The diseases notifiable to local authority proper officers under the Health
Protection (Notification) Regulations 2010 are:

 Acute encephalitis (A5B2CDEFHI2L2M4PR2S3T3VWY)

 Acute infectious hepatitis
 Acute meningitis
 Acute poliomyelitis
 Anthrax
 Botulism
 Brucellosis
 Cholera
 Diphtheria
 Enteric fever (typhoid or paratyphoid fever)
 Food poisoning
 Haemolytic uraemic syndrome (HUS)
 Infectious bloody diarrhoea
 Invasive group A streptococcal disease
 Legionnaires’ disease
 Leprosy
 Malaria
 Measles
 Meningococcal septicaemia
 Mumps
 Plague
 Rabies
 Rubella
 Severe Acute Respiratory Syndrome (SARS)
 Scarlet fever
 Smallpox
 Tetanus
 Tuberculosis
 Typhus
 Viral haemorrhagic fever (VHF)
 Whooping cough
 Yellow fever

Virulence factors are molecules produced by organisms that contribute to the pathogenicity of the
organism and enable them to achieve one or more of the following:
  Colonisation of a niche of the host (e.g. attachment to cells)
 Evasion of the host’s immune response (immunoevasion)
 Inhibition of the host’s immune response (immunosuppression)
 Entry into and exit out of cells (if the pathogen is intracellular)
 Obtain nutrition from the host

Virulence factor Example organisms

IgA protease secretion Neisseria meningitides
Haemophilus influenzae
Streptococcus pneumoniae
Protein A Staphylococcus aureus
M protein  Streptococcus pyogenes
Lecthinase alpha toxin Clostridium perfringens
Toxin mediated epithelial Vibrio cholerae
irritation
Spore formation Clostridium perfringens
Clostridium tetani
Bacillus anthracis
Bacillus cereus
Flagella Vibrio cholerae
Helicobacter pylori
Campylobacter jejuni
Salmonella typhi
Escherichia coli

Type of bacteria Notable examples

Facultative anaerobe Listeria spp.
Escherichia coli
Staphylococcus spp.
Streptococcus spp.

Obligate aerobe Mycobacterium tuberculosis

Pseudomonas aeruginosa
Bacillus spp.
Obligate anaerobe Bacteroides spp.
Clostridium spp.
Treponema spp.
Actinomyces spp.
Micro-aerophile Campylobacter jejuni
Helicobacter pylori
 Facultative anaerobic bacteria make ATP via aerobic respiration and are also capable of switching to
fermentation.

Obligate aerobic bacteria are bacteria that require oxygen to grow.

Obligate anaerobic bacteria are bacteria that live and grow in the absence of oxygen.

Micro-aerophilic bacteria are bacteria that require oxygen to survive, but require environments
containing lower levels of oxygen than are present in the atmosphere.

Route of transmission Example organisms

Aerosol (airborne particle < 5 µm) Mycobacterium tuberculosis
Varicella zoster virus
Measles virus
Droplet (airborne particle > 5 µm) Neisseria meningitides
Bordatella pertussis
Influenza virus
Parainfluenza virus
Respiratory syncytial virus
Faeco-oral Salmonella enteritidis
Escherichia coli
Vibrio cholerae
Ascaris lumbricoides
Hepatitis A
Poliovirus
Rotavirus
Sexual Neisseria gonorrhoea
Chlamydia trachomatis
Trepenoma pallidum
HIV
Hepatitis B
Human papillomavirus
Direct contact Staphylococcus aureus
Streptococcus pyogenes
Trichophyton rubrum
Human papillomavirus
Vertical Trepenoma pallidum
HIV
Hepatitis B
Vector-borne Plasmodium falciparum
 Borrelia burgdorferi
Trypanosoma cruzi
Coxiella burnetti
Leishmania donovani

The commonest cause of meningitis by patient group is summarized in the table below:

Patient group Commonest organisms

Neonates
Infants and children
Adolescents and young adults
Older adults
Immunocompromised
Group B Streptococcus
Escherichia coli
Escherichia coli
Listeria monocytogenes
Haemophilus influenza  type B
Streptococcus pneumoniae
Neisseria meningitidis
Streptococcus pneumoniae
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenza type B
Listeria monocytogenes
Listeria monocytogenes

Hepatitis A is infectious from 2 weeks before until 1 week after jaundice starts.

Measles is infectious from the initial onset of symptoms until 5 days after the rash appears.

Mumps is infectious for 3 days before until 1 week after the onset of salivary gland swelling.

Rubella is infectious from 1 week before until 5 days after the rash appears.

Chickenpox is infectious from 5 days before the rash appears until the last vesicle has crusted over.

Whooping cough is infectious from 3 days before until 3 weeks after the start of the symptoms.
Erythromycin reduces the infectious period to 3 days after the start of the course.

Scarlet fever is infectious for 10-21 days from the onset of symptoms. This is reduced to 1 day if the
patient is taking penicillin.

 
  

Anatomical site Organisms present in nearly 100% Organisms present in approx. 25%

Skin Staphylococcus epidermidis Staphylococcus aureus

Corynebacterium spp. Mycobacterium spp.
Nasopharynx Staphylococcus epidermidis Staphylococcus aureus
Staphylococcus salivarius Streptococcus pyogenes
Corynebacterium spp. Neisseria meningitidis
Haemophilus influenzae
Proteus spp
Mouth Staphylococcus epidermidis Staphylococcus aureus
Staphylococcus salivarius Enterococcus faecalis
Streptococcus mitis Neisseria meningitides
Streptococcus mutans Haemophilus influenzae
Lactobacillus spp. Proteus spp.
Corynebacterium spp.
Lower GI tract Staphylococcus aureus Staphylococcus epidermidis
Enterococcus faecalis Proteus spp.
Clostridium spp. Corynebacterium spp.
Bacteroides spp.
Lactobacillus spp
Anterior urethra Staphylococcus epidermidis Streptococcus mitis
Enterococcus faecalis
Proteus spp.

