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# Chapter 9

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
•
haemolytic anaemia secondary to cold agglutins (IgM)
•
a maculopapular, pruritic rash develops in around 99% of patients who take 
ampicillin/amoxicillin whilst they have infectious mononucleosis
Drug-induced rash is usually pruritic and is prolonged, in contrast to the viral 
rash of EBV infectious mononucleosis.
Early infectious mononucleosis may present with a maculopapular generalized 
rash.It is nonpruritic and rapidly disappears.
•
Because leukocytosis is the rule in infectious mononucleosis, the presence of a
normal or decreased WBC count should suggest an alternative diagnosis. 
•
Lymphocytosis
Relative lymphocytosis (≥ 60%) plus atypical lymphocytosis (≥ 10%) are the 
characteristic findings of EBV infectious mononucleosis. 
•
presence of 50% lymphocytes with at least 10% atypical lymphocytes
Atypical lymphocytes

most commonly seen in patients who have infectious 
mononucleosis. 

Other causes
drug reactions (phenytoin), 
stress, 
viral or bacterial infections, 
allergies,
autoimmune diseases, thyroid problems 
malignancy.
•
ESR is most useful in differentiating group A streptococcal pharyngitis from EBV 
infectious mononucleosis. 
(ESR elevated with EBV infectious mononucleosis, not elevated in group A 
streptococcal pharyngitis). 
atypical lymphocytosis point towards a viral illness
Diagnosis
•
heterophile antibody test (Monospot test) (immunoglobulin IgM to EBV)
the initial screening test 
sensitivity 85% and specificity 100%.
Cytomegalovirus is a herpesvirus that causes infectious 
mononucleosis with a negative monospot test.
•
EBV serological tests
Definitive diagnosis
should be obtained in patients with a mononucleosis-like illness and a 
negative finding on the Monospot test. 
Management is supportive and includes:
•
rest during the early stages, drink plenty of fluid, avoid alcohol
•
simple analgesia for any aches or pains
•
consensus guidance in the UK is to avoid playing contact sports for 8 weeks 
after having glandular fever to reduce the risk of splenic rupture
•
unfortunately on clinical appearances it is not possible to distinguish bacterial from 
viral or throat infections with any degree of reliability.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

•
If the child has EBV infection, then the administration of Amoxicillin will give 
an erythematous rash. Non-vomiting patients can be treated with oral penicillin-v.'
•
Patients with EBV infectious mononucleosis who have positive throat cultures for 
group A streptococci should not be treated because this represents colonization 
rather than infection
•
complicated EBV infectious mononucleosis : 
Short courses of corticosteroids are indicated for EBV infectious 
mononucleosis with:

hemolytic anemia, 

thrombocytopenia, 

CNS involvement, or 

extreme tonsillar enlargement (impending airway obstruction).
In which structure is the immune response most likely localized? Paracortex
•
immune response to the virus takes place through T-cell mediated immune 
responses, which take place in the lymphocyte-rich areas of the lymph node, 
namely the paracortex.
•
A biopsy of the lymph node of this patient would show reactive hyperplasia due to 
increased activity of the paracortex.
____________________________________________________
Parvovirus B19 
Pathogen: Parvovirus B19 is a single-strand DNA virus. 
Transmission: particularly via airborne infection
Pathology 
•
Primarily infects progenitor cells of erythrocytes in bone marrow and endothelial cells
•
Attaches to P antigen on RBCs and endothelial cells → cell destruction
Diseases
•
erythema infectiosum 
The most widely known clinical manifestation of parvovirus B19 is erythema 
infectiosum ('slapped cheek syndrome'), a mild viral illness of childhood 
characterised by a classic exanthema in which both cheeks appear bright red as 
though they had been slapped.
•
Aplastic crisis in patients with hemolytic anemias (e.g. sickle cell disease, thalassemias)
•
Parvovirus B19-associated arthritis
most commonly in adults, particularly in women
affect the small joints of the hands and feet. Knees or elbows are rarely involved.
may mimic rheumatoid arthritis. Unlike rheumatoid arthritis, the post-infectious 
arthritis associated with parvovirus B19 does not cause permanent damage to bones 
or joints.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
•
Pure red blood cell aplasia
•
The virus has a tropism for rapidly dividing erythrocyte precursors which they infect and 
destroy. Thus, no reticulocytes (immature erythrocytes) are available to replace aging or 
damaged erythrocytes as they are cleared by the reticuloendothelial system. This may not 
have any significant impact on otherwise healthy individuals, but can trigger an aplastic 
crisis - particularly in patients with haemoglobinopathies.
____________________________________________________
Leishmaniasis
•
Leishmaniasis is caused by the intracellular protozoa Leishmania, (intramacrophage protozoa)
•
transmitted to humans by phlebotomine sand flies. 
•
There are four main clinical syndromes: cutaneous, muco-cutaneous, visceral (also 
known as kala-azar) and post kala-azar dermal leishmaniasis.
Cutaneous leishmaniasis
•
caused by Leishmania tropica or Leishmania mexicana
•
crusted lesion at site of bite
•
present with ulcers or nodules. 
•
usually heal spontaneously, but slowly, in immuncompetent individuals with resultant 
disfiguring scars.
Mucocutaneous leishmaniasis
•
caused by Leishmania braziliensis
•
skin lesions may spread to involve mucosae of nose, pharynx etc
•
characterised by progressively destructive ulcerations of the mucosa extending from 
the nose and mouth to the pharynx and larynx, 
•
are not self-healing.
Visceral leishmaniasis (kala-azar)
•
mostly caused by Leishmania donovani
•
caused by the Leishmania donovani complex 
(L. donovani sensu stricto in East Africa and India, 

