidazole increases the anticoagulant effect of warfarin.
418
Q: How should a patient be screened for MRSA?
A: By taking a nasal swab and swabbing skin lesions or wounds. The swab should be wiped around the inside rim of the patient's nose for 5 seconds, and the microbiology form must be labeled 'MRSA screen.'
419
Q: What is the recommended treatment for suppression of MRSA in carriers?
A: For the nose: mupirocin 2% in white soft paraffin, applied tds for 5 days. For the skin: chlorhexidine gluconate, applied od for 5 days, focusing on areas like the axilla, groin, and perineum.
420
Q: Which antibiotics are commonly used to treat MRSA infections?
A: Vancomycin, teicoplanin, and linezolid.
421
Q: Which antibiotics should not generally be used alone for MRSA due to resistance concerns?
A: Rifampicin, macrolides, tetracyclines, aminoglycosides, and clindamycin.
422
Q: What are some newer antibiotics used for resistant MRSA cases?
A: Linezolid, quinupristin/dalfopristin combinations, and tigecycline.
423
Q: What virus causes mumps?
A: Mumps is caused by an RNA paramyxovirus.
424
Q: How is mumps spread?
A: Mumps is spread by respiratory droplets, affecting respiratory tract epithelial cells, then the parotid glands, and can spread to other tissues.
425
Q: What are the clinical features of mumps?
A: Clinical features include fever, malaise, muscular pain, and parotitis (initially unilateral, becoming bilateral in 70% of cases).
426
Q: What is the management of mumps?
A: Management includes rest and paracetamol for high fever or discomfort. It is a notifiable disease.
427
Q: What are common complications of mumps?
A: Complications include orchitis (uncommon in pre-pubertal males, but occurs in 25-35% of post-pubertal males), hearing loss (usually unilateral and transient), meningoencephalitis, and pancreatitis.
428
Q: What causes atypical pneumonia often affecting younger patients?
A: Mycoplasma pneumoniae.
429
Q: What are some complications of Mycoplasma pneumoniae?
A: Complications include cold agglutinins (causing hemolytic anemia and thrombocytopenia), erythema multiforme, erythema nodosum, meningoencephalitis, Guillain-Barre syndrome, bullous myringitis, pericarditis/myocarditis, gastrointestinal issues (hepatitis, pancreatitis), and renal problems (acute glomerulonephritis).
430
Q: What are the typical symptoms of Mycoplasma pneumoniae infection?
A: Symptoms typically include a prolonged and gradual onset, flu-like symptoms followed by a dry cough, and bilateral consolidation on x-ray.
431
Q: How is Mycoplasma pneumoniae diagnosed?
A: Diagnosis is generally made through Mycoplasma serology and may show positive cold agglutination test with red blood cell agglutination on peripheral blood smear.
432
Q: What is the treatment for Mycoplasma pneumoniae infection?
A: The treatment includes doxycycline or a macrolide (e.g., erythromycin or clarithromycin).
433
Q: What is necrotising fasciitis?
A: Necrotising fasciitis is a medical emergency that involves severe soft tissue infection, often affecting deep fascial planes, and is difficult to recognize in the early stages.
434
Q: How is necrotising fasciitis classified?
Type 1: caused by mixed anaerobes and aerobes, often post-surgery in diabetics (most common).
Type 2: caused by Streptococcus pyogenes.
435
Q: What are common risk factors for necrotising fasciitis?
A: Risk factors include recent trauma, burns, soft tissue infections, diabetes mellitus (especially with SGLT-2 inhibitors), intravenous drug use, and immunosuppression.
436
Q: What is the most commonly affected site in necrotising fasciitis?
A: The most commonly affected site is the perineum, leading to Fournier's gangrene.
437
Q: What are the key features of necrotising fasciitis?
A: Features include acute onset, pain, swelling, erythema, rapidly worsening cellulitis, and pain out of proportion to physical findings. Late signs include skin necrosis, crepitus (gas gangrene), and hypoaesthesia to light touch. Fever and tachycardia may be absent or occur late.
438
Q: What is the management of necrotising fasciitis?
A: Management includes urgent surgical referral for debridement and intravenous antibiotics.
439
Q: What is non-gonococcal urethritis (NGU)?
A: Non-gonococcal urethritis (NGU) refers to urethritis where gonococcal bacteria are not identified in the initial swab, typically involving purulent urethral discharge and dysuria.
440
Q: What is the most common cause of non-gonococcal urethritis?
A: The most common cause is Chlamydia trachomatis.
441
Q: What is the typical management for non-gonococcal urethritis?
A: Management includes contact tracing and antibiotics such as oral azithromycin or doxycycline as recommended by BNF and BASHH.
442
Q: What are the common symptoms of Norovirus infection?
A: Symptoms include nausea, vomiting, diarrhoea, and may be accompanied by headaches, low-grade fevers, and myalgia.
443
Q: How is Norovirus transmitted?
A: Norovirus is transmitted via the faecal-oral route, including aerosolized particles from vomiting, direct contact with infected surfaces, and food preparation.