The typical CSF findings in different causes of meningitis is shown in the table below: 

  Normal Bacterial Viral Tuberculous

Pressure (cmH2O) 5-20 > 30 Usually normal Variable
Appearance Clear Turbid/cloudy Clear Fibrin web
Protein (g/L) 0.18-0.45 >1 <1 0.1-0.5
Glucose (mmol/L) 2.5-3.5 <2.2 Normal 1.5-2.5
WBC count (per mm3) 0-5 > 500 < 1000 100-500
Cell type N/A Polymorphs Lymphocytes Lymphocytes
Gram stain Negative Positive in 60-90% Negative Negative
This patient has a CSF sample consistent with a diagnosis of viral meningitis. The coxasackie and
echovirus groups of enteroviruses are the most common cause of viral meningitis. It can also be caused,
less commonly, by the herpes simplex virus and the varicella zoster virus.

Endocarditis is inflammation of the inner layer of the heart and often involves the heart valves. It can
be infective or non-infective (marantic endocarditis).

Risk factors for infective endocarditis include:

 Prosthetic heart valves
 Congenital heart defects
 Prior history of endocarditis
 Rheumatic fever
 Illicit intravenous drug use

The presentation of endocarditis is highly variable but the following triad is often quoted:
 Persistent fever
 Embolic phenomena
 New or changing murmur

Other features that may be present include heart failure, splenomegaly, finger clubbing, renal features
(haematuria, proteinuria, nephritis), and vasculitic features (splinter haemorrhages, Osler’s nodes,
Janeway lesions, Roth’s spots).

The following table summarises the BNF advised treatment regimes for the various causes of infective
endocarditis:

Causative organism BNF advised therapy

‘Blind’ therapy Flucloxacillin and gentamicin
Vancomycin plus rifampicin plus gentamicin (if the
patient is penicillin allergic, has a cardiac prostheses
present, or if MRSA is suspected)
Staphylococci e.g. Staphylococcus aureus Flucloxacillin plus rifampcin (in prosthetic valve endocarditis)
Vancomycin plus rifampicin (if penicillin allergy or MRSA)

Streptococci e.g.  Streptococcus viridans Benzylpenicillin plus gentamicin (if large vegetation present,
less-sensitive organism or prosthetic valve)
Vancomycin (if penicillin allergy)
Enterococci e.g.  Enterococcus faecalis Amoxicillin plus gentamicin
Vancomycin plus gentamicin (if penicillin allergic)
‘HACEK’ microorganisms ( Haemophilus, Amoxicillin plus low-dose gentamicin
Actinobacillus, Cardiobacterium, Eikenella,   Ceftriaxone plus low-dose gentamicin (if amoxicillin resistant)
and   Kingella spp .)

According to the current NICE guidelines people with the following cardiac conditions are at
increased risk for infective endocarditis :
 Acquired valvular heart disease with stenosis or regurgitation
 Valve replacement
 Structural congenital disease (excluding ASD or fully repaired VSD or PDA)
 Previous infective endocarditis
 Hypertrophic cardiomyopathy

Vaccine type Examples

Live, attenuated Measles,Mumps,Rubella (MMR)
Polio (OPV sabin)
Yellow fever
Influenza (nasal spray)
Rotavirus
Varicella (chicken pox)
BCG
Zoster (shingles)
Killed / Inactivated Polio (IPV salk)
Hepatitis A
Rabies
Toxoid (inactivated toxin) Diptheria (as part of DTaP)
Tetanus (as part of DTaP)
Botulism
Subunit/conjugate/Genetically Hepatitis B
engineered Haemophilus influenza  type B
Influenza ( injection)
Pertussis (as part of DTaP)
Pneumococcal
Meningococcal
Human papillomavirus (HPV)

Tuberculosis is treated in two phases, an initial phase using 4 drugs and a continuation phase using 2
drugs.

1. The initial phase lasts 2 months and the treatment combination of choice is isoniazid,

rifampicin, pyrazinamide, and ethambutol

2. The continuation phase usually lasts 4 months and the combination of choice is isoniazid and
rifampicin
Streptomycin is rarely used in the UK but may be used as an alternative treatment in the initial phase of
treatment if resistance to isoniazid has been established before treatment is commenced.

All vaccines are recommended, whether live or inactivated, in patients with asplenia. 

A history of anaphylaxis following any vaccination would be a contraindication to having that vaccine
again. BCG is a live vaccine.

Live vaccinations are generally contraindicated in the following situations:

 Pregnancy
 HIV, whether asymptomatic or symptomatic
 If less than 3 weeks after another live vaccine (although 2 live vaccinations can be given together
at different sites of the body)
 Other illnesses causing severe compromise of the immune system
 Haematological malignancies

All vaccines are contraindicated in individuals who have had:

 A confirmed anaphylactic reaction to a previous dose of a vaccine containing the same
antigens
 A confirmed anaphylactic reaction to another component in the relevant vaccine e.g.
streptomycin or neomycin

There is no evidence of harm to pregnant women or fetus from vaccination with inactivated vaccine or
toxoids. Live attenuated vaccines, however, are contraindicated in pregnancy but vaccination may be
performed if the risks of infection exceed the risks of vaccination.