L. infantum in Europe, North Africa and Latin America).
•
incubation period of 2-6 months 
•
patients present with persistent systemic infection (fever, sweating, rigor, malaise, 
loss of appetite and weight loss) (*occasionally patients may report increased 
appetite with paradoxical weight loss)
•
parasitic infection of the blood and reticulo-endothelial system lymphadenopathy, 
massive splenomegaly and hepatomegaly
•
grey skin - 'kala-azar' means black sickness
•
investigations 
pancytopaenia secondary to hypersplenism
There is also often marked polyclonal hypergammaglobulinaemia.
Visualisation of the parasite (amastigote form) from lymph nodes, bone 
marrow or spleen is used as a confirmatory test.
PCR can be used to detect the parasite in the blood.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

Anti-leishmanial antibodies can be detected, but they remain positive up to 
several years after cure and therefore cannot be used to detect relapse.
•
Treatment
First line antimonials are sodium stibogluconate and meglumine antimoniate. 
Adverse effects influde cardiac arrhythmias and acute pancreatitis. 
Amphotericin B is increasingly being used. 
Post kala-azar dermal leishmaniasis
•
a complication of visceral leishmaniasis 
•
characterised by a macular, maculo-papular or nodular rash   
•
frequently observed after treatment.It can also occur in immunosuppressed 
individuals.
•
highly infectious.
____________________________________________________
Leptospirosis (Also known as Weil's disease*)
•
*the term Weil's disease is sometimes reserved for the most severe form

If the infection causes jaundice, kidney failure and bleeding, it is then known 
as Weil's disease.
If it affects the lung and causes pulmonary haemorrhage, then it is known as 
severe pulmonary haemorrhage syndrome.
•
leptospirosis is commonly seen in questions referring to sewage workers, farmers, 
vets or people who work in abattoir. 
•
It is caused by the spirochaete Leptospira interrogans (serogroup L 
icterohaemorrhagiae),
•
classically being spread by contact with infected rat urine. 
•
Weil's disease should always be considered in high-risk patients with hepato-renal 
failure
Features
•
fever
•
flu-like symptoms
•
renal failure (seen in 50% of patients)
•
jaundice
•
headache, may herald the onset of meningitis
•
subconjunctival haemorrhage
•
Haemorrhagic tendencies with purpura or petechiae
•
Enlargement of liver and spleen.
•
Presentation with heart failure is uncommon but has been described in severe 
leptospirosis.
Management
•
high-dose benzylpenicillin or doxycycline
•
other options:  cefotaxime or ceftriaxone.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
____________________________________________________
Lyme disease
Aetiology
•
Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by 
ticks of the genus Ixodes
Ixodes ricinus is predominantly responsible for its transmission in 
Europe.
Ixodes pacificus and Ixodes scapularis are the ticks responsible for 
transmission of in the USA.
Features
Early features
•
erythema chronicum migrans (small papule often at site of the tick bite which 
develops into a larger annular lesion with central clearing, 'bulls-eye'. Occurs in 70% 
of patients)
Erythema migrans is often the presenting sign of Lyme disease
•
systemic symptoms: malaise, fever, arthralgia
Later features
•
CVS: heart block, myocarditis
•
neurological: (Neuroborreliosis): cranial nerve palsies, meningitis
•
polyarthritis
Investigation
•
serology: antibodies to Borrelia burgdorferi (ELISA test for antibodies to Borrelia 
burgdorferi)
Serological tests are the most appropriate first line investigation for 
diagnosing Lyme disease. 
ELISA tests are preferred to Western blots as they are more sensitive.
Management
•
Early disease:
doxycycline is the drug of choice for 2 – 3 weeks
Amoxicillin is an alternative if doxycycline is contraindicated (e.g. pregnancy)
•
Disseminated disease:
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)
MRCPUK-part-1-September 2013 exam: H/O returning from a camping holiday in the New 
Forest. C/O lethargy, arthralgia, rash consistent with erythema chronicum migrans. What is 
the most appropriate test to perform given the likely diagnosis? 
ELISA test for antibodies to Borrelia burgdorferi