444
Q: How is Norovirus diagnosed?
A: Diagnosis is based on clinical history, stool culture, and viral PCR.
445
Q: What are the differentiating features of Salmonella infection compared to Norovirus?
A: Salmonella has a 6-72 hour incubation period, often causes bloody diarrhoea, and is associated with high fever.
446
Q: What is the resolution and potential complication of Norovirus infection?
A: Norovirus infection is self-limiting in immunocompetent patients, resolving within 72 hours, but dehydration and electrolyte imbalances may occur.
447
Q: What is another name for erythema infectiosum caused by Parvovirus B19?
A: Fifth disease or slapped-cheek syndrome.
448
Q: What is the characteristic rash seen in erythema infectiosum?
A: A rose-red rash that makes the cheeks appear bright red, often described as "slapped cheeks."
449
Q: What triggers the recurrence of the rash in erythema infectiosum?
A: Warm baths, sunlight, heat, or fever may trigger a recurrence of the bright red cheeks and rash.
450
Q: Is school exclusion necessary for children with erythema infectiosum?
A: No, children are no longer infectious once the rash appears, so school exclusion is unnecessary.
451
Q: How is Parvovirus B19 spread?
A: It is spread through the respiratory route and a person is infectious 3 to 5 days before the rash appears.
452
Q: What are the potential complications of Parvovirus B19 in pregnant women?
A: Hydrops fetalis, which leads to severe anaemia, heart failure, and accumulation of fluid in fetal serous cavities (ascites, pleural and pericardial effusions).
453
Q: What is the treatment for hydrops fetalis caused by Parvovirus B19 in pregnancy?
A: Intrauterine blood transfusions.
454
Q: What are some other presentations of Parvovirus B19?
A: Asymptomatic, pancytopaenia in immunosuppressed patients, and aplastic crises in conditions like sickle-cell disease.
455
Q: How does Parvovirus B19 affect erythropoiesis?
A: Parvovirus B19 suppresses erythropoiesis for about a week, leading to aplastic anaemia in some cases, especially in chronic haemolytic anaemia.
456
Q: What is the most common cause of community-acquired pneumonia (CAP)?
A: Streptococcus pneumoniae (pneumococcus) accounts for around 80% of CAP cases.
457
Q: Which organism is classically associated with pneumonia in alcoholics?
A: Klebsiella pneumoniae is classically associated with pneumonia in alcoholics.
458
Q: What is the post-exposure prophylaxis for HIV?
A: Oral antiretrovirals (e.g., Tenofovir, Emtricitabine, Lopinavir, Ritonavir) should be given as soon as possible (within 1-2 hours, up to 72 hours following exposure) for 4 weeks. Serological testing should be done at 12 weeks.
459
Q: What is the most sensitive diagnostic test for hyposplenism?
A: The most sensitive diagnostic test is a radionucleotide-labelled red cell scan.
460
Q: Why does hyposplenism increase the risk of post-splenectomy sepsis?
A: Hyposplenism increases the risk due to the spleen's role in detecting and responding to encapsulated organisms, leading to impaired immunity.
461
Q: What vaccines should be administered before or after splenectomy to prevent post-splenectomy sepsis?
A: Pneumococcal, Haemophilus type b, and Meningococcal type C vaccines should be administered two weeks before or after splenectomy.
462
Q: What is the recommended schedule for Meningococcal and Haemophilus influenzae type b (Hib) vaccines after splenectomy?
A: Men C and Hib vaccines should be given at two weeks post-splenectomy, and the MenACWY vaccine one month later. Children under 2 may need a booster at 2 years.
463
Q: What vaccine should be administered annually to individuals who have undergone splenectomy?
A: Annual influenza vaccination is recommended for all splenectomy patients.
464
Q: What is the antibiotic prophylaxis recommended for individuals post-splenectomy?
A: Penicillin V is recommended, typically for at least 2 years or until the patient is 16 years old, though some patients may require lifelong antibiotic prophylaxis.
465
Q: What type of bacteria is Pseudomonas aeruginosa?
A: Pseudomonas aeruginosa is an aerobic Gram-negative rod.
466
Q: What infections are commonly caused by Pseudomonas aeruginosa?
A: Pseudomonas aeruginosa causes chest infections (especially in cystic fibrosis), skin infections (burns, wound infections, 'hot tub' folliculitis), otitis externa, and urinary tract infections.
467
Q: What is pyrexia of unknown origin (PUO)?
A: PUO is defined as a prolonged febrile illness with temperatures exceeding 38.3°C on several occasions over at least 3 weeks, with no established diagnosis after one week of inpatient investigation.
468
Q: What are the types of PUO?
Classical PUO: Often due to infections, malignancies, or non-infectious inflammatory diseases.
Hospital-acquired PUO: Fevers developing in hospitalized patients, often due to nosocomial infections, thromboembolic diseases, or drug fevers.
Neutropenic PUO: Seen in neutropenic patients (e.g., chemotherapy), typically due to infections.
HIV-associated PUO: Seen in HIV patients, caused by opportunistic infections, malignancies, or HIV itself.