HIV positive patients should not receive BCG, yellow fever or oral typhoid vaccinations, and in those with
impaired immunity (i.e. low CD4 count), MMR and varicella should be avoided until immunity improves

Fluenz tetra is a live attenuated vaccine that is administered as a nasal spray. It has been shown to
provide greater protection against influenza in children aged 2 to 18 than injectable influenza vaccine
containing inactivated virus. Current advice is that children with a history of egg allergy can be safely
vaccinated with Fluenz tetra unless they have previously had severe anaphylaxis to egg requiring
intensive care.

Premature infants, and also those with heart and lung diseases, should be vaccinated according to the
usual immunisation schedule. Premature infants should be immunised at the normal times
recommended for full-term babies and there should be no correction for gestational age implemented.

Concurrent antibiotic therapy is not a contraindication to vaccination.

Hepatitis B vaccination isn't routinely available as part of the NHS vaccination schedule. It is only
offered to those thought to be at increased risk of hepatitis B or its complications.
 The Hepatitis B vaccine is a conjugate vaccine that contains a surface antigen of the hepatitis virus
(HBsAg), on an aluminium adjuvant to increase immunogenicity. It is made via a recombinant DNA
technique.

 In adults and older children the preferred site of injection is the deltoid muscle. The anterolateral thigh
is preferred in younger children. Gluteal injection is not recommended as reduced efficacy has been
reported.

 The standard regime is three primary doses (the initial dose, then further doses at one and six months
later) with a booster at five years if still at risk. The accelerated regime for post-exposure prophylaxis is a
vaccination at the time of exposure, then repeat doses at one and two months later. 

Hepatitis B immunoglobulin can be given up to 7 days after high-risk exposure. Ideally immunoglobulin
should be given within 12 hours but the BNF recommends use up to 7 days after exposure.

The hepatitis B vaccine contains the viral envelope protein, hepatitis B surface antigen (HBsAg).
Vaccination results in the generation of the antibody anti-HBsAg. The vaccine is currently recommended
for all healthcare professionals working in the UK.

Blood titres are taken 1 month after the third dose of the vaccine and levels > 100 mIU/ml is regarded
as adequate. This generally provides immunity for at least 5 years. At 5 years after the initial injection a
booster can be given.

There is no substantiated association with Guillain-Barre syndrome.

The vaccine should be stored between 2 and 8 degrees C as freezing destroys its efficacy. 

The presence of the Australia antigen indicates current Hepatitis B infection. The Australia
antigen is the surface antigen of the Hepatitis B virus (HBsAg).
 
 

Indications for hepatitis B vaccination include:

 All health care professional’s working in the UK
 Other professions with occupational risks (foster carers, staff of custodial institutions,
morticians etc)
 Babies of mothers with hepatitis B during pregnancy
 Close family contacts of a case or carrier
 IV drug abusers
 Individuals with haemophilia
 Individuals with chronic renal failure
  Sex workers and individuals with frequently changing sexual partners

Hepatitis B surface antigen (HBsAg) is a protein on the surface of hepatitis B virus. It can be
detected in high levels in serum during acute or chronic hepatitis B virus infection. The
presence of HBsAg indicates that the person is infectious. The body normally produces
antibodies to HBsAg as part of the normal immune response to infection. HBsAg is the
antigen used to make hepatitis B vaccine.
 
Hepatitis B surface antibody (anti-HBs) indicates recovery and immunity from the hepatitis
B virus infection. Anti-HBs also develops in a person who has been successfully vaccinated
against hepatitis B.
 
Total hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute
hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing
infection with hepatitis B virus in an undefined time frame. It is not present following
hepatitis B vaccination.
 
IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicate recent infection with
hepatitis B virus (<6 months). Its presence indicates acute infection.
 
The following table summarises the presence of hepatitis B markers according to each
situation:
 
Marker Result Situation
HBsAg Negative
Anti-HBc Negative Susceptible to infection
Anti-HBs Negative
HBsAg Negative
Immune due to natural
Anti-HBc Positive
infection
Anti-HBs Positive
HBsAg Negative
Immune due to
Anti-HBc Negative
vaccination
Anti-HBs Positive
HBsAg Positive
Anti-HBc Positive
Acute infection
Anti-HBs Negative
IgM anti-HBc Positive
HBsAg Positive
Anti-HBc Positive
Chronic infection
Anti-HBs Negative
IgM anti-HBc Negative

Tetanus prone wounds include:

 Puncture wounds
 Wounds over 6 hours old
 Dirty wounds
 Wounds with significant devitalized tissue
 Avulsions
 Open fractures
 Gunshot wounds
 Crush injuries
 Burns

Tetanus prone wounds only require tetanus immunoglobulin (TIG) if there is an unknown history of
tetanus prophylaxis, less than 3 doses of tetanus toxoid have been given in the past or it is over 5 years
since the last dose.

The preventative dose of tetanus immunoglobulin is 250 IU in most cases, unless over 24 hours have
passed since the injury or the wound is heavily contaminated, then 500 IU should be given.
Anaphylaxis or encephalopathy following previous doses, are the only contraindications to the
administration of tetanus toxoid administration.

TIG and tetanus toxoid should not be given at the same site

community-acquired pneumonia
A 50-year-old man presents with a cough productive of green sputum that has been present for the past
2 days. On examination he is febrile, with a temperature of 38.0°C and has coarse right basal crackles on
chest examination. He has a confirmed allergy to penicillin.

