Infectious Disease Flashcards

1
Q

what is the commonest causes of bacterial intestinal disease in the UK

A

Campylobacter
The majority of cases are caused by the Gram-negative bacillus Campylobacter jejuni. It is spread by the faecal-oral route and has an incubation period of 1-6 days.

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2
Q

Features of campylobacter?

A

prodrome: headache malaise
diarrhoea: often bloody
abdominal pain: may mimic appendicitis

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3
Q

Management of Campylobacter?

A

usually self-limiting
the BNF advises treatment if severe or the patient is immunocompromised. Antibiotics are recommended if severe symptoms (high fever, bloody diarrhoea, or more than eight stools per day) or symptoms have lasted more than one week
the first-line antibiotic is clarithromycin
ciprofloxacin is an alternative although the BNF states that ‘Strains with decreased sensitivity to ciprofloxacin isolated frequently’

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4
Q

complications of campylobacter?

A

Guillain-Barre syndrome may follow Campylobacter jejuni infections
reactive arthritis
septicaemia, endocarditis, arthritis

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5
Q

management of Legionella pneumonia?

A

treat with erythromycin/clarithromycin

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6
Q

What is Granuloma Inguinale?

A

Granuloma inguinale, also known as Donovanosis, is a sexually transmitted infection caused by the bacterium Klebsiella granulomatis. It presents with painless genital ulcers and can progress to cause significant tissue destruction if left untreated.

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7
Q

What are the symptoms of HIV seroconversion?

A

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

Features
sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis

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8
Q

mechanism of action of ahminoglycosides and adverse effects?

A

Binds to 30S subunit causing misreading of mRNA

adverse effects - Nephrotoxicity, Ototoxicity

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9
Q

Mechanism of action of tetracyclines? and adverse effects?

A

Binds to 30S subunit blocking binding of aminoacyl-tRNA

Adverse effects Discolouration of teeth, photosensitivity

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10
Q

mechanism of action of clindamycin?

A

Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site)

Adverse effects - common cause of c.diff

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11
Q

Mechanism of action of macrocodes?

A

Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site)

adverse effects
Nausea (especially erythromycin), P450 inhibitor, prolonged QT interval

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12
Q

what is Orf and how does it present?

A

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

generally affects the hands and arms
initially small, raised, red-blue papules
later may increase in size to 2-3 cm and become flat-topped and haemorrhagic

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13
Q

what are the different types of tape worm?

A

Cysticercosis
Hydatid disease

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14
Q

what is the cause of cysticercosis and what is the management?

A

caused by Taenia solium (from pork) and Taenia saginata (from beef)
management: niclosamide

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15
Q

What is the cause of Hydatid disease and what is the management?

A

caused by the dog tapeworm Echinococcus granulosus
life-cycle involves dogs ingesting hydatid cysts from sheep liver
often seen in farmers
may cause liver cysts
management: albendazole

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16
Q

What is Chikungunya virus?

A

Alphavirus disease caused by infected mosquitoes. Areas affected are Africa, Asia and Indian subcontinent but in recent years there has been seen in a few cases in Southern Europe. Tanzania had the first reported case.

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17
Q

what are the symptoms and treatment of chikungunya ?

A

severe joint pain
high fever
flu like illness

Treatment: Relief of symptoms. No specific treatment.

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18
Q

what is the most common cause of diaeehowa in travellers?

A

Worldwide, enterotoxigenic E. coli (ETEC) is the most common cause of diarrhoea in travellers. There is, however, geographical variation - Campylobacter is more common in travellers in South East Asia.

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19
Q

post exposure prophylaxis for Hep B

A

HBsAg positive source
if the person exposed is a known responder to the HBV vaccine then a booster dose should be given
if they are a non-responder (anti-HBs < 10mIU/ml 1-2 months post-immunisation) they need to have hepatitis B immune globulin (HBIG) and a booster vaccine
unknown source
for known responders the HBV vaccine the Green Book advises considering a booster dose of HBV vaccine
for known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated should have an accelerated course of HBV vaccine

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20
Q

post exposure prophylaxis for Hep A

A

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

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21
Q

post exposure prophylaxis for Hep C

A

monthly PCR - if seroconversion then interferon +/- ribavirin

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22
Q

post exposure prophylaxis for varicella zoster?

A

VZIG for IgG negative pregnant women/immunosuppressed

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23
Q

what kind of virus is HIV?

A

HIV is a RNA retrovirus of the lentivirus genus (lentiviruses are characterized by a long incubation period)

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24
Q

what are the two variants of HIV?