469
Q: What are the causes of PUO?
Infections (30%): e.g., tuberculosis, abscesses.
Malignancies (20%): e.g., lymphoma, hypernephroma, leukaemia, atrial myxoma.
Non-infectious inflammatory diseases: e.g., systemic lupus erythematosus, temporal arteritis, rheumatoid arthritis.
Miscellaneous (50%): e.g., drug fevers, factitious fever.
470
Q: What is the diagnostic approach to PUO?
History and physical examination: Focus on travel, occupational, animal exposures, medical history, and medication use.
Laboratory tests: Full blood count, ESR/CRP, HIV test, blood cultures, urine analysis, and chest radiography.
Imaging: CT scans, MRI, and PET scans.
Biopsies and specialized tests: Depending on clinical suspicion, targeted biopsies and bone marrow examination may be required.
471
Q: What is Q fever and what causes it?
A: Q fever is caused by Coxiella burnetii, a rickettsia. The source of infection is typically an abattoir, cattle/sheep, or inhalation of infected dust.
472
Q: What are the clinical features of Q fever?
Prodrome: fever, malaise
Pyrexia of unknown origin
Transaminitis (elevated liver enzymes)
Atypical pneumonia
Endocarditis (culture-negative)
473
Q: What is the management for Q fever?
A: Doxycycline is the treatment for Q fever.
474
Q: What virus causes Rabies and what is its structure?
A: Rabies is caused by the rabies virus, which is an RNA rhabdovirus (specifically a lyssavirus) with a bullet-shaped capsid.
475
Q: How is Rabies transmitted?
A: Rabies is primarily transmitted through dog bites, but it may also be transmitted by bat, raccoon, and skunk bites.
476
Q: What are the clinical features of Rabies?
Prodrome: headache, fever, agitation
Hydrophobia: water-provoking muscle spasms
Hypersalivation
Negri bodies: cytoplasmic inclusion bodies found in infected neurons
477
Q: What respiratory pathogen is associated with Bronchiolitis?
A: Respiratory syncytial virus.
478
Q: Which virus is most commonly associated with Croup?
A: Parainfluenza virus.
479
Q: What pathogen causes the common cold?
A: Rhinovirus.
480
Q: What is the most common cause of community-acquired pneumonia?
A: Streptococcus pneumoniae.
481
Q: What pathogen is the most common cause of bronchiectasis exacerbations?
A: Haemophilus influenzae.
482
Q: Which pathogen causes acute epiglottitis?
A: Haemophilus influenzae.
483
Q: What pathogen is associated with pneumonia, particularly after influenza?
A: Staphylococcus aureus.
484
Q: What pathogen causes atypical pneumonia and is known for flu-like symptoms followed by a dry cough, with complications like haemolytic anaemia and erythema multiforme?
A: Mycoplasma pneumoniae.
485
Q: Which pathogen causes atypical pneumonia, often spread through air-conditioning systems, and may present with dry cough, lymphopenia, deranged liver function tests, and hyponatraemia?
A: Legionella pneumophilia.
486
Q: What is a common cause of pneumonia in HIV patients, where patients often have few chest signs and develop exertional dyspnoea?
A: Pneumocystis jiroveci.
487
Q: Which pathogen causes tuberculosis, with a wide range of presentations from asymptomatic to disseminated disease, and includes symptoms like cough, night sweats, and weight loss?
A: Mycobacterium tuberculosis.
488
Q: What is Rifampicin commonly used to treat?
A: Tuberculosis (in combination with other medications) and meningitis (prophylaxis after close contact).
489
Q: What are the common adverse effects of Rifampicin?
Potent CYP450 liver enzyme inducer
Hepatitis
Orange secretions
Flu-like symptoms
490
Q: What is the causative organism of rubella?
A: Rubella is caused by the togavirus.
491
Q: When are individuals with rubella infectious?
A: Individuals with rubella are infectious from 7 days before symptoms appear to 4 days after the onset of the rash.
492
Q: What are the typical features of rubella?
Prodrome: Low-grade fever
Rash: Maculopapular, initially on the face and spreading to the body, usually fading by 3-5 days
Lymphadenopathy: Suboccipital and postauricular
493
Q: What are the potential complications of rubella?
Arthritis
Thrombocytopaenia
Encephalitis
Myocarditis
494
Q: What serious condition can result if rubella is contracted during pregnancy?
A: Congenital rubella syndrome.
495
Q: What are the acute symptoms of schistosomiasis?
Swimmer's itch
Acute schistosomiasis syndrome (Katayama fever)
Fever
Urticaria/angioedema
Arthralgia/myalgia
Cough
Diarrhoea
Eosinophilia
496
Q: What are the chronic manifestations of Schistosoma haematobium infection?
Frequency
Haematuria
Bladder calcification
Obstructive uropathy
Kidney damage
Risk factor for squamous cell bladder cancer
497
Q: How is Schistosoma haematobium diagnosed?
A: Diagnosis is confirmed by urine or stool microscopy looking for eggs, or serum schistosome antibodies for asymptomatic patients.