This patient has symptoms and signs consistent with a community-acquired pneumonia (CAP). The
commonest cause of CAP in an adult patient that is otherwise well is  Streptococcus pneumoniae.

The first-line antibiotic of choice for community-acquired pneumonia is amoxicillin. The NICE guidelines
recommend the use of a macrolide (e.g. clarithromycin) or a tetracycline (e.g. doxycycline) for patients
who are allergic to penicillin. 

  hospital acquired pneumonia

The current recommendations by NICE and the BNF on the treatment are:
Early onset infection  (less than 5 days after admission to hospital):
 co-amoxiclav or cefuroxime for 7 days

Late-onset infection  (more than 5 days after admission to hospital):

 antipseudomonal penicillin (e.g. piperacillin with tazobactam)
 broad-spectrum cephalosporin (e.g. ceftazidime)
 quinolone (e.g. ciprofloxacin)

Atypical pneumonia
This patient has symptoms and signs consistent with an atypical pneumonia, most likely secondary
to Mycoplasma pneumoniae infection.

The clinical features of Mycoplasma pneumoniae infection include:

 Flu-like illness preceding respiratory symptoms
  Fever
 Myalgia
 Headache
 Diarrhoea
 Cough (initially dry but often becomes productive)
 Focal chest signs develop later in the illness

Mycoplasma pneumoniae  is commonly associated with the development of erythema multiforme and
can also cause Steven-Johnson syndrome. The rash of erythema multiforme characteristically comprises
multiple red lesions on the limbs that develop ‘target lesions’ a few days after the onset of the rash.

Another clue also for the diagnosis is the evidence of haemolytic anaemia with cold agglutinins, which
can both complicate Mycoplasma pneumoniae infections.

The first line antibiotic to use in this case would be a macrolide, such as clarithromycin. Doxycycline can
also be used but is generally considered a second-line agent.

In a child with a non-blanching rash meningococcal septicaemia should always be suspected. That is
especially true if one or more of the following are present:

1. An ill-looking child
2. Lesions larger than 2 mm in diameter (purpura)
3. Capillary refill time of  >   3 seconds
4. Neck stiffness

In the UK, most cases of meningococcal septicaemia are caused by   Neisseria meningitidis   group B.  

10-20% of the UK population are colonized with  Neisseria meningitidis.

Droplets and secretions from an infected patient are considered to be infectious from the onset of the
illness until completion of 24 hours treatment with systemic antibiotics.

The vaccination programme for   Neisseria meningitidis   group C has made this type much less common.
A vaccine for group B disease has recently been introduced for infants.

  The child in this case is clearly very sick and is demonstrating signs of septic shock. A single dose of
benzylpenicillin should be given without delay and the child transferred immediately via ambulance to
the nearest Emergency Department.  

The recommended doses of benzylpenicillin according to age are:

 Infants < 1 year of age: IM or IV benzylpenicillin 300 mg
 Children 1 to 9 years of age: IM or IV benzylpenicillin 600 mg
 Children and adults 10 years or older: IM or IV benzylpenicillin 1.2 g
Whooping cough is an upper respiratory tract infection caused by the Gram-negative
bacteria Bordatella pertussis. The disease is highly contagious and is transmitted to approximately 90%
of close household contacts.

The Health Protection Agency has identified two sets of priority groups for public health action in the
contact management of whooping cough:

Group 1. At increased risk of severe or complicated infection (vulnerable):

 Infants under 1 year who have received less than 3 doses of pertussis vaccine

Group 2. At increased risk of transmitting infection to individuals in Group 1:

 Pregnant women at greater than 32 weeks gestation

 Healthcare workers working with infants and pregnant women

 Individuals working with infants too young to be vaccinated (< 4 months old)

 Individuals sharing a household with infants too young to be vaccinated (< 4 months old)

Current guidance states that antibiotic prophylaxis with a macrolide antibiotic, such as erythromycin,
should only be offered to close contacts when both of the following criteria have been met:

1. Onset of disease in the index case is within the preceding 21 days and;

2. There is a close contact in one of the two priority groups

When these two criteria have been met ALL contacts, regardless of vaccination status and age, should
be offered chemoprophylaxis.

Immunisation or a booster dose (depending on current vaccination status) should also be considered for
those who have been offered chemoprophylaxis.

Whooping cough is an upper respiratory tract infection caused by the Gram-negative

bacteria Bordatella pertussis. Transmission is via respiratory droplets and the incubation period
is approximately 7-21 days. The disease is highly contagious and is transmitted to
approximately 90% of close household contacts.

The clinical course of whooping cough occurs in two stages:

1. Catarrhal stage:
This phase presents similarly to any mild respiratory infection with low-grade pyrexia and
coryzal symptoms. A cough can be present but it is usually mild and nowhere near as
pronounced as during the paroxysmal phase. The catarrhal phase usually lasts around a week.

2. Paroxysmal stage:

The typical paroxysmal cough develops in this phase as the catarrhal symptoms start to settle.
The coughing occurs in paroxysmal spasms, typically preceded by an inspiratory ‘whoop’
followed by a rapid succession of expiratory hacking coughs. There may be vomiting and
patients often develop subconjunctival haemorrhages and petechiae. Patients are generally well
between spasms and there are usually no chest signs present. This phase can be very
protracted, lasting up to 3 months. There is usually a gradual recovery over this period and the
latter stages are sometimes referred to as the ‘convalescent stage’.

Documented complications of whooping cough include:

 Secondary pneumonia
 Rib fractures
 Herniae
 Syncopal episodes
 Encephalopathy
 Seizures.