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

____________________________________________________
Lymphadenopathy
There are many causes of generalised lymphadenopathy
Infective
•
infectious mononucleosis
•
HIV, including seroconversion illness
•
eczema with secondary infection
•
rubella
•
toxoplasmosis
•
CMV
•
tuberculosis
•
roseola infantum
Neoplastic
•
leukaemia
•
lymphoma
Others
•
autoimmune conditions: SLE, rheumatoid arthritis
•
graft versus host disease
•
sarcoidosis
•
drugs: phenytoin and to a lesser extent allopurinol, isoniazid
____________________________________________________
Malaria 
Malaria: Falciparum
•
P. falciparum typically presents within the first three months of return from an endemic 
area.
In the slide shown, the blood film 
shows ring forms within erythrocytes; 
some erythrocytes contain two to 
three parasites per cell - typical of 
falciparum; other forms of malaria 
seldom have more than one parasite 
per red cell.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
Feature of severe 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) (Respiratory rate 30 per minute)
hypoglycaemia
disseminated intravascular coagulation (DIC)
Uncomplicated falciparum malaria
•
strains resistant to chloroquine are prevalent in certain areas of Asia and Africa
•
the 2010 WHO guidelines recommend artemisinin-based combination therapies (ACTs) as 
first-line therapy
•
examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate 
plus mefloquine, artesunate plus sulfadoxine-pyrimethamine, dihydroartemisinin plus 
piperaquine
Severe falciparum malaria
•
a parasite counts of more than 2% will usually need parenteral treatment irrespective of 
clinical state
•
Hyperparasitemia, where more than 5% of the red blood cells are infected by malaria 
parasites
In 2010, WHO defined hyperparasitemia as >2%/100 000/µL in low intensity 
transmission areas or >5% or 250 000/µL in areas of high stable malaria 
transmission intensity.
•
intravenous artesunate is now recommended by WHO in preference to intravenous quinine
I.V quinine is reserved for severe or cerebral malaria (most deaths from M. 
falciparum occur in first 96 hours of starting treatment).
The initial dose should NOT be reduced in those severely ill with renal/hepatic 
impairment.
High doses of quinine in pregnancy are teratogenic in the first trimester. However in 
malaria, the benefit of treatment outweighs the risk.
WHO Guidelines (2006) recommend artemisinins are first line in the second and 
third trimester. In the first trimester, both artesunate and quinine are considered 
treatment options. 
Hypoglycaemia is an important side effect of quinine

Quinine ↑ insulin secretion and the sensitivity of cells to insulin 
hypoglycaemia

Malaria itself can cause hypoglycaemia too, so blood glucose should be
monitored every 2 h.
•
if parasite count > 10% then exchange transfusion should be considered
•
shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic 
collapse
Malaria: non-falciparum

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

•
P. vivax:
The most common cause of non-falciparum malaria is Plasmodium vivax, with 
Plasmodium ovale and Plasmodium malariae accounting for the other cases.
The incubation period of P. vivax can go up to six months or more with malaria 
being caused by hypnozoites.  

P. falciparum incubation is normally around six days though it can go till 14 
days or more.
The Duffy antigen on RBCs acts as a receptor for P. vivax. facilitate the 
entry of P. vivax in to RBCs.

Duffy negative individuals are therefore resistant to this strain

West Africans lack the Duffy blood group and therefore P. ovale replaces P. 
vivax in this region.
•
P. ovale:

it is quite rare
The incubation period is similar to that of P. vivax but on the thick film the parasites 
are more compact and smaller. On the thin film the red blood cells appear oval with 
ragged ends.
•
P. malariae:
it is rare. 
Its incubation could go up to14 days like P. falciparum. 
The thick film will show a few compact rings or small neat schizonts or small round 
gametocytes with yellow-brown pigment. The thin film will show red blood cells in 
band forms.
•
Plasmodium vivax is often found in Central America and the Indian Subcontinent 
whilst Plasmodium ovale typically comes from Africa
•
Both P. vivax and P. ovale have a liver hypnozoite stage which can cause repeated 
relapses.
May present six months after return from an endemic area 
Features
•
fever, 
Plasmodium vivax/ovale: cyclical fever every 48 hours.
Plasmodium malariae: cyclical fever every 72 hours
•
headache, 
•
splenomegaly
•
Plasmodium malariae: is associated with nephrotic syndrome
Investigations
•
Plasmodium ovale,
all stages of the parasite and not just trophozoites and gametocytes are visible 
in the peripheral blood.
•
In P. falciparum malaria, only trophozoite-ring forms and gametocytes are usually seen.
Treatment
•
non-falciparum malarias are almost always chloroquine sensitive
•
patients with ovale or vivax malaria should be given primaquine following acute treatment 
with chloroquine to destroy liver hypnozoites and prevent relapse.
all individuals should be screened for glucose-6-phosphate dehydrogenase (G6PD) 
deficiency, as primaquine may cause haemolysis in those without the enzyme.

Chapter 9

Infectious diseases
 
fast-acting
intermediate-acting
slow-acting
high-efficacy blood 
schizonticides that may be 
effective as monotherapy
low-efficacy schizonticides that 
normally need to be 
administered in combination.
Artemesinin
Mepacrine
Pyrimethamine
Doxycycline is also a very 
slow-acting antimalarial.
Pyrimethamine
Quinine
Mefloquine
•
used in the treatment of uncomplicated malaria, particularly for chloroquine-resistant P. 
falciparum.
•
It acts on both the erythrocytic and hepatic phases of infection.
•
It inhibits dihydrofolate reductase in the parasite thus preventing the biosynthesis of purines 
and pyrimidines, and thereby halting the processes of DNA replication, cell division and 
reproduction.
•
It is normally used alongside a sulfonamide. 
Malaria: prophylaxis
•
around 75% of malaria in patients returning from endemic countries are caused by the 
potentially fatal Plasmodium falciparum protozoa.  
•
The majority of patients who develop malaria did not take prophylaxis.
•
It should also be remembered that UK citizens who originate from malaria endemic areas 
quickly lose their innate immunity.
Drug
Side-effects + notes
Atovaquone + 
proguanil 
(Malarone)
GI upset
1 - 2 days
7 days
Chloroquine
Headache
Contraindicated in epilepsy
Taken weekly
Doxycycline
Photosensitivity
Oesophagitis
Mefloquine (Lariam)
Dizziness
Neuropsychiatric disturbance
Contraindicated in epilepsy
and mental illnesses 
Taken weekly
Proguanil 
(Paludrine)
Proguanil + 
chloroquine
See above
1 week
4 weeks
Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

Time to begin 
before travel
Time to end after travel
1 week
4 weeks
1 - 2 days
4 weeks
2 - 3 weeks
4 weeks
1 week
4 weeks

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

•
Which drug?
In certain parts of South-East Asia there is widespread chloroquine resistance. 
Chemoprophylaxis using atovaquone + proguanil (Malarone), mefloquine 
(Lariam) or doxycycline is therefore recommended.
Doxycycline prophylaxis is the safest option with less resistance in many 
parts of the world compared to the other options available. 