498
Q: What is the management for schistosomiasis?
A: The management involves a single oral dose of praziquantel.
499
Q: What is the quickSOFA (qSOFA) score and its criteria?
The qSOFA score helps identify patients at heightened risk of mortality in suspected infection. Criteria include:
Respiratory rate ≥ 22/min
Altered mentation
Systolic blood pressure ≤ 100 mm Hg
500
Q: What is the SOFA score used for?
A: The SOFA score is used to assess organ dysfunction, grading abnormality by organ system and considering clinical interventions.
501
Q: What are the Red flag criteria for sepsis according to NICE?
Systolic BP ≤ 90 mm Hg
Heart rate > 130 per minute
Respiratory rate ≥ 25 per minute
Non-blanching rash, mottled/ashen/cyanotic skin
Lactate ≥ 2 mmol/l
Acute confusional state or unresponsive
502
Q: What are the components of the sepsis six management?
Administer oxygen (aim for saturations >94%)
Take blood cultures
Give broad-spectrum antibiotics
Give intravenous fluid challenges
Measure serum lactate
Measure accurate hourly urine output
503
Q: What does a SOFA score of 2 or more indicate?
A: A SOFA score of 2 or more reflects an overall mortality risk of approximately 10% in a general hospital population with suspected infection.
504
Q: What is the most common cause of genital herpes?
A: Genital herpes is most often caused by herpes simplex virus (HSV) type 2. Primary attacks are severe, often associated with fever, while subsequent attacks are less severe and localized.
505
Q: What is the primary symptom of syphilis?
A: The primary symptom of syphilis is a painless ulcer (chancre), which appears after an incubation period of 9-90 days.
506
Q: What causes chancroid and what is its characteristic feature?
A: Chancroid is caused by Haemophilus ducreyi, leading to painful genital ulcers with a sharply defined, ragged, undermined border and unilateral, painful inguinal lymphadenopathy.
507
Q: What is Lymphogranuloma venereum (LGV) and how is it treated?
LGV is caused by Chlamydia trachomatis and involves three stages:
Small painless pustule forming an ulcer
Painful inguinal lymphadenopathy
Proctocolitis
Treatment: Doxycycline.
508
Q: What are other causes of genital ulcers besides herpes and syphilis?
Behcet's disease
Carcinoma
Granuloma inguinale (caused by Klebsiella granulomatis)
509
Q: What is a spinal epidural abscess (SEA)?
A: Spinal epidural abscess (SEA) is a collection of pus located superficial to the dura mater, covering the spinal cord, and is an emergency that requires urgent investigation and treatment to prevent spinal cord damage.
510
Q: What is the most common causative organism of spinal epidural abscess (SEA)?
A: The most common causative organism of SEA is Staphylococcus aureus.
511
Q: What are the typical symptoms of spinal epidural abscess (SEA)?
Fever
Back pain
Focal neurological deficits, depending on the segment of the spinal cord affected.
512
Q: What is the treatment for spinal epidural abscess (SEA)?
Broad-spectrum antibiotics initially, refined based on culture results
Surgical evacuation of the abscess if it is large, compressive, causing neurological deficits, or not responding to antibiotics alone.
513
Q: What infections are patients at increased risk for following a splenectomy?
Pneumococcus
Haemophilus influenzae
Meningococcus
Capnocytophaga canimorsus (typically from dog bites)
514
Q: What vaccinations are recommended before a splenectomy?
Vaccinations to be done 2 weeks prior to an elective splenectomy include:
Hib (Haemophilus influenzae type b)
Meningitis A & C
Annual influenza vaccine
Pneumococcal vaccine (every 5 years)
515
Q: What is the recommended antibiotic prophylaxis following a splenectomy?
Penicillin V is recommended for antibiotic prophylaxis.
Duration: Generally, for at least 2 years or until 16 years of age; some patients are given lifelong prophylaxis.
516
Q: What changes occur in the blood following a splenectomy?
Platelets rise initially (especially in ITP, where treatment is given after splenic artery clamping)
Howell-Jolly bodies appear on the blood film in the following weeks
Other changes include target cells and Pappenheimer bodies
517
Q: What are the CDC diagnostic criteria for Staphylococcal Toxic Shock Syndrome?
Fever: Temperature > 38.9ºC
Hypotension: Systolic blood pressure < 90 mmHg
Diffuse erythematous rash
Desquamation of rash, especially on palms and soles
Involvement of three or more organ systems, such as:
Gastrointestinal (diarrhoea and vomiting)
Mucous membrane erythema
Renal failure
Hepatitis
Thrombocytopenia
518
Q: What is the management for Staphylococcal Toxic Shock Syndrome?
Removal of the infection focus (e.g., retained tampon)
IV fluids
IV antibiotics
519
Q: What is Strongyloides stercoralis?
A: Strongyloides stercoralis is a human parasitic nematode worm that causes strongyloidiasis.
520
Q: What are the typical features of strongyloidiasis?