Nasopharyngeal swabs can be cultured in the Bordet-Gengou medium, a type of agar plate
containing blood, potato extract and glycerol with an antibiotic that is used to
isolate Bordetella pertussis.

1. Testing in infants under 12 months of age:

 Hospitalised patients should be investigated with PCR testing

 Non-hospitalised patients within 2 weeks of onset of 48 hours of antibiotic therapy

should be investigated with culture of nasopharyngeal swab or aspirate

 Non-hospitalised patients presenting over 2 weeks after onset should be investigated

with serology for anti-pertussis toxin IgG antibody levels 

2. Testing in children over 12 month of age and adults:

 Patients within 2 weeks of onset of 48 hours of antibiotic therapy should be investigated

with culture of nasopharyngeal swab or aspirate

 Patients aged 5 to 16 that have not received the vaccine within the last year, presenting
over 2 weeks after onset should have oral fluid testing for anti-pertussis toxin IgG
antibody levels
  Patients aged under 5 or over 17 presenting over 2 weeks after onset should be
investigated with serology for anti-pertussis toxin IgG antibody levels.

The Mantoux test replaced the Heaf test as the TB screening test in the UK in 2005. It involves
the injection of 5 Tuberculin units (0.1mL) intradermally. The result is read 2-3 days later and
interpreted as follows:

 Mantoux negative – Induration less than 6 mm

 Mantoux positive – Induration 6 mm or greater

 Mantoux strongly positive – Induration 15 mm or greater

This patient has a diagnosis of malaria, which is an infectious disease transmitted by female of
the Anopheles genus of mosquito. It is a parasitic infection caused by the genus Plasmodium.
Five species are recognized as causing disease in humans: Plasmodium
falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae and Plasmodium
knowlesi.

The classic symptom of malaria is the malarial paroxysm, a cyclical occurrence of a cold
phase, where the patient experiences intense chills, a hot stage, where the patient feels
extremely hot and finally a sweating stage, where the fever declines and the patient sweats
profusely. On examination the patient may show signs of anaemia, jaundice and have
hepatosplenomegaly without evidence of lymphadenopathy. The full blood count in malaria
often shows the classic combination of anaemia and thrombocytopenia.

Plasmodium falciparum is the most serious form and is responsible for most deaths. Severe or
complicated malaria is suggested by the presence of impaired consciousness, seizures,
hypoglycaemia, anaemia, renal impairment, respiratory distress and spontaneous
bleeding. Plasmodium falciparum is the most likely type in this case in view of the presentation.

Thick and thin blood films are the ‘gold-standard’ investigation for malaria. Patients can have
malaria despite a negative film and in cases where the blood film is negative at least two further
films should be obtained over the subsequent 48 hours before the diagnosis can be excluded.

Malaria is usually diagnosed using the Indirect Fluorescence Antibody Test (IFAT).

Haemoglobinuria and renal failure following treatment is suggestive of blackwater fever, which is
caused by Plasmodium falciparum. An autoimmune reaction between the parasite and quinine
causes haemolysis, haemoglobinuria, jaundice and renal failure. This can be fatal.
The benign malarias: P.vivax, P. malariae and P.ovale are usually treated with chloroquine. A
course of primaquine is also required in P.vivax and P.ovale infection. Artesunate is the drug
treatment of choice for Plasmodium falciparum malaria. Quinine can still be used where
artesunate is not available. Often combination therapy with drugs such as doxycycline or
fansidar is also required. In severe or complicated cases (such as the one outlined in this
question), where artesunate is not available, IV quinine hydrochloride would be the first-line
drug.

The Epstein-Barr virus (EBV), also known as human herpes virus 4 (HHV-4), is a commonly
encountered virus that is best known as the cause of infectious mononucleosis (glandular fever). As with
other herpes virus infections, EBV infection is life-long, although most patients have no further
symptoms after the first few weeks of infection. EBV infects and subsequently lays dormant within B-
lymphocytes.

EBV infection is associated with an increased risk of several cancers including nasopharyngeal cancer,
Burkitt lymphoma, Hodgkin lymphoma and gastric cancer. EBV-related cancers occur most commonly in
Africa and in parts of Southeast Asia. Overall, very few patients that have been infected with EBV will go
on to develop cancer and this risk is very low.

Hepatitis B and C are both linked with the development of hepatocellular cancer but there is no
established link with hepatitis A.

Adenovirus is currently being explored as a possible anti-cancer treatment due to its oncolytic potential.
A genetically modified H101 strain of adenovirus has gained approval from China’s State Food and Drug
Administration (SFDA) for the treatment of head and neck cancer.
 HIV

A normal CD4 count ranges from 500-1000 cells/mm3. In patients with a diagnosis of HIV the CD4 count
is typically checked every 3-6 months. The CD4 count can vary from day to day. It also varies depending
upon the time that the blood test is taken and can be affected by the presence of other infections or
illnesses.

At CD4 count of less than 350 cells/mm3 treatment with anti-retroviral therapy should be considered.

A CD4 count of less than 200 cells/mm3 is AIDS defining.

This man is at risk of HIV due to his history of intravenous drug abuse and shared needles. Any patient
with a flu-like illness and a history of risk factors should be suspected of experiencing an HIV
seroconversion illness. 

Approximately 20-60% of patients that contract HIV undergo a seroconversion illness. It typically occurs
between 1 and 6 weeks after exposure and presents with a flu-like illness. Common clinical features
include:
 Fever
 Malaise
 Myalgia
 Pharyngitis
 Diarrhoea
 Headaches
 Maculopapular rash
 Lymphadenopathy

Antibody tests will be negative at this stage of the disease but a diagnosis of HIV can be made at this via
a P24 antigen test or by measuring HIV RNA levels. CD4 and CD8 counts are also typically normal at this
stage.