Atovaquone and proguanil are used for prophylaxis especially where there are high 
levels of resistance against most of the other drugs.
Proguanil should not be used alone as malaria could develop resistance to it.
•
Pregnant women 
Pregnant women should be advised to avoid travelling to regions where malaria is 
endemic. Diagnosis can also be difficult as parasites may not be detectable in the 
blood film due to placental sequestration. However, if travel cannot be avoided:

chloroquine can be taken

proguanil: folate supplementation (5mg od) should be given

Malarone (atovaquone + proguanil): the BNF advises to avoid these drugs 
unless essential. If taken then folate supplementation should be given

mefloquine: caution advised

doxycycline is contraindicated
•
Children 
It is again advisable to avoid travel to malaria endemic regions with children if 
avoidable. However, if travel is essential then children should take malarial 
prophylaxis as they are more at risk of serious complications.

diethyltoluamide (DEET) 20-50% can be used in children over 2 months of 
age

doxycycline is only licensed in the UK for children over the age of 12 years
MRCPUK-part-1-May 2013 exam: H/O vivax malaria treated initially with chloroquine then 
later given primaquine. What is the benefit of the primaquine? 
Destroy liver hypnozoites and prevent relapse
MRCPUK-part-1-May 2014 exam: A 25-year-old man with a history of epilepsy presents for 
advice regarding malarial prophylaxis. Next month he plans to travel to Vietnam. What is 
the most appropriate medication to prevent him developing malaria? 
Atovaquone + proguanil
____________________________________________________
Measles
Overview
•
RNA paramyxovirus
•
spread by droplets
•
infective from prodrome until 4 days after rash starts
•
incubation period = 10-14 days
Features
•
prodrome: irritable, conjunctivitis, fever
Patients present with the three C's: cough, coryza, and conjunctivitis.

Rash usually develops on the head and torso, typically sparing the wrists and 
hands.
•
Koplik spots (before rash): white spots ('grain of salt') on buccal mucosa
Koplik's spots are small, irregular, bright red spots with blue-white centres, 
occurring on the inside of the cheek next to the premolars.Seen only in 
measles, they are diagnostic.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
The spots usually occur briefly after the fever begins and a couple of days 
before the generalised rash appears. 
Not infrequently, the spots disappear as the eruption develops.
•
rash: starts behind ears then to whole body, discrete maculopapular rash becoming 
blotchy & confluent
Koplik spots
Complications
•
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
•
giant cell pneumonia
•
keratoconjunctivitis, corneal ulceration
•
diarrhoea
•
increased incidence of appendicitis
•
myocarditis
The rash typically starts behind the ears and then spreads to the whole body

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

Management of contacts
•
if a child not immunized against measles comes into contact with measles then 
MMR should be offered (vaccine-induced measles antibody develops more rapidly 
than that following natural infection)
•
this should be given within 72 hours
____________________________________________________
Rubella 
•
also known as german measles.
•
RNA virus , part of the togavirus family
rubella has positive single-stranded RNA.
rubeola virus (measles) contains negative single-stranded RNA  
•
affects unimmunized children and presents with a rash that begins at the head and 
moves down with postauricular lymphadenopathy.
•
A positive rubella haemagglutination inhibition (HAI) combined with a negative 
rubella IgM is consistent with:
1. Early acute infection with rubella

The IgM may take several days to rise and the test should be 
repeated one to two weeks later.
2. Previous vaccination, or
3. Previous rubella infection.
___________________________________________________________________________
Parotitis
Causes 
•
Bacterial parotitis 
Commonly unilateral
more common in older patients. 
The most common bacterial cause of parotitis is Staphylococcus aureus.
The risk is increased by agents that have an atropine-like action, including 
medications prescribed to reduce excess respiratory secretions. 
A ductal stone, with consequent pooling of infected secretions, should be 
excluded, and ultrasound is an appropriate investigation to perform for this. 
Antibiotics should be selected that cover typical mouth flora.
•
Viral parotitis
Mumps parotitis is usually bilateral
Parotitis, orchitis, aseptic meningitis, and pancreatitis are symptoms 
of mumps virus infection.
•
autoimmune disease, Sjogren's syndrome.
•
Bulimia nervosa
____________________________________________________
Parotid swelling 
•
causes of bilateral parotid swelling include:
Infection with viruses, including mumps, parainfluenza virus type 3, Coxsackie 
viruses and influenza A virus
Metabolic diseases, such as:

diabetes mellitus 

uraemia

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
Drugs, such as:

phenylbutazone 

thiouracil
•
Other conditions associated with chronic parotid swelling include:
Alcoholic liver disease
Sarcoidosis
Sjögren syndrome
Lymphoma
Infection with HIV
____________________________________________________
Orf
Orf is generally a condition found in sheep and goats although it can be transmitted to 
humans. It is caused by the parapox virus.
In animals
•
'scabby' lesions around the mouth and nose
In humans
•
generally affects the hands and arms
•
initially small, raised, red-blue papules
•
later may increase in size to 2-3 cm and become flat-topped and haemorrhagic
____________________________________________________
Pelvic inflammatory disease(PID)
Definition
•
infection and inflammation of the female pelvic organs including the uterus, fallopian 
tubes, ovaries and the surrounding peritoneum. 
•
It is usually the result of ascending infection from the endocervix
Causative organisms
•
Chlamydia trachomatis - the most common cause
•
Neisseria gonorrhoeae
•
Mycoplasma genitalium
•
Mycoplasma hominis
one of the most frequently isolated mycoplasma in the genital tract. 
It is an opportunistic pathogen which may cause pelvic inflammatory disease 
in immunocompromised patients.
Clindamycin is used in the treatment 
Features
•
lower abdominal pain
•
fever
•
deep dyspareunia
•
dysuria and menstrual irregularities may occur
•
vaginal or cervical discharge
•
cervical excitation
Investigation
•
screen for Chlamydia and Gonorrhoea

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

Management
•
due to the difficulty in making an accurate diagnosis, and the potential complications 
of untreated PID, consensus guidelines recommend having a low threshold for 
treatment
•
Consensus guidelines recommend treatment once a diagnosis of pelvic 
inflammatory disease is suspected, rather than waiting for the results of swabs
•
oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline 
+ oral metronidazole
•
RCOG guidelines suggest that in mild cases of PID intrauterine contraceptive 
devices may be left in. The more recent BASHH guidelines suggest that the 
evidence is limited but that ' Removal of the IUD should be considered and may be 
associated with better short term clinical outcomes'
Complications
•
infertility - the risk may be as high as 10-20% after a single episode
•
chronic pelvic pain
•
ectopic pregnancy
•
Fitz-Hugh-Curtis syndrome
is a rare complication of pelvic inflammatory disease, resulting in liver capsule 
inflammation.
It is most often caused by untreated sexually transmitted infections 
including Chlamydia trachomatis and Neisseria gonorrhoeae. 
a patient may present with septic shock secondary to the untreated liver 
capsule infection.
____________________________________________________
Psittacosis (ornithosis)
•
Chlamydia psittaci is endemic in birds including psittacine birds, canaries, finches, 
pigeons and poultry.
•
Pet owners, vets and zoo keepers are most at risk. It is rare in children.
•
Person to person transmission occurs especially in a hospital environment.
•
Sputum Gram stain reveals a few leucocytes and no predominant bacteria. 
•
There are few signs and few laboratory/x ray findings.
•
Positive serology is with complement-fixing antibodies.
•
It is treated with tetracycline.
____________________________________________________
Pyogenic liver abscess
•
The most common organisms found in pyogenic liver abscesses are Staphylococcus 
aureus in children and Escherichia coli in adults.
Management
•
amoxicillin + ciprofloxacin + metronidazole
•
if penicillin allergic: ciprofloxacin + clindamycin
January 2018 exam: What is the most appropriate antibiotic therapy to accompany 
drainage of liver abscess?
Amoxicillin + ciprofloxacin + metronidazole

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
____________________________________________________
Pyrexia of unknown origin
indium labelled leukocyte study:
•
useful for detecting occult abscesses in patients with pyrexia of unknown origin where 
conventional scans have failed to detect a source of infection.
Definition
•
Defined as a prolonged fever of > 3 weeks which resists diagnosis after a week in hospital
Neoplasia
•
lymphoma
•
hypernephroma
•
preleukaemia
•
atrial myxoma
Infections
•
abscess
•
TB
Connective tissue disorders
____________________________________________________
Q fever
Q fever - Coxiella burnetti
Overview
•
Q fever is a zoonotic disease caused by Coxiella burnetii an obligate gram-negative 
intracellular bacterium.
•
The organism is very resistant to drying.
•
does not grow on standard culture media.
Transmission
•
The organism is usually inhaled from infected dust (animal products)
•
acquired through contact with animals.
Cattle, sheep and goats are the primary reservoirs of C. burnetii.
•
drinking unpasteurised milk from infected cows.
Risk factors
•
It is not notifiable, but can occur in outbreaks in farming communities and in abattoirs. and 
therefore an occupational history is very important.
Features:
•
high fevers, chills, sweats 
•
severe headache, (typically retrobulbar)
•
general malaise, myalgia, 
•
confusion, 
•
sore throat, , 
•
non-productive cough, 
•
nausea, vomiting, diarrhoea, abdominal pain
•
chest pain.
•
Between 30% and 50% of patients with a symptomatic infection will develop pneumonia.
•
may be complicated by immune complex-mediated glomerulonephritis