A

two variants - HIV-1 and HIV-2
HIV-2 is more common in west Africa, has a lower transmission rate and is thought to be less pathogenic with a slower progression to AIDS

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25
What is the structure of HIV?
spherical in shape with two copies of single-stranded RNA enclosed by a capsid of the viral protein p24 a matrix composed of viral protein p17 surrounds the capsid envelope proteins: gp120 and gp41 pol gene encodes for viral enzymes reverse transcriptase, integrase and HIV protease
26
How does HIV enter cells?
HIV can infect CD4 T cells, macrophages and dendritic cells gp120 binds to CD4 and CXCR4 on T cells and CD4 and CCR5 on macrophages mutations in CCR5 can give immunity to HIV after entering a cell the enzyme reverse transcriptase creates dsDNA from the RNA for integration into the host cell's genome
27
what is Leishmaniasis?
Leishmaniasis is caused by the intracellular protozoa Leishmania, which are spread by the bites of sandflies. Cutaneous, mucocutaneous leishmaniasis and visceral forms are seen
28
what is cutaneous Leishmanisis?
caused by Leishmania tropica or Leishmania mexicana crusted lesion at the site of bite there may be an underlying ulcer it is typically diagnosed by doing a punch biopsy from the edge of the lesion allowing for both histology and culture cutaneous leishmaniasis acquired in South or Central America merits treatment due to the risk of mucocutaneous leishmaniasis whereas disease acquired in Africa or India can be managed more conservatively
29
what is mucocutaneous Leishmaniasis?
caused by Leishmania braziliensis skin lesions may spread to involve mucosae of nose, pharynx etc
30
what causes Visceral Leishmaniasis? what are the symptoms what is the treatment?
mostly caused by Leishmania donovani occurs in the Mediterranean, Asia, South America, Africa fever, sweats, rigors massive splenomegaly. hepatomegaly poor appetite*, weight loss occasionally patients may report increased appetite with paradoxical weight loss grey skin - 'kala-azar' means black sickness pancytopaenia secondary to hypersplenism the gold standard for diagnosis is bone marrow or splenic aspirate management the BNF recommends sodium stibogluconate, an organic pentavalent antimony compound amphotericin B may be used with or after treatment with an antimony compound
31
what is botulism caused by?
Clostridium botulinum gram positive anaerobic bacillus 7 serotypes A-G produces botulinum toxin, a neurotoxin which irreversibly blocks the release of acetylcholine may result from eating contaminated food (e.g. tinned) or intravenous drug use neurotoxin often affects bulbar muscles and autonomic nervous system
32
features of botulism?
Features patient usually fully conscious with no sensory disturbance flaccid paralysis diplopia ataxia bulbar palsy
33
treatment for botulism?
botulism antitoxin and supportive care antitoxin is only effective if given early - once toxin has bound its actions cannot be reversed
34
features of Legionella ?
Features flu-like symptoms including fever (present in > 95% of patients) dry cough relative bradycardia confusion lymphopaenia hyponatraemia deranged liver function tests pleural effusion: seen in around 30% of patients
35
how is viral meningitis managed?
supportive care Antivirals are of no benefit in the treatment of confirmed viral meningitis
36
what causes bacterial vaginosis ?
Bacterial vaginosis (BV) describes an overgrowth of predominately anaerobic organisms such as Gardnerella vaginalis This leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH.
37
what criteria is used for diagnosing BV?
Amsel's criteria for diagnosis of BV - 3 of the following 4 points should be present thin, white homogenous discharge clue cells on microscopy: stippled vaginal epithelial cells vaginal pH > 4.5 positive whiff test (addition of potassium hydroxide results in fishy odour)
38
how is BV managed?
if asymptomatic - dont need treatment unless pregnant Oral metronidazole
39
what may cause progressive multifocal leukoencephalopathy?
Progressive multifocal leukoencephalopathy is caused by the JC virus or BK virus JC virus affects significantly immunosuppressed patients. It causes demyelination and significant white matter changes and the clinical syndrome of PML which can include cognitive and behavioural abnormalities, sensory and motor deficits, ataxia, aphasia and cortical visual changes.
40
what are the clinical features of progressive multifocal leukoencephalopathy?
cognitive and behavioural abnormalities, sensory and motor deficits, ataxia, aphasia and cortical visual changes. Seizures are a common feature.
41
what would an MRI show in progressive multifocal leukoencephalopathy?
The MRI findings of cerebral white matter change without gadolinium enhancement are typical of progressive multifocal leukoencephalopathy (PML). CT brain would likely be performed first in this scenario but findings may be non specific and an MRI would be subsequently be performed. .
42
how should people who have been exposed to a confirmed case of bacteria meningitis be managed>?
should be given prophylactic antibiotics if they have close contact within the 7 days before onset oral ciprofloxacin or rifampicin may be used.
43