Diarrhoea
Abdominal pain/bloating
Papulovesicular lesions at the site where larvae penetrate the skin (e.g. soles of feet, buttocks)
Larva currens: Pruritic, linear, urticarial rash
If larvae migrate to the lungs, they can cause a pneumonitis similar to Loeffler's syndrome.
521
Q: What is the treatment for Strongyloides stercoralis infection?
A: Ivermectin and albendazole are used to treat Strongyloides stercoralis infection.
522
Q: What are some adverse effects of co-trimoxazole?
Hyperkalaemia
Headache
Rash, including Steven-Johnson Syndrome.
523
Q: What is syphilis caused by?
A: Syphilis is caused by the spirochaete Treponema pallidum.
524
Q: What are the primary features of syphilis?
Chancre: A painless ulcer at the site of sexual contact
Local non-tender lymphadenopathy
In women: Often not seen, as the lesion may be on the cervix.
525
Q: What are the secondary features of syphilis?
Secondary features occur 6-10 weeks after primary infection and include:
Systemic symptoms: Fevers, lymphadenopathy
Rash: On the trunk, palms, and soles
Buccal 'snail track' ulcers (30%)
Condylomata lata: Painless, warty lesions on the genitalia.
526
Q: What are the features of congenital syphilis?
Blunted upper incisor teeth (Hutchinson's teeth)
'Mulberry' molars
Rhagades: Linear scars at the angle of the mouth
Keratitis
Saber shins
Saddle nose
Deafness.
527
Q: What are the two types of serological tests used to diagnose syphilis?
Non-treponemal tests:
Not specific for syphilis and may result in false positives.
Assess the quantity of antibodies produced in response to a cardiolipin-cholesterol-lecithin antigen.
Examples: Rapid Plasma Reagin (RPR), Venereal Disease Research Laboratory (VDRL).
Becomes negative after treatment.
Treponemal-specific tests:
More specific for syphilis, but more complex and expensive.
Reported as 'reactive' or 'non-reactive'.
Examples: TP-EIA (T. pallidum enzyme immunoassay), TPHA (T. pallidum HaemAgglutination test).
TP-EIA has become increasingly popular.
528
Q: What is the typical testing algorithm for syphilis diagnosis?
A: The typical testing algorithm involves a combination of a non-treponemal test and a treponemal-specific test.
529
Q: What are some causes of false-positive non-treponemal tests?
Causes of false positives include:
Pregnancy
SLE (Systemic Lupus Erythematosus), anti-phospholipid syndrome
Tuberculosis
Leprosy
Malaria
HIV
530
Q: What does a positive non-treponemal test + positive treponemal test indicate?
A: This combination is consistent with active syphilis infection.
531
Q: What does a positive non-treponemal test + negative treponemal test indicate?
A: This combination is consistent with a false-positive syphilis result, which may be due to conditions like pregnancy or SLE.
532
Q: What does a negative non-treponemal test + positive treponemal test indicate?
A: This combination is consistent with successfully treated syphilis.
533
Q: What is the first-line management for syphilis?
A: The first-line management for syphilis is intramuscular benzathine penicillin.
534
Q: What is an alternative treatment for syphilis?
A: An alternative treatment for syphilis is doxycycline.
535
Q: How should nontreponemal titres (e.g., RPR or VDRL) be used in syphilis management?
A: Nontreponemal titres should be monitored after treatment to assess the response. A fourfold decline in titres (e.g., 1:16 → 1:4 or 1:32 → 1:8) is often considered an adequate response to treatment.
536
Q: What is the Jarisch-Herxheimer reaction and what causes it?
A: The Jarisch-Herxheimer reaction is a reaction sometimes seen following syphilis treatment, characterized by fever, rash, and tachycardia after the first dose of antibiotic. It is thought to be due to the release of endotoxins following bacterial death.
537
Q: How should the Jarisch-Herxheimer reaction be managed?
A: The Jarisch-Herxheimer reaction typically does not require treatment other than antipyretics if needed. It usually occurs within a few hours of treatment.
538
Q: What distinguishes the Jarisch-Herxheimer reaction from anaphylaxis?
A: Unlike anaphylaxis, the Jarisch-Herxheimer reaction does not involve wheeze or hypotension.
539
Q: What causes tetanus?
A: Tetanus is caused by the tetanospasmin exotoxin released from Clostridium tetani.
540
Q: What are some clinical features of tetanus?
Prodrome: fever, lethargy, headache
Trismus (lockjaw)
Risus sardonicus (facial spasms)
Opisthotonus (arched back, hyperextended neck)
Spasms (e.g., dysphagia)
541
Q: What is the management of tetanus?
Supportive therapy (including ventilatory support and muscle relaxants)
Intramuscular human tetanus immunoglobulin for high-risk wounds (e.g., compound fractures, delayed surgical intervention)
Metronidazole (preferred over benzylpenicillin) as the antibiotic of choice.
542
Q: What are common examples of tetracyclines?
Doxycycline
Tetracycline
543
Q: What are notable adverse effects of tetracyclines?
Discolouration of teeth (should not be used in children < 12 years)
Photosensitivity
Angioedema
Black hairy tongue
544
Q: What is the usual animal reservoir for Toxoplasma gondii?