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

•
Chronic infection can manifest as hepatitis, osteomyelitis or endocarditis.
•
In Q fever endocarditis:
the aortic valve is involved in over 80% of cases. 
A murmur is not always present, but augmentation of an existing murmur may occur. 
Low-grade fever (or no fever),
signs of heart failure, 
hepatosplenomegaly, 
clubbing, 
arterial emboli, 
leukocytoclastic vasculitic rash.
Diagnosis:
•
Confirmed by serological testing for C. burnetii. 
phase I antibody titre to Coxiella burnetti (IgG and/or IgA) greater than 1:200 is 
virtually diagnostic of Q fever.
•
chest X-ray might show multilobar consolidation. 
•
Anaemia 
•
Thrombocytopenia
•
Elevated ESR
•
Hypergammaglobulinaemia 
•
liver function tests 
abnormal in the majority of patients and some will develop hepatitis.
•
Microscopic haematuria may be present.
Treatment :
•
Most patients will recover within a few months with no treatment.
•
Doxycycline is the treatment of choice for acute Q fever. OR prolonged courses of 
tetracyclines.
Prognosis
•
Only 1–2% of people with acute Q fever die of the disease. 
•
Chronic Q fever
Endocarditis with negative culture findings and seropositivity is the main clinical 
presentation of chronic Q fever,

usually occurring in patients with preexisting cardiac disease including valve 
defects, rheumatic heart disease, and prosthetic valves.
____________________________________________________
Rabies
Overview
•
Rabies is a viral disease that causes an acute encephalitis. 
•
The rabies virus is classed as a RNA rhabdovirus and has a bullet shaped capsid. 
•
It is commonly transmitted by bat, raccoon and skunk bites. 
•
Following a bite the virus travels up the nerve axons towards the central nervous 
system in a retrograde fashion.
Features
•
prodrome: headache, fever, agitation
•
hydrophobia: water-provoking muscle spasms
•
hypersalivation
•
Negri bodies: cytoplasmic inclusion bodies found in infected neurons

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
 
There is now considered to be 'no risk' of developing rabies following an animal bite in the 
UK and the majority of developed countries. 
Following an animal bite in at risk countries:
•
if an individual is already immunised then 2 further doses of vaccine should be given
•
if not previously immunised then human rabies immunoglobulin (HRIG) should be 
given along with a full course of vaccination
•
Lyssaviruses such as rabies cannot cross intact skin and humans are regarded as 
an end-host (outside of transplantation-associated transmission). Therefore, only 
standard infection-prevention precautions such as gloves and gowns are 
required.
____________________________________________________
Scabies
Scabies should be suspected in any sexually active young person who presents with 
generalised pruritus without any specific signs.
Overview
•
Scabies is caused by the mite Sarcoptes scabiei and is spread by prolonged skin contact. 
•
It typically affects children and young adults.
Pathophysiology
•
The scabies mite burrows into the skin, laying its eggs in the stratum corneum. 
•
The intense pruritus associated with scabies is due to a delayed type IV hypersensitivity 
reaction to mites/eggs which occurs about 30 days after the initial infection.
Features
•
widespread pruritus
•
linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
The tiny erythematous burrows in the web spaces of the fingers are almost 
pathognomonic
•
in infants the face and scalp may also be affected
•
secondary features are seen due to scratching: excoriation, infection
Investigation
•
Skin scrapings demonstrate Sarcoptes scabiei
Management
•
first-line is permethrin 5% 
•
second-line is malathion 0.5% 
•
Application should be repeated seven days after initial treatment to kill any mites hatched 
from eggs in that time
•
give appropriate guidance on use (see below)
•
pruritus persists for up to 4-6 weeks post eradication
Patient guidance on treatment (from Clinical Knowledge Summaries)
•
avoid close physical contact with others until treatment is complete
•
all household and close physical contacts should be treated at the same time, even if 
asymptomatic
Re-infection most likely means Other household members were not treated

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

•
launder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill 
off mites.
Patients should be given the following instructions:
•
The BNF advises to apply the insecticide to all areas, including the face and scalp, contrary 
to the manufacturer's recommendation. 
•
apply the insecticide cream or liquid to cool, dry skin
•
pay close attention to areas between fingers and toes, under nails, armpit area, creases of 
the skin such as at the wrist and elbow
•
allow to dry and leave on the skin for 8-12 hours for permethrin, or for 24 hours for 
malathion, before washing off
•
reapply if insecticide is removed during the treatment period, e.g. If wash hands, change 
nappy, etc
•
repeat treatment 7 days later
Crusted (Norwegian) scabies
•
Crusted scabies is seen in patients with suppressed immunity, especially HIV.
•
The crusted skin will be teeming with hundreds of thousands of organisms.
•
Ivermectin is the treatment of choice and isolation is essential

Chapter 9

Infectious diseases
____________________________________________________
Helminths
Nematodes (roundworms)
Worm
Notes
Treatment
Larvae are present in soil and gain access to the body by 
penetrating the skin
Strongyloides 
stercoralis
Features include diarrhoea, abdominal pain, 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
Enterobius 
vermicularis
(pinworm)
asymptomatic in 90% of cases, possible features include 
perianal itching, particularly at night; girls may have vulval 
symptoms
Diagnosis may be made by the applying sticky plastic tape to 
the perianal area and sending it to the laboratory for 
microscopy to see the eggs
Larvae penetrate skin of feet; gastrointestinal infection → 
anaemia
Thin-shelled ova
Ancylostoma 
duodenale, Ne
cator 
americanus(h
ookworms)
Loa loa
Transmission by deer fly and mango fly
Causes red itchy swellings below the skin called 'Calabar 
swellings', may be observed when crossing conjunctivae
Typically develops after eating raw pork.
Features include fever, periorbital oedema and myositis 
(larvae encyst in muscle)
Trichinella 
spiralis
Causes 'river blindness'. Spread by female blackflies
Onchocerca 
volvulus
Features include blindness, hyperpigmented skin and possible 
allergic reaction to microfilaria
Transmission by female mosquito
Wuchereria 
bancrofti
Causes blockage of lymphatics → elephantiasis
Transmitted through ingestion of infective eggs.
Toxocara 
canis (dog 
roundworm)
Features include visceral larva migrans and retinal 
granulomas
VISCious dogs → blindness
Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