how is bacterial meningitis managed ?
< 3 months - IV cefotaxime + amoxicillin (or ampicillin) 3 months - 50 years - IV Cefotaxime > 50 years - IV cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin) Meningococcal - IV ben pen or cefotaxime Pneumococcal - IV cefotaxime H.ifluenzae - IV cefotaxime Lesteria - amoxicillin and gentamicin
44
Management of Lyme disease?
If asymptomatic - do not need treatment doxycycline if early disease. Amoxicillin is an alternative if doxycycline is contraindicated (e.g. pregnancy) people with erythema migrans should be commenced on antibiotic without the need for further tests ceftriaxone if disseminated disease Jarisch-Herxheimer reaction is sometimes seen after initiating therapy: fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)
45
features of Lyme disease
erythema migraines - bulls eye rash, typically presents 1-4 weeks after initial bite, usually painless Systemic features - headache, lethargy, fever, arthralgia Later features - heart block, peri/myocarditis, neurological (facial never palsy, radicular pain, meningitis)
46
investigations for Lyme disease?
NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present erythema migrans is therefore an indication to start antibiotics enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test if negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test. If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done if positive or equivocal then an immunoblot test for Lyme disease should be done
47
management of toxoplasmosis in immunocompetent patients?
Most infections are asymptomatic. Symptomatic patients usually have a self-limiting infection, often having clinical features resembling infectious mononucleosis (fever, malaise, lymphadenopathy). Other less common manifestations include meningoencephalitis and myocarditis. Serology is the investigation of choice. No treatment is usually required unless the patient has a severe infection or is immunosuppressed.
48
Toxoplasmosis in Immunosupressed patients?
Cerebral toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV constitutional symptoms, headache, confusion, drowsiness CT: usually single or multiple ring-enhancing lesions, mass effect may be seen management: pyrimethamine plus sulphadiazine for at least 6 weeks
49
how does toxoplasmosis infect the body?
Toxoplasma gondii is an obligate intracellular protozoan that infects the body via the gastrointestinal tract, lung or broken skin. It's oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.
50
management of Gonorrhoea?
IM cerftriaxone If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given if ceftriaxone is refused (e.g. needle-phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used
51
what causes typhoid?
Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia.
52
how is typhoid spread?
typhoid is transmitted via the faecal-oral route (also in contaminated food and water)
53
features of enteric fever?
initially systemic upset as above relative bradycardia abdominal pain, distension constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
54
complications of enteric fever?
osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens) GI bleed/perforation meningitis cholecystitis chronic carriage (1%, more likely if adult females)
55
what is the cause of acute epiglottis?
Acute epiglottitis is rare but serious infection caused by Haemophilus influenzae type B.
56
what are the features of acute epiglottis?
rapid onset high temperature, generally unwell stridor drooling of saliva 'tripod' position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position
57
how is acute epiglottis diagnosed
Diagnosis is made by direct visualisation (only by senior/airway trained staff, see below). However, x-rays may be done, particularly if there is concern about a foreign body: a lateral view in acute epiglottis will show swelling of the epiglottis - the 'thumb sign' in contrast, a posterior-anterior view in croup will show subglottic narrowing, commonly called the 'steeple sign'
58
how is acute epiglottis managed?
immediate senior involvement, including those able to provide emergency airway support (e.g. anaesthetics, ENT) endotracheal intubation may be necessary to protect the airway if suspected do NOT examine the throat due to the risk of acute airway obstruction the diagnosis is made by direct visualisation but this should only be done by senior staff who are able to intubate if necessary oxygen intravenous antibiotic
59
when is the tetanus vaccine given?
2 months 3 months 4 months 3-5 years 13-18 years
60
what is considered a tetanus prone wound and a high risk tetanus prone wound?
tetanus prone wound puncture-type injuries acquired in a contaminated environment e.g. gardening injuries wounds containing foreign bodies compound fractures wounds or burns with systemic sepsis certain animal bites and scratches High risk tetanus prone wound heavy contamination with material likely to contain tetanus spores e.g. soil, manure wounds or burns that show extensive devitalised tissue wounds or burns that require surgical intervention
61
when is tetanus vaccine required following wound?