According to the CDC definition, a patient can be diagnosed with AIDS if he or she is co-
infected with HIV and has:

 A CD4 T-cell count of less than 200 cells/mm 3 or;

 A CD4 T-cell percentage of total lymphocytes of less than 15% or;
 An AIDS defining infection

Staphylococci are part of the Micrococcaceae family. It is a genus of Gram-positive bacteria that appear

round (cocci) on microscopy and form in grape-like clusters.
Staphylococcus aureus is commonly carried asymptomatically in the nose, respiratory tract, and on the
skin of healthy people (up to 40% of people). It produces coagulase, which catalyses the conversion of
fibrinogen to fibrin and is thought to form a protective barrier for the organism. It also has receptors for
the host cell surface and matrix proteins that help the organism to adhere.

Transmission is by airborne transmission and direct person-to-person contact (e.g. from the hands of

healthcare professionals).

Staphylococcus aureus causes a wide range of clinical infections including:

 Skin infections: boils, follicullitis, impetigo, cellulitis

 Pneumonia: rare, but may follow influenza and has high mortality
 Endocarditis: particularly in IV drug abusers
 Bacteraemia: associated with intravascular devices, catheters etc

Staphylococcus aureus  grows readily on most laboratory media, is usually coagulase-positive and has a

typical ‘cluster of grapes’ morphology.

Staphylococcus aureus is capable of secreting several exotoxins, which can be categorised into four
groups:

1. Superantigens: these have superantigen activities that induce toxic shock syndrome (TSS). An
example is TSST-1 enterotoxin type B, which causes TSS associated with tampon use.

2. Exfoliative (EF) toxins: EF toxins are implicated in the disease staphylococcal scalded-skin
syndrome (SSSS), which most commonly occurs in infants and young children.

3. Cell membrane toxins: examples include the alpha, beta and delta toxins, which increase
invasiveness and virulence

4. Biocomponent toxins: an example is Panton-Valentine leukocidin (PVL), which is associated with

severe necrotising pneumonia in children.

Historically the treatment of choice for Staphylococcus aureus  infection was penicillin, however,
penicillin resistance is now very common and first-line therapy is usually a penicillinase-resistant beta-
lactam antibiotic, such as the methacillin-related agent flucloxacillin.

Methacillin-resistant  Staphylococcus aureus (MRSA) has become troublesome in hospitals and other

healthcare institutions over recent years. MRSA is any strain of Staphylococcus aureus that has
developed resistance to beta-lactam antibiotics, which include penicillins and cephalosporins. Resistance
is caused by possession of the mecA gene, which codes for a low-affinity penicillin-binding protein. It is
usually sensitive to teicoplanin and vancomycin.
Skin infections are the most common form of S. aureus infection and these can manifest in a number of
ways including boils, impetigo, cellulitis and more severe, invasive infections. It is the commonest cause
of soft tissue infections in intravenous drug users and can also cause pneumonia, septic arthritis,
endocarditis, and bacteraemia.

S. aureus  is usually sensitive to flucloxacillin and macrolide antibiotics, such as erythromycin.

Combination therapy with gentamicin is sometimes used for more serious infections, such as
endocarditis.

This child has a diagnosis of staphylococcal scalded skin syndrome. This is caused by Staphylococcus
aureus, which releases extoxins (epidermolytic toxins A and B) that damage the outer layer of the skin
causing it to be shed.

Staphylococcal scalded skin syndrome is most commonly seen in children younger than 5 years. Lifelong
protective antibodies are usually acquired during childhood, making it much less common in older
children and adults.

The clinical features of staphylococcal scalded skin syndrome include:

 Fever
 Irritability (children often do not want to be touched)
 Widespread blistering rash (which is painful)
 Skin peels leaving painful, raw patches

It is usually treated with intravenous flucloxacillin. The skin needs to be gently cleansed at least once per
day and the application of greasy moisturizers help to soothe the skin and prevent it from sticking .

Species of Streptococcus are classified on the basis of their haemolytic properties. Alpha-haemolytic

species cause oxidation of iron in haemoglobin molecules within red blood cells, giving it a greenish
colour on blood agar.

In clinical practice the two most important groups of alpha-haemolytic  Streptococci are:

 Streptococcus pneumoniae 
 Streptococcus viridans

Streptococcus pneumoniae is a leading cause of bacterial pneumonia and can also cause otitis media,
sinusitis, meningitis, and peritonitis.

Beta-haemolytic  Streptococci are sub-classified by the Lancefield grouping.

 Streptococcus pyogenes (group A)
  Streptococcus agalactiae (group B)
 Enterococcus faecalis (group D).
Most cases of erysipelas are caused by Streptococcus pyogenes.

Erysipelas is an infection of dermis and upper subcutaneous tissue that is most frequently caused
by Streptococcus pyogenes. It can also, more rarely, be caused by other beta-haemolytic streptococci or
staphylococci.

Patients are usually systemically unwell with fever and rigors common. The infected area is red, hot and
tender. Local oedema produces a raised, well-defined edge that enables it to be distinguished from
cellulitis clinically.

Streptococcus pneumoniae is a Gram-positive, alpha-haemolytic, facultative anaerobic bacteria. It is

typically seen in lanceolate pairs.