Ivermectin and -
bendazoles are 
used
-bendazoles
-bendazoles
Diethylcarbamazine
-bendazoles
Ivermectin
rIVERblindness 
= IVERmectin
Diethylcarbamazine
Diethylcarbamazine

Worm
Notes
Treatment
Ascaris 
lumbricoides(
giant 
roundworm)
•
the most common nematode parasite of humans.
•
Eggs are visible in faeces
•
large roundworm, growing up to 35 cm in length 
•
result of pneumonitis caused by the worm's migration 
through the lungs 
•
May cause intestinal obstruction and occasional migrate to 
lung (Loffler's syndrome)
•
biliary/pancreatic duct obstruction.
Cestodes (tapeworms)
Worm
Notes
Treatment
•
Responsible for hydatid disease
•
Transmission through ingestion of eggs in dog faeces. 
•
Definite host is dog, which ingests hydatid cysts from 
sheep, who act as an intermediate host. 
•
Often seen in farmers.
•
Features include liver cysts and anaphylaxis if cyst 
ruptures (e.g. during surgical removal)
•
the most appropriate next step in diagnosis?
ELISA testing for Echinococcus
Echinococcus 
granulosus
Taenia solium
Often transmitted after eating undercooked pork. Causes 
cysticercosis and neurocysticercosis, mass lesions in the brain 
'swiss cheese appearance'
May cause biliary obstruction
Triclabendazole
Fasciola 
hepatica (the 
liver fluke)
Trematodes (flukes)
Worm
Notes
Treatment
Hosted by snails, which release cercariae that penetrate skin.
Causes 'swimmer's itch' - frequency, haematuria. Risk factor 
for squamous cell bladder cancer
Schistosoma 
haematobium
Caused by undercooked crabmeat, results in secondary 
bacterial infection of lungs
Paragonimus 
westermani
Clonorchis 
sinensis
Caused by undercooked fish
Features include biliary tract inflammation. 
Known risk factor for cholangiocarcinoma
Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

-bendazoles
Piperazine is the 
treatment of 
choice in patients 
presenting with 
bowel obstruction;
mebendazole may 
be used to treat 
other infections.
•
bendazoles 
alone
(For smaller 
cysts)
•
albendazole 
combined with 
surgical 
excision.
•
(for larger 
cysts)
-bendazoles
Praziquantel
Praziquantel
Praziquantel

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
___________________________________________________
Schistosomiasis
Schistosoma haematobium causes haematuria
Schistosomiasis, or bilharzia, is a parasitic flatworm infection. 
Types
•
Schistosoma mansoni and Schistosoma intercalatum: intestinal schistosomiasis
•
Schistosoma haematobium: urinary schistosomiasis
This typically presents as a 'swimmer's itch' in patients who have recently returned 
from Africa. Schistosoma haematobium is a risk factor for squamous cell bladder 
cancer
Features
•
frequency
•
haematuria
•
bladder calcification
Management
•
single oral dose of praziquantel
•
Praziquantel is the treatment of choice for all Schistosoma species. 
•
CNS involvement
S. japonicum

Praziquantel 60 mg/kg per day for 6 days and prednisolone 1 mg/kg per 
day

Praziquantel 60 mg/kg per day for six days is recommend for S. japonicum 
with a maximum dose of 5 grams per day with prednisolone 1 mg/kg. 
S. mansoni and S. haematobium.

Praziquantel 40 mg/kg per day for three days is recommended for S. mansoni 
and S. haematobium.
Since some of the pathology in neuroschistosomiasis is secondary to 
hypersensitivity reactions there is need to use a steroid, in this case prednisolone 1 
mg/kg per day. There is no consensus about when it should be started or stopped.
Complications:
•
S. mansoni Eggs can migrate to liver through the portal venous system where they can 
elicit a granulomatous fibrosing reaction venous blockade Portal venous hypertension 
varicies and upper GIT bleeding.
•
S. haematobium leads to granulomatous inflammation, ulceration of the vesicle and 
ureteral walls. Subsequent fibrosis can cause bladder neck obstruction, hydroureter and 
hydronephrosis. These changes can cause a chronic renal impairment and predispose to 
secondary bacterial infection as well as squamous cell carcinoma.
•
all schistosome species can result in immune complex deposition in the kidneys leading 
to a proteinuria and nephrotic syndrome.
•
S. japonicum:

is prevalent in China, Indonesia, Thailand and the Philippines mainly. 
It is the commonest cause of Schistosoma encephalitis. 
Its eggs are smaller unlike those of S. masoni and S. haematobiumwhich are more 
likely to cause spinal cord schistosomiasis because of their larger size and spikes 
which do not enable them get to the brain hence the infection in the spinal cord.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

____________________________________________________
Strongyloides stercoralis
•
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.
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
____________________________________________________
Tape worms
•
Tape worms are made up of repeated segments called proglottids. These are often present 
in faeces and are useful diagnostically
Cysticercosis
•
caused by Taenia solium (from pork) and Taenia saginata (from beef)
•
These may affect any tissue in the body but are commonest in subcutaneous tissues and 
(CNS) patient with a palpable nodule who has an epileptic seizure
•
management: niclosamide
Hydatid disease
•
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
____________________________________________________
Trypanosomiasis
•
Two main form of this protozoal disease are recognised:
1.
African trypanosomiasis (sleeping sickness) and 
2. American trypanosomiasis (Chagas' disease)
1. African trypanosomiasis, or sleeping sickness
Two forms of African trypanosomiasis, or sleeping sickness, are seen:
1) Trypanosoma brucei gambiense in West Africa

West African trypanosomiasis has a slower course. Symptoms start 
several weeks or even months after the tsetse fly bite.
2) Trypanosoma brucei rhodesiense in East Africa. 