Patient has had a full course of tetanus vaccines, with the last dose < 10 years ago no vaccine nor tetanus immunoglobulin is required, regardless of the wound severity Patient has had a full course of tetanus vaccines, with the last dose > 10 years ago if tetanus prone wound: reinforcing dose of vaccine high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue): reinforcing dose of vaccine + tetanus immunoglobulin If vaccination history is incomplete or unknown reinforcing dose of vaccine, regardless of the wound severity for tetanus prone and high-risk wounds: reinforcing dose of vaccine + tetanus immunoglobulin
62
what is strongyloides steracoralis?
Strongyloides stercoralis is a human parasitic nematode worm. The larvae are present in soil and gain access to the body by penetrating the skin. Infection with Strongyloides stercoralis causes strongyloidiasis.
63
what are the features and treatment of Strongyloides stercoralis?
Features diarrhoea abdominal pain/bloating papulovesicular lesions where the skin has been penetrated by infective larvae e.g. soles of feet and buttocks larva currens: pruritic, linear, urticarial rash if the larvae migrate to the lungs a pneumonitis similar to Loeffler's syndrome may be triggered Treatment ivermectin and albendazole are used
64
What abx are commonly used to treat MSRA ?
vancomycin teicoplanin linezolid
65
what is Lymphogranuloma venereum?
Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis serovars L1, L2 and L3*.
66
Risk factors of Lymphogranuloma venereum?
men who have sex with men the majority of patients who present in developed countries have HIV historically was seen more in the tropics
67
How does Lymhogranuloma venereum present?
Typically infection comprises of three stages: stage 1: small painless pustule which later forms an ulcer stage 2: painful inguinal lymphadenopathy may occasionally form fistulating buboes stage 3: proctocolitis
68
how is Lymphogrannuloma venereum treated?
Doxycycline
69
what is Pneumocystis Jiroveci Pneumonia?
Pneumocystis jiroveci (AKA PCP) is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa common opportunistic infection in AIDS all patients with a CD4 count < 200/mm³ should receive PCP prophylaxis
70
Features of Pneumocystis Jiroveci pneumonia?
dyspnoea dry cough fever very few chest signs Pneumothorax is a common complication of PCP. Extrapulmonary manifestations are rare (1-2% of cases), may cause hepatosplenomegaly lymphadenopathy choroid lesions ## Footnote It classically presents with a fever, dyspnoea, dry cough, exercise-induced desaturation and very few chest signs
71
Investigations for PCP?
CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings e.g. lobar consolidation. May be normal exercise-induced desaturation sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate PCP (silver stain shows characteristic cysts)
72
management of PCP?
Management co-trimoxazole IV pentamidine in severe cases aerosolized pentamidine is an alternative treatment for Pneumocystis jiroveci pneumonia but is less effective with a risk of pneumothorax steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)
73
key things in pneumonia causes....
 Streptococcus pneumoniae --> cold sores  Staph. Aureus --> followed by infection with H. Influenza  H. Influenza --> Infective exacerbation of COPD  Mycoplasma pneumonia --> Cold hemagglutination, deranged LFTs  Klebsiella pneumonia --> Alcoholics and causes cavitation  Legionella pneumonia --> history of traveling, swimming, living in hotels, presents with hyponatremia and deranged LFTs
74
what are the diagnostic criteria for staphylococcal toxic shock syndrome?
fever: temperature > 38.9ºC hypotension: systolic blood pressure < 90 mmHg diffuse erythematous rash desquamation of rash, especially of the palms and soles involvement of three or more organ systems: e.g. gastrointestinal (diarrhoea and vomiting), mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. confusion)
75
what vaccinations should be given to patients having splenectomy?
Vaccination if elective, should be done 2 weeks prior to operation Hib, meningitis A & C annual influenza vaccination pneumococcal vaccine every 5 years
76
Indications for splenectomy?
Trauma: 1/4 are iatrogenic Spontaneous rupture: EBV Hypersplenism: hereditary spherocytosis or elliptocytosis etc Malignancy: lymphoma or leukaemia Splenic cysts, hydatid cysts, splenic abscesses
77
What is Immune reconstitution inflammatory syndrome?
Immune reconstitution inflammatory syndrome is a condition generally associated with HIV/immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
78
what are examples of live attenuated vaccines
TB - BCG Yellow fever Oral polio Intranasal influenza Varicella Measles, mumps and rubella (MMR) Should not be given in
79
what are examples of inactivated vaccines?
employ pathogens that have been killed, often by heat or chemicals, to elicit an immune response might require booster doses to maintain immunity as the induced immune response is generally weaker than live attenuated vaccines examples: rabies hepatitis A influenza (intramuscular)
80
What are examples of toxoid vaccines?
tetanus diphtheria pertussis
81
what are examples of subunit and conjugate vaccines?