A: The usual animal reservoir for Toxoplasma gondii is the cat, although other animals such as rats may also carry the disease.
545
Q: What are the typical symptoms of Toxoplasmosis in immunocompetent patients?
A: In immunocompetent patients, Toxoplasmosis is often asymptomatic. If symptomatic, it typically presents with fever, malaise, and lymphadenopathy, resembling infectious mononucleosis. Less common manifestations include meningoencephalitis and myocarditis.
546
Q: What is the investigation of choice for Toxoplasmosis?
A: Serology is the investigation of choice for diagnosing Toxoplasmosis.
547
Q: When is treatment required for Toxoplasmosis in immunocompetent patients?
A: Treatment is not usually required for immunocompetent patients unless the infection is severe or the patient is immunosuppressed.
548
Q: What is the presentation of cerebral toxoplasmosis in HIV/immunosuppressed patients?
A: In HIV/immunosuppressed patients, cerebral toxoplasmosis presents with constitutional symptoms, headache, confusion, and drowsiness. CT scans show single or multiple ring-enhancing lesions with possible mass effect.
549
Q: What is the treatment for cerebral toxoplasmosis in HIV/immunosuppressed patients?
A: The treatment for cerebral toxoplasmosis is pyrimethamine plus sulphadiazine for at least 6 weeks.
550
Q: What are the characteristics of latent tuberculosis?
A: Latent tuberculosis patients are asymptomatic and non-infectious. They are diagnosed with a positive tuberculin skin test or Interferon-Gamma Release Assay (IGRA), combined with a normal chest x-ray to exclude active tuberculosis.
551
Q: How is latent tuberculosis treated according to NICE guidelines?
NICE offers two treatment options for latent tuberculosis:
3 months of isoniazid (with pyridoxine) and rifampicin, or
6 months of isoniazid (with pyridoxine).
552
Q: Why are there two treatment options for latent tuberculosis?
3 months of isoniazid and rifampicin is recommended for people under 35 years if hepatotoxicity is a concern after assessing liver function and risk factors.
6 months of isoniazid is preferred when rifamycin interactions are a concern, such as in HIV-positive patients or those with a transplant.
553
Q: Can patients with latent tuberculosis transmit the disease to others?
A: No, patients with latent tuberculosis cannot transmit the disease. Therefore, there are no restrictions on employment, etc., unless the patient develops active tuberculosis.
554
Q: What is the standard therapy for treating active tuberculosis?
Initial phase (first 2 months):
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol (added routinely in the 2006 NICE guidelines, previously only added if drug-resistant tuberculosis was suspected)
Continuation phase (next 4 months):
Rifampicin
Isoniazid
555
Q: What are some complications of tuberculosis treatment?
Complications include:
Immune reconstitution disease: Occurs 3-6 weeks after starting treatment, often presenting with enlarging lymph nodes.
Drug adverse effects:
Rifampicin: Potent liver enzyme inducer, hepatitis, orange secretions, flu-like symptoms.
Isoniazid: Peripheral neuropathy (prevent with pyridoxine), hepatitis, agranulocytosis, liver enzyme inhibitor.
Pyrazinamide: Hyperuricaemia causing gout, arthralgia, myalgia, hepatitis.
Ethambutol: Optic neuritis (check visual acuity before and during treatment).
556
Q: What investigations are used to diagnose active tuberculosis?
Diagnosis of active tuberculosis involves:
Chest x-ray: Upper lobe cavitation is a classical finding of reactivated TB, with bilateral hilar lymphadenopathy.
Sputum smear: Requires 3 specimens, stained for acid-fast bacilli (Ziehl-Neelsen stain). Sensitivity is 50-80%, reduced to 20-30% in HIV-infected individuals.
Sputum culture: The gold standard for diagnosis, more sensitive than smear or nucleic acid amplification tests, can assess drug sensitivities. It takes 1-3 weeks (longer if using solid media).
Nucleic acid amplification tests (NAAT): Provides a rapid diagnosis (24-48 hours), more sensitive than smear but less sensitive than culture.
557
Q: What is primary tuberculosis and how does it develop?
A: Primary tuberculosis occurs when a non-immune host is exposed to Mycobacterium tuberculosis. A small lung lesion, known as a Ghon focus, develops, made up of tubercle-laden macrophages. The Ghon complex is the combination of the Ghon focus and affected hilar lymph nodes. In immunocompetent individuals, the lesion typically heals by fibrosis, but in immunocompromised individuals, disseminated disease (miliary TB) may develop.
558
Q: What is secondary (post-primary) tuberculosis and what causes reactivation?
A: Secondary tuberculosis occurs when the initial infection is reactivated, often due to immunocompromise. This typically happens in the apex of the lungs but can spread locally or to distant sites. Causes of immunocompromise include:
Immunosuppressive drugs (e.g., steroids)
HIV
Malnutrition
559
Q: What is urethritis and how does it typically present in men?
A: Urethritis refers to inflammation of the urethra, typically in men, presenting with dysuria (painful urination) and/or urethral discharge. It is asymptomatic in up to 30% of men.