Streptococcus pneumoniae is a major cause of worldwide infection, is a leading cause of bacterial

pneumonia and can also cause otitis media, sinusitis, meningitis, and peritonitis.

It is a normal commensal of the respiratory tract and resides asymptomatically in the nasopharynx of

healthy carriers. Transmission in disease is via close person-to-person contact via respiratory droplets.

The polysaccharide capsule of Streptococcus pneumoniae is the main determinant of its pathogenicity.

It serves to protect the pneumococci from phagocytes. Its cell wall components are pro-inflammatory
and it also has a variety of adhesions that mediate colonisation by binding to cell surface carbohydrates.

Infection is more likely in individuals under the age of 2 and over the age of 65. Severe infection is
predisposed to by the following factors:

 Complement deficiency
 Agammaglobulinaemia
 HIV infection
 Splenectomy
 Alcoholism
Streptococcus pneumoniae was once universally susceptible to penicillin but significant numbers have
now developed resistance through a genetically modified penicillin-binding gene. It is also susceptible to
macrolide antibiotics, cephalosporins, and tetracyclines.

Streptococcus pyogenes is a Gram-positive, group A beta-haemolytic, facultative anaerobic bacteria.

It is carried asymptomatically in the pharynx in between 5 and 30% of the population. In disease it
is transmitted by the aerosol route and also by direct person-to-person contact. Infection can occur at
any age, but is most common in children.

It carries a group A carbohydrate antigen (Lancefield’s antigen) and is surrounded by the M protein
antigen, which prevents leucocyte phagocytosis. Antibodies to particular M proteins are protective
against further infection with the same M type.

Streptococcus pyogenes  is associated with three distinct types of disease:

1. Infection: It is the commonest cause of bacterial pharyngitis and also causes erysipelas,
impetigo, cellulitis, wound infections, and rarely necrotizing fasciitis or pneumonia.
Streptococcus pyogenes infections are characterised by rapid onset, local tissue destruction, and
a spreading nature.

2. Toxin-mediated disease: These can occur with both systemic and localized infections. Examples
include erythrogenic toxin, which causes scarlet fever, and pyrogenic toxin, which causes
streptococcal shock.

3. Post-infectious immune-mediated disease: Rheumatic fever, glomerulonephritis, and erythema

nodosum are all thought to occur due to an immune-mediated process whereby antibodies to
bacterial structures cross-react with host tissues.

Benzylpenicillin is the mainstay of treatment and no resistance is currently reported. Amoxicillin can be
sued for oral therapy in less severe infections and macrolides are a suitable alternative in patients with a
history of penicillin allergy.

Klebsiella pneumoniae  is most commonly seen in alcohol dependent patients. It is more common in
men than women and typically presents after the age of 40.
Clinical features include:
 Fevers and rigors
 Pleuritic chest pain
 Purulent sputum(Rusty)
 Haemoptysis (more frequently than with other bacterial pneumonias)

It tends to involve the upper lobes and commonly leads to cavitating lesions.

Cavitation can also occur with Staphylococcus aureus but is generally multilobar and not restricted to
the upper lobes.

Other causes of cavitating pneumonia include:

 Pseudomonas aeruginosa
 Mycobacterium tuberculosis
 Legionella pneumophila (rare)

Klebsiella is a genus of non-motile, Gram-negative, rod-shaped bacteria with a prominent

polysaccharide-based capsule. They are routinely found in the nose, mouth and gastrointestinal tract as
normal flora, however, they can also behave as opportunistic pathogens.

Infections with Klebsiella spp. are usually nocosomial. They are an important cause of ventilator-

associated pneumonia (VAP), urinary tract infection, wound infection and bacteraemia. Outbreaks of
infections with Klebsiella spp. in high-dependency units have been described and are associated with
septicaemia and high mortality rates. Length of hospital stay and performance of invasive procedures
are risk factors for Klebsiella infections.

Primary pneumonia with  Klebsiella pneumoniae  is a rare,  severe, community-acquired infection

associated with a poor outcome.

Klebsiella rhinoscleromatis causes a progressive granulomatous infection of the nasal passages and

surrounding mucous membranes. This infection is mainly seen in the tropics.

Klebsiella ozanae is a recognised cause of chronic bronchiectasis.

Klebsiella  organisms are resistant to multiple antibiotics including penicillins. This is thought to be a

plasmid-mediated property. Agents with high intrinsic activity against Klebsiella  pneumoniae should be
selected for severely ill patients. Examples of such agents include third-generation cephalosporins (e.g
cefotaxime), carbapenems (e.g. imipenem), aminoglycosides (e.g. gentamicin), and quinolones (e.g.
ciprofloxacin). These agents may be used as monotherapy or combination therapy. Aztreonam may be
used in patients who are allergic to beta-lactam antibiotics.

Species with ESBLs (Extended spectrum beta-lactamase) are resistant to penicillins and also
cephalosporins such as cefotaxime and ceftriaxone.
This child has a clinical diagnosis of measles. The classical presentation is of a high fever with coryzal
symptoms and photophobia with conjunctivitis often being present. The rash that is associated is a
widespread erythematous maculopapular rash. Koplik spots are pathognomonic for measles, and are
the presence of white lesions on the buccal mucosa.

Public Health England recommends that children with measles be kept away from school, nursery or
childminders for 4 days from the onset of the rash.