Subunit and conjugate vaccines are often grouped together. Subunit means that only part of the pathogen is used to generate an immunogenic response. A conjugate vaccine is a particular type that links the poorly immunogenic bacterial polysaccharide outer coats to proteins to make them more immunogenic pneumococcus (conjugate) haemophilus (conjugate) meningococcus (conjugate) hepatitis B human papillomavirus ,
82
HIV drug types?
HIV drugs, rule of thumb: Nucleoside analogue reverse transcriptase inhibitors (NRTIs) end in 'ine' Protease inhibitors (PI): end in 'vir' Non-nucleoside reverse transcriptase inhibitors (NNRTI): nevirapine, efavirenz
83
How is chlamydia diagnosed?
nuclear acid amplification tests (NAATs) are now the investigation of choice urine (first void urine sample), vulvovaginal swab or cervical swab may be tested using the NAAT technique for women: the vulvovaginal swab is first-line for men: the urine test is first-line Chlamydiatesting should be carried out two weeks after a possible exposure
84
what are examples of viral hemorrhagic fevers?
Flaviviridae: dengue, yellow fever Arenaviridae: Lassa fever Filoviridae: Ebola virus, Marburg virus Bunyaviridae: Hantaviruses, Crimean-Congo haemorrhagic fever, Rift Valley fever
85
what are features of viral haemorrhagic fevers?
flu-like symptoms abdominal pain haemorrhage petechiae, bruising bloody diarrhoea, haematemesis, haemoptysis disseminated intravascular coagulation multiorgan failure
86
how is Lassa fever contracted and what is the treatment?
Lassa fever is contracted by contact with the excreta of infected African rats (Mastomys rodent) or by person-to-person spread. ribavirin is used to treat Lassa fever
87
what kind of virus is measles?
RNA paramyxovirus
88
How is measles spread and what is the incubation person? How long are the infective?
spread by aerosol transmission infective from prodrome until 4 days after rash starts incubation period = 10-14 days
89
what are the features of Measles?
Features prodromal phase irritable conjunctivitis fever Koplik spots typically develop before the rash white spots ('grain of salt') on the buccal mucosa rash starts behind ears then to the whole body discrete maculopapular rash becoming blotchy & confluent desquamation that typically spares the palms and soles may occur after a week diarrhoea occurs in around 10% of patients
90
Investigations for measles?
IgM antibodies can be detected within a few days of rash onset
91
how is measles managed?
mainly supportive admission may be considered in immunosuppressed or pregnant patients notifiable disease → inform public health
92
complications of measles?
otitis media: the most common complication pneumonia: the most common cause of death encephalitis: typically occurs 1-2 weeks following the onset of the illness) subacute sclerosing panencephalitis: very rare, may present 5-10 years following the illness febrile convulsions keratoconjunctivitis, corneal ulceration diarrhoea increased incidence of appendicitis myocarditis
93
management of contacts of patients with measles?
if a child not immunized against measles comes into contact with measles then MMR should be offered (vaccine-induced measles antibody develops more rapidly than that following natural infection) this should be given within 72 hours
94
treatment of UTI in pregnancy?
should be treated with an antibiotic for 7 days first-line: nitrofurantoin (should be avoided near term) second-line: amoxicillin or cefalexin trimethoprim is teratogenic in the first trimester and should be avoided during pregnancy
95
what is anthrax?
Bacillus anthracis (anthrax) is a spore-forming, aerobic gram-positive bacillus.
96
how does anthrax present?
causes painless black eschar (cutaneous 'malignant pustule', but no pus) typically painless and non-tender may cause marked oedema anthrax can cause gastrointestinal bleeding
97
what is the management of anthrax?
the current Health Protection Agency advice for the initial management of cutaneous anthrax is ciprofloxacin further treatment is based on microbiological investigations and expert advice
98
what is cat scratch disease and what are the features?
Cat scratch disease is generally caused by the Gram negative rod Bartonella henselae Features fever history of a cat scratch regional lymphadenopathy headache, malaise
99
management of active TB?
nitial phase - first 2 months (RIPE) Rifampicin Isoniazid Pyrazinamide Ethambutol (the 2006 NICE guidelines now recommend giving a 'fourth drug' such as ethambutol routinely - previously this was only added if drug-resistant tuberculosis was suspected) Continuation phase - next 4 months Rifampicin Isoniazid
100
management of latent TB?
The treatment for latent tuberculosis is 3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)
101
when is direct observed therapy indicated in TB treatment?
Directly observed therapy with a three times a week dosing regimen may be indicated in certain groups, including: homeless people with active tuberculosis patients who are likely to have poor concordance all prisoners with active or latent tuberculosis
102
how long do patients with meningeal TB require treatment for?
Patients with meningeal tuberculosis are treated for a prolonged period (at least 12 months) with the addition of steroids
103
complications of TB treatment?