560
Q: What are the two types of urethritis and their causes?
Urethritis is divided into:
Gonococcal urethritis (caused by Neisseria gonorrhoeae)
Non-gonococcal urethritis (NGU), also called non-specific urethritis (NSU), commonly caused by:
Chlamydia trachomatis
Ureaplasma urealyticum
Mycoplasma genitalium
561
Q: How is urethritis investigated?
Investigation typically includes a urethral swab that is Gram stained to look for:
Leukocytes
Gram-negative diplococci (indicating gonococcal infection)
Additionally, Chlamydia is increasingly diagnosed using urinary nucleic acid amplification tests (NAAT).
562
Q: What are the complications of urethritis?
epididymitis
Subfertility
Reactive arthritis
563
Q: What is the management for urethritis?
Oral doxycycline for 7 days
Alternatively, a single dose of oral azithromycin
564
Q: Who should not use a urine dipstick for diagnosing a lower UTI?
Women over 65 years
Men
Catheterised patients
565
Q: When should a urine culture be sent for a suspected lower UTI?
Women aged over 65 years
Recurrent UTIs (2 episodes in 6 months or 3 in 12 months)
Pregnant women
Men
Visible or non-visible haematuria
566
Q: How should non-pregnant women with a lower urinary tract infection (UTI) be managed?
Non-pregnant women should be treated according to local antibiotic guidelines. NICE recommends trimethoprim or nitrofurantoin for 3 days. A urine culture should be sent if:
Aged > 65 years
Visible or non-visible haematuria
567
Q: What is the management of a pregnant woman with a lower urinary tract infection?
A urine culture should be sent in all cases.
First-line treatment: Nitrofurantoin (avoid near term)
Second-line treatment: Amoxicillin or Cefalexin
Trimethoprim is teratogenic in the first trimester and should be avoided.
For asymptomatic bacteriuria:
A urine culture should be done at the first antenatal visit.
Treat with nitrofurantoin, amoxicillin, or cefalexin for 7 days.
Test of cure: Send a urine culture after treatment.
568
Q: What should be done for women who suffer recurrent UTIs following sexual intercourse?
Women with recurrent UTIs after sexual intercourse can be offered post-coital antibiotic prophylaxis:
Single dose of trimethoprim or nitrofurantoin is used first-line.
569
Q: How should men with lower urinary tract infection (UTI) be managed?
Offer an immediate antibiotic prescription for 7 days.
First-line treatment: Trimethoprim or nitrofurantoin (unless prostatitis is suspected).
A urine culture should be sent in all cases before antibiotics.
Referral to urology is not routinely required for men with one uncomplicated UTI.
570
Q: How should catheterised patients with a urinary tract infection (UTI) be managed?
Do not treat asymptomatic bacteriuria.
If symptomatic, treat with an antibiotic.
A 7-day course is recommended (not 3 days).
Consider removing or changing the catheter if it has been in place for >7 days.
571
Q: What is the management of acute pyelonephritis?
Hospital admission should be considered.
Local antibiotic guidelines should be followed.
The BNF recommends a broad-spectrum cephalosporin or a quinolone (for non-pregnant women) for 10-14 days.
572
Q: What are live attenuated vaccines, and who should avoid them?
A: Live attenuated vaccines use a weakened form of the pathogen to stimulate an immune response similar to natural infection, without causing the disease. They are typically not recommended for individuals with compromised immune systems.
Examples:
BCG
MMR (measles, mumps, rubella)
Influenza (intranasal)
Oral rotavirus
Oral polio
Yellow fever
Oral typhoid
573
Q: What are inactivated vaccines and how do they work?
Inactivated vaccines use pathogens that have been killed (by heat or chemicals) to elicit an immune response. These vaccines might require booster doses to maintain immunity as their induced immune response is generally weaker than live vaccines.
Examples:
Rabies
Hepatitis A
Influenza (intramuscular)
574
Q: What are toxoid vaccines and why do they require booster doses?
Toxoid vaccines are based on the toxin produced by certain bacteria that is rendered harmless and used to stimulate an immune response. Booster doses are needed because the immune response can wane over time.
Examples:
Tetanus
Diphtheria
Pertussis
575
Q: What are subunit and conjugate vaccines?
Subunit vaccines use only part of the pathogen to generate an immune response. Conjugate vaccines link bacterial polysaccharide outer coats (that are poorly immunogenic) to proteins, making them more immunogenic.
Examples:
Pneumococcus (conjugate)
Haemophilus (conjugate)
Meningococcus (conjugate)
Hepatitis B
Human papillomavirus
576
Q: What are common adverse effects of vancomycin?
Nephrotoxicity (kidney damage)
Ototoxicity (hearing damage)
Thrombophlebitis (inflammation of veins)
Red man syndrome (occurs with rapid infusion, leading to a red rash, hypotension, and flushing)
577
Q: What are the common clinical features of viral meningitis?
Headache
Neck stiffness
Photophobia (less severe than in bacterial meningitis)
Confusion
Fever
578
Q: How is viral meningitis managed?