Trypanosoma rhodesiense tends to follow a more acute course.

progression is more rapid - starting within days of infection. Death may 
occur within weeks or months.

Rash is a more prominent feature and lymphadenopathy is less 
frequently present.
Both types are spread by the tsetse fly.
Clinical features include:

Trypanosoma chancre - painless subcutaneous nodule at site of infection

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases

intermittent fever

enlargement of posterior cervical lymph nodes

later: central nervous system involvement e.g. somnolence, headaches, mood 
changes, meningoencephalitis

The reversal of the sleep wake cycle is typical and can be accompanied by 
behavioural changes.
Stages

The first stage of disease is haematolymphatic spread and is accompanied 
by fever, and lymphadenopathy (discrete, rubbery, non-tender nodes). A rash 
sometimes occurs and mild hepatosplenomegaly may develop.

The second stage is the meningoencephalitic stage. This occurs months or 
years after the acquisition of infection. Manifestations include personality 
change and progressive indifference with daytime somnolence. 
Extrapyramidal signs and ataxia are common.
Management

early disease: IV pentamidine or suramin

later disease or central nervous system involvement: IV melarsoprol
2. American trypanosomiasis, or Chagas' disease
caused by the protozoan Trypanosoma cruzi.
Transmitted by triatomine bug bite. 
Features:

acute phase: 
asymptomatic (95%) 
chagoma (an erythematous nodule at site of infection) 
periorbital oedema

Chronic Chagas' disease mainly affects the heart, gastrointestinal tract and 
CNS.
Cardiac feature myocarditis may lead to dilated cardiomyopathy 
(with apical atophy) and arrhythmias.
Cardiac involvement is the leading cause of death in 
patients with Chagas' disease
GIT feature:
Mega-oesophagus (causing dysphagia) 
Mega-colon (causing constipation)
CNS feature meningoencephalitis 
Management

treatment is most effective in the acute phase using azole or nitroderivatives 
such as benznidazole or nifurtimox

chronic disease management involves treating the complications e.g., heart 
failure.

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad

____________________________________________________
Nematodes
•
most common cause of cutaneous larva migrans Ancylostoma braziliense
•
commonest cause of visceral larva migrans Toxocara canis
Ancylostoma braziliense
•
most common cause of cutaneous larva migrans
•
common in Central and Southern America
•
The infection is acquired by direct contact with dog or cat faeces - often acquired when 
sunbathing on contaminated sand, etc. The larvae burrow in the dermo-epidermal junction.
•
Symptoms include pruritus and a raised, serpiginous erythematous rash that migrates at a 
rate of up to 1 cm/day.
•
Treatment i
The disease is self-limiting but the duration of disease varies considerably

Oral ivermectin in a single dose of 200 µg/kg body weight is the main treatment. 
Other treatment options include oral albendazole or topical thiabendazole.
Strongyloides stercoralis
•
acquired percutaneously (e.g. walking barefoot)
•
causes pruritus and larva currens - this has a similar appearance to cutaneous larva 
migrans but moves through the skin at a far greater rate
•
abdo pain, diarrhoea, pneumonitis
•
may cause Gram negative septicaemia due carrying of bacteria into bloodstream
•
eosinophilia sometimes seen
•
management: thiabendazole, albendazole. Ivermectin also used, particularly in chronic 
infections
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
cutaneous larva migrans
cutaneous larva migrans

Notes & Notes for MRCP                          
By Dr. Yousif Abdallah Hamad
Chapter 9

Infectious diseases
____________________________________________________
Filariasis
•
Manifestations of filariasis
Remember 3 L's:

Lymphatic filariasis (caused by Wuchereria bancrofti and Brugia 
malayi)

Loiasis (caused by Loa loa)

Light (light, sight, blindness - river blindness caused by Onchocerca 
volvulus)
Tropical eosinophilia:

Tropical eosinophilia is an allergic reaction to microfilaria of Wuchereria 
bancrofti. 

Characteristic features include: 
myalgia; fatigue; 
weight loss; 
cough and dyspnoea with wheeze; 
fever; 
current or previous residence in an area endemic for filariasis 
(southern Asia, Africa, India, South America); 
lymphadenopathy; 
marked peripheral blood eosinophilia 
high titres of anti-filarial antibodies.

The chest x ray shows bilateral reticulonodular shadowing. 

This condition is commonly accompanied by false positive serological 
tests for syphilis and high titres of cold agglutinins. 

There is typically a rapid response to treatment with 
diethylcarbamazine.
•
Diagnosis
finger prick test

identifying microfilariae on Giemsa stained, thin and thick blood film 
smears,
"Filariasis fills the blood at night." 
To remember that Microfilaria can be demonstrated in peripheral smear only 
at night.

W. bancrofti, whose vector is a mosquito; night is the preferred time for 
blood collection.

Loa loa's vector is the deer fly; daytime collection is preferred.
•
Which immune mechanisms does the body employ against the live filarial 
worms ?
Antibody-dependent cell-mediated cytotoxicity