mmune reconstitution disease occurs typically 3-6 weeks after starting treatment often presents with enlarging lymph nodes Drug adverse effects rifampicin potent liver enzyme inducer hepatitis, orange secretions flu-like symptoms isoniazid peripheral neuropathy: prevent with pyridoxine (Vitamin B6) hepatitis, agranulocytosis liver enzyme inhibitor pyrazinamide hyperuricaemia causing gout arthralgia, myalgia hepatitis ethambutol optic neuritis: check visual acuity before and during treatment
104
mechanism of action of rifampicin?
Inhibits RNA synthesis
105
how to differentiate between lymphoma and toxoplasmosis?
Differentiating between toxoplasmosis and lymphoma is an important aspect of managing neurocomplications relating to HIV. Given the more limited availablity of SPECT compared to CT many patients are treated empirically on the basis of scoring systems, for example there is a 90% likelihood of toxoplasmosis if all of the following criteria are met: toxoplasmosis IgG in the serum CD4 < 100 and not receiving prophylaxis for toxoplasmosis multiple ring enhancing lesions on CT or MRI Toxoplasmosis - multiple lesions, ring or nodular enhancement, Thallium SPECT negative Lymphoma - single lesion, solid
106
Symptoms of toxoplasmosis? what is seen on CT head? how is it managed?
accounts for around 50% of cerebral lesions in patients with HIV constitutional symptoms, headache, confusion, drowsiness CT: usually single or multiple ring enhancing lesions, mass effect may be seen management: sulfadiazine and pyrimethamine
107
Primary CNS lymphoma in HIV what is it associated with what does CT head show? what is the treatment?
Primary CNS lymphoma accounts for around 30% of cerebral lesions associated with the Epstein-Barr virus CT: single or multiple homogenous enhancing lesions treatment generally involves steroids (may significantly reduce tumour size), chemotherapy (e.g. methotrexate) + with or without whole brain irradiation. Surgical may be considered for lower grade tumours
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HIV - neurocomplication cryptococcus: Features CSF results CT scan
most common fungal infection of CNS headache, fever, malaise, nausea/vomiting, seizures, focal neurological deficit CSF high opening pressure elevated protein reduced glucose normally a lymphocyte predominance but in HIV white cell count many be normal India ink test positive CT: meningeal enhancement, cerebral oedema meningitis is typical presentation but may occasionally cause a space-occupying lesion
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features of mycoplasma pneumonia?
the disease typically has a prolonged and gradual onset flu-like symptoms classically precede a dry cough bilateral consolidation on x-ray complications may occur as below
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complications of mycoplasma pneumonia?
cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia erythema multiforme, erythema nodosum meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases bullous myringitis: painful vesicles on the tympanic membrane pericarditis/myocarditis gastrointestinal: hepatitis, pancreatitis renal: acute glomerulonephritis
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investigations and management of mycoplasma pneumoniae?
Investigations diagnosis is generally by Mycoplasma serology positive cold agglutination test → peripheral blood smear may show red blood cell agglutination Management doxycycline or a macrolide (e.g. erythromycin/clarithromycin)
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What is Meliodosis?
Melioidosis, also called Whitmore's disease, is an infection caused by the gram-negative bacteriumBurkholderia pseudomallei. This organism is a widely distributed environmental saprophyte in soil and fresh surface water in endemic regions. ## Footnote Endemic in tropics and subtropics climates, mainly in Southeast Asia (e.g Thailand, Malaysia) and Northern America.
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How is meliodosis transmitted?
Percutaneous inoculation: contact with contaminated soil or water (most common) Inhalation, aspiration, or ingestion of contaminated dust or water Person-to-person transmission is rare
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Risk factors for Meliodosis?
Diabetes mellitus (the strongest risk factor) Chronic renal, liver, or lung disease (e.g., cystic fibrosis) Immunocompromised states (e.g., malignancy, long-term glucocorticoid use) Occupational exposure: agricultural work
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Signs and symptoms of Meliodosis?
Sign and symptoms: Incubation period: 1-21 days ( mean around 9 days) Symptomatic cases can be acute, chronic (> 2 months), or reactivations of latent infection. Clinical features depend on the infected organ: Acute pulmonary infection (most common): wide range of presentations (mild to severe) - Localized infection: skin ulcer, nodule, or abscess. - Visceral abscesses: especially in the prostate, spleen, kidney, and liver. - Disseminated infection: occurs in ˆ¼ 55% of cases and has a 20% mortality rate. Manifests with fever and septic shock.
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How to diagnose Meliodosis?
Culture: the mainstay of diagnosis. Gram stain of sputum or abscess pus Imaging: Chest radiography: may show signs of acute pneumonia