A: Treatment is supportive, and if there is concern about bacterial meningitis or encephalitis, broad-spectrum antibiotics (e.g., ceftriaxone and aciclovir) are given while awaiting lumbar puncture results. Aciclovir is used if HSV is suspected. Viral meningitis is generally self-limiting, with improvement in 7-14 days in immunocompetent patients.
579
Q: When should broad-spectrum antibiotics be started in viral meningitis?
A: Broad-spectrum antibiotics should be started if there is any concern for bacterial meningitis or encephalitis, especially in patients with risk factors such as being elderly or immunocompromised.
580
Q: What is yellow fever?
A: Yellow fever is a viral hemorrhagic fever caused by a zoonotic infection transmitted by Aedes mosquitoes.
581
Q: What are the clinical features of yellow fever?
Mild flu-like illness lasting less than a week
Sudden onset of high fever, rigors, nausea, and vomiting
Bradycardia may develop
Brief remission followed by jaundice, haematemesis, and oliguria
582
Q: What may occur in severe cases of yellow fever?
A: In severe cases, jaundice and haematemesis may occur.
583
Q: What are Councilman bodies?
A: Councilman bodies are inclusion bodies that may be seen in the hepatocytes of patients with yellow fever.
584
Which cause of diarrhoea is linked to lactose intolerance/milk
giardiasis
585
Which cause of diarrhoea is linked to floating stool
giardiasis
586
Difference between chancroid and syphilis
chancroid has painful ulcer whereas syphillis doesnt
587
Painless genital pustule → ulcer → painful inguinal lymphadenopathy → proctocolitis
lymphogranuloma venereum
588
Q: What is the primary use of trimethoprim?
A: Trimethoprim is mainly used in the management of urinary tract infections.
589
Q: How might trimethoprim interact with methotrexate?
A: Both trimethoprim and methotrexate inhibit dihydrofolate reductase, which may lead to an interaction.
590
Q: What are the adverse effects of trimethoprim?
Myelosuppression
Transient rise in creatinine (due to competitive inhibition of tubular secretion of creatinine)
Hyperkalaemic distal renal tubular acidosis (type 4) (due to blocking the ENaC channel in the distal nephron)
591
Q: How does trimethoprim affect creatinine levels?
A: Trimethoprim competitively inhibits the tubular secretion of creatinine, resulting in a temporary increase in creatinine levels, which reverses upon stopping the drug.
592
Q: What are the features of trichomoniasis in women?
Vaginal discharge: Offensive, yellow/green, frothy
Vulvovaginitis
Strawberry cervix
pH > 4.5
593
Q: How is trichomoniasis diagnosed?
A: Trichomoniasis is diagnosed by microscopy of a wet mount showing motile trophozoites.
594
Q: What is the management of trichomoniasis?
A: The management of trichomoniasis involves oral metronidazole for 5-7 days, although a one-off dose of 2g metronidazole is also supported by the BNF.
595
What cause of diarrhoea is linked to reheated rice
bacillus
596
What do you do if after giving hep B vaccine, patient has inadequate results from testing a month after vaccine
give another booster
597
Relative bradycardia + diarrhoea
typhoid
598
Relative bradycardia + cough
Legionella
599
What causes pneumonia especially in cystic fibrosis patients
pseudomonas
600
Most common organism in central line infections
staph epidermidis
601
needlestick injury from hep b positive source. person is previously vaccinated but bloods show inadequate anti hbs
Hepatitis B immune globulin (HBIG) + a booster vaccine
602
most common complication in mumps
orchitis
603
india ink stain is used for what
cryptococcus
604
What does gas gangrene in C. perfringens look like
black blisters which produce foul smelling discharge
605
in asymptomatic patients, when should hiv testing be done after exposure
4 weeks
606
Patient has symptoms of temporal arteritis, but biopsy is normal. they are on pred. what do you do?
skip lesions can cause normal biopsy, continue pred
607
If combined test for HIV shows positive results, what should you do
repeat test in 12 weeks to confirm and start anti retroviral treatment today
608
How to differentiate between warts and herpes
herpes - ulcerated
warts - 'fleshy' and protruding
609
Negative nitrates on dipstick
no UTI
610
Atypical pneumonia with neuro signs cause
mycoplasma
611
What is the purpose of the BCG vaccine
protective against severe diseases in children, particularly TB meningitis and disseminated TB in children
612
What causes bacterial vaginosis
Gardnerella vaginalis
613
how long can HIV post exposure prophylaxis be given until
72 hours post exposure
614
what does ground-glass hepatocytes on light microscopy point towards regarding hep B infection
chronic infection
615
When is the shingles vaccine available
70-79 years old
616
what is the most common HIV opportunistic infection
PCP pneumonia
617
treatment for epididymitis
single shot of ceftriaxone 1 g, followed by doxycycline 2 × 100 mg/day for two weeks.
618
When you get a needlestick infection, what should you do initially
encourage bleeding from the site
619
what makes c diff particularly difficult to destroy
spore formation
620