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Treatment of Meliodosis?
Initial intensive therapy: IV ceftazidime, imipenem, or meropenem for 10-14 days Followed by eradication therapy: oral TMP/SMX (plus doxycycline) for 3-6 months Adjunct therapy: abscess drainage.
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Prevention of Meliodosis?
In endemic areas, contact with soil and standing water should be avoided (e.g., agricultural workers should wear boots) Health care and laboratory workers should wear masks, gloves, and gowns to prevent infection. No vaccination available
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what kind of bacteria in Gardnerella vaginalis?
gram positive coccobacilli
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What is mycobacerium avium complex?
Mycobacterium avium complex (MAC) is an atypical mycobacterial infection seen in HIV patients. It is caused by both Mycobacterium avium and Mycobacterium intracellulare, and is often referred to as Mycobacterium avium-intracellulare (MAI). Over 95% of MAC infections in patients with HIV are caused by Mycobacterium avium. MAC is generally seen when the CD4 count is less than 50 cells/mm³
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Featues of Mycobacterium avium complex?
fever, sweats abdominal: pain, diarrhoea lung: dyspnoea, cough anaemia lymphadenopathy hepatomegaly/deranged LFTs
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Diagnosis of mycobacterium avium complex?
blood cultures bone marrow aspirate
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Prophylaxsis and management of mycobacterium avium complex?
Prophylaxis clarithromycin or azithromycin when CD4 is less than 100 cells/mm³ Management rifampicin + ethambutol + clarithromycin
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Shigella Features? Treatment?
causes diarrhoea (may be bloody), abdominal pain severity depends on type: S sonnei (e.g. from UK) may be mild, S. flexneri or S. dysenteriae from abroad may cause severe disease Shigella infection is usually self-limiting and does not require antibiotic treatment antibiotics (e.g. ciprofloxacin) are indicated for people with severe disease, who are immunocompromised or with bloody diarrhoea
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what is Q fever?
Q fever is caused by Coxiella burnetii, a rickettsia. The source of infection is typically an abattoir, cattle/sheep or it may be inhaled from infected dust
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Features and management of Q fever?
Features typically prodrome: fever, malaise causes pyrexia of unknown origin transaminitis atypical pneumonia endocarditis (culture-negative) Management doxycycline
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What is non-gonococcal urethritis?
Non-gonococcal urethritis (NGU, sometimes referred to as non-specific urethritis) is a term used to describe the presence of urethritis when a gonococcal bacteria are not identifiable or the initial swab. A typical case would be a male who presented to a GUM clinic with a purulent urethral discharge and dysuria. A swab would be taken in clinic, microscopy performed which showed neutrophils but no Gram-negative diplococci (i.e. no evidence of gonorrhoea). ## Footnote No cause is found in around half of cases. Possible causative organisms include: Chlamydia trachomatis most common cause Mycoplasma genitalium thought to cause more symptoms than Chlamydia less common causes Ureaplasma urealyticum Trichomonas vaginalis Escherichia coli
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Management of non-gonococcal urethritis?
contact tracing the BNF and British Association for Sexual Health and HIV (BASHH) both recommend either oral azithromycin or doxycycline
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What is Tularaemia?
Tularaemia is a zoonotic infection involving the microorganism F. tularensis commonly transmitted through lagomorphs such as rabbits, hares and pikas but also in aquatic rodents - beavers and muskrat - and ticks. It can present in a variety of forms. Commonly, it produces an erythematous papulo-ulcerative lesion at the site of the bite with reactive and ulcerating regional lymphadenopathy. It is treated with antibiotics such as doxycycline.
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What is Erysipelas?
Erysipelas is an acute infection typically with a skin rash, usually on any of the legs and toes, face, arms and fingers. It is primarily caused by Streptococcus pyogenes, also known as Group A Streptococcus (GAS). The characteristic features of erysipelas are a well-demarcated erythematous rash with raised borders and systemic symptoms such as fever.
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commonest cause of visceral larva migrans?
**Toxocara canis** commonly acquired by ingesting eggs from soil contaminated by dog faeces commonest cause of visceral larva migrans other features: eye granulomas, liver/lung involvement
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causes of cutaneous larva migrans?
**Ancylostoma braziliense** most common cause of cutaneous larva migrans common in Central and Southern America
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Management of genital herpes in pregnancy?
elective caesarean section at term is advised if a primary attack of herpes occurs during pregnancy at greater than 28 weeks gestation women with recurrent herpes who are pregnant should be treated with suppressive therapy and be advised that the risk of transmission to their baby is low
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clinical features of malaria falciparum
Falciparum malaria typically presents with symptoms suggestive of a flu-like illness. The classical triad of symptoms includes paroxysms of fever, chills, and sweating. These symptoms may occur every 48 hours corresponding to the erythrocytic cycle of the Plasmodium falciparum parasite. Fever is often high, intermittent, and may be accompanied by rigors. Initial manifestations can be non-specific and include malaise, headache, and myalgia, which might be mistaken for a viral syndrome. General features of falciparum malaria fever: The hallmark of malaria, typically cyclical, often accompanied by sweating and sometimes rigors. gastrointestinal: anorexia, nausea, vomiting, and abdominal pain are frequent diarrhoea can occasionally be a feature, more commonly in children patients may exhibit mild jaundice and occasional pruritus respiratory: Cough and, in some cases, mild tachypnoea may occur, though primary respiratory complications are rare in non-severe cases. musculoskeletal: Generalised body aches and joint pains are common. neurological: headache is prominent and often severe. dizziness and sleep disturbances may also be observed. cardiovascular: Tachycardia may be evident, and although hypotension is more typical of severe malaria, it can occasionally be seen in non-severe cases as well. haematological: thrombocytopaenia is the most significant haematological finding and can occur in the absence of severe disease. mild anaemia may also be present. renal: While acute kidney injury is associated with severe malaria, non-severe cases might show mild to moderate increases in creatinine or blood urea nitrogen levels.
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Features of severe malaria falciparum and complications?
Feature of severe falciparum malaria schizonts on a blood film parasitaemia > 2% hypoglycaemia acidosis temperature > 39 °C severe anaemia complications as below Complications cerebral malaria: seizures, coma acute renal failure: blackwater fever, secondary to intravascular haemolysis, mechanism unknown acute respiratory distress syndrome (ARDS) hypoglycaemia disseminated intravascular coagulation (DIC)
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Managament of malaria falciparum?
artemisinin-based combination therapies (ACTs) as first-line therapy examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine, artesunate plus sulfadoxine-pyrimethamine, dihydroartemisinin plus piperaquine Severe falciparum malaria a parasite counts of more than 2% will usually need parenteral treatment irrespective of clinical state intravenous artesunate is now recommended by WHO in preference to intravenous quinine if parasite count > 10% then exchange transfusion should be considered shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic collapse
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what is black water fever?
Blackwater fever is a rare complication of malaria which can be fatal. It is caused by large intravascular haemolysis resulting in haemoglobinuria, anaemia, jaundice and acute kidney injury. Urine is classically black or dark red in colour.The cause of the massive haemolysis is unknown. The treatment is with antimalarials, intravenous fluids and in some cases dialysis. Urinalysis reveals blood which is not seen on microscopy as it is haemoglobinuria.
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what is primary TB?
A non-immune host who is exposed to M. tuberculosis may develop a primary infection of the lungs. A small lung lesion known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages. The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex In immunocompetent people, the initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).
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What is secondary TB?
if the host becomes immunocompromised the initial infection may become reactivated The lungs remain the most common site for secondary tuberculosis. Extra-pulmonary infection may occur in the following areas: central nervous system (tuberculous meningitis - the most serious complication) vertebral bodies (Pott's disease) cervical lymph nodes (scrofuloderma) renal gastrointestinal tract
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Mucocutaneous ulceration following travelling?
Mucocutaneous ulceration following travel? - Leishmania brasiliensis
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what kind of abx are cephalosporins?
Cephalosporins are a type of β-lactam antibiotic which are bactericidal. They are less susceptible to penicillinases than penicillins. β-lactam antibiotics work by disrupting the synthesis of bacterial cell walls, by inhibiting peptidoglycan cross-linking.
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