Incubation period of less than 1 week include:

 Staphylococcal enteritis (1-6 hours)
 Salmonella enteritis (12-24 hours)
 Botulism (18-36 hours)
 Gas gangrene (6 hours to 4 days)
 Scarlet fever (1-4 days)
 Diphtheria (2-5 days)
 Gonorrhoea (3-5 days)
 Yellow fever (3-6 days)
 Cholera (12 hr-6 days)
 Meningococcaemia (1-7 days)

Diseases that have an incubation period of between 1 and 3 weeks include:

 Whooping cough (7-10 days)

 Leptospirosis (7-10 days)
 Brucellosis (7-20 days)
 Chickenpox (7-20 days)
 Typhoid (8-20 days)
 Measles (10-20 days)
  Mumps (14-20 days)
 Rubella (14-20 days)
 Malaria (7-40 days depending on strain)

Falciparum malaria usually has an incubation period of 7-14 days.

Other infectious disease that have an incubation period longer than 3 weeks include:
 Hepatitis A (3-5 weeks)
 Hepatitis B (6 weeks to 6 months)
 HIV (3 weeks to 3 months)
 Infectious mononucleosis  (4-6 weeks)

Acute bacterial prostatitis is an acute focal or diffuse suppurative inflammation of the prostate gland.

The most common causative organisms are:

 Escherichia coli
 Streptococcus faecalis
 Staphylococcus aureus
 Neisseria gonorrhoea

The prostate is usually involved as a consequence of:

 Direct extension from the posterior urethra or urinary bladder
 Distant spread in the blood or lymphatics
 Occasionally, infection may spread from the rectum

NICE suggest that acute prostatitis should be suspected in a man who presents with:
 A feverish illness of sudden onset (which may be associated with rigors, arthralgia, or
myalgia).
 Irritative urinary voiding symptoms (dysuria, frequency, urgency) or acute urinary retention.
 Perineal or suprapubic pain (penile pain, low back pain, pain on ejaculation, and pain during
bowel movements can also occur).
 Exquisitely tender prostate on rectal examination.
 Urine dipstick test showing white blood cells, and urine culture confirming urinary infection.

The current recommendations by NICE and the BNF on the treatment of acute prostatitis are:
 Ciprofloxacin or ofloxacin (suggested duration of treatment 28 days)
 Trimethoprim as an alternative (suggested duration of treatment 28 days)
Pelvic inflammatory disease (PID) is an infection of the upper part of the female reproductive
system. It usually arises from ascending infection from the cervix. The most commonly implicated
organisms are Neisseria gonorrhoea and Chlamydia trachomatis.

The current recommendations by NICE and the BNF on the treatment of PID are:

 Doxycycline plus metronidazole (suggested duration of treatment 14 days days) plus single dose
IM ceftiaxone

otitis externa (swimmer’s ear), which is infection and inflammation of the ear canal. Common
symptoms include pain, itching and discharge from the ear. Otoscopy will reveal erythema of the ear
canal with pus and debris present.

Various conditions can predispose to otitis externa including skin conditions, such as psoriasis and
eczema. It is also more prevalent in people that have regular exposure to water in the ear canal, such as
swimmers.

The commonest causative organisms are:

 Pseudomonas aeruginosa (50%)
 Staphylococcus aureus (23%)
 Gram negative bacteria e.g. E.coli (12%)
 Aspergillus and Candida species (12%)

It can generally be treated with topical antibiotic and corticosteroid mix such as Betnesol-N or Sofradex.
Occasionally when persistent it requires referral to ENT for auditory toilet and insertion of an antibiotic
saturated wick.

Complement deficiencies comprise 1-10% of all primary immunodefiencies and tend to predispose to
infection with encapsulated bacteria including:

 Neisseria meningitidis
 Haemophilus influenzae
 Group B  Streptococcus
 Streptococcus pneumoniae
 Klebsiella pneumoniae
 Salmonella typhi
 Patients with hypertension are only eligible for the seasonal influenza vaccination if they
have co-existent cardiac complications.
 
The UK national policy is that the Seasonal influenza vaccine should be offered to the
following groups:
 All those aged 65 years and older
 Children aged 2 to 7 years
 Residents of nursing and residential homes for the elderly (and other long-stay
facilities)
 Carers of persons whose welfare may be at risk if the carer falls ill
 All those aged 6 months or older in a clinical risk group
 
The following table outlines the clinical risk groups that are considered eligible for the
vaccine:
 
Category Examples of eligible groups
COPD
Interstitial lung disease
Respiratory disease
Cystic fibrosis
Asthma (requiring oral or inhaled steroids)
Congenital heart disease
Chronic heart failure
Heart disease Coronary heart disease (requiring medication
and/or follow-up)
Hypertension with cardiac complications
Chronic kidney disease
Kidney disease Nephrotic syndrome
Renal transplant patients
Liver cirrhosis
Liver disease Chronic hepatitis
Biliary atresia
Cerebrovascular accident
Neurological disease
Transient ischaemic attack
Endocrine disease Type 1 and 2 diabetes
Patients undergoing chemotherapy
Patients taking immunosuppressive drug
Immunosuppression therapy (including systemic steroids)
Asplenia or splenic dysfunction
HIV infection
Pregnancy All pregnant women
The photo above demonstrates the presence of a dendritic ulcer in an eye that has been stained with
fluorescein drops.

Two infectious agents can cause this condition.

 Herpes simplex virus (type I) (80%)

 Herpes zoster virus (20%)

The patient should receive the following treatment:

 Aciclovir ointment 5 times daily topically for 10 days

 Prednisolone 0.5% drops 2-4 times daily
 Oral high dose vitamin C (which can reduce healing time)

Clostridium tetani is a Gram positive, rod shaped, obligate anaerobic bacterium.

The incubation period is quoted as anywhere between 4-21 days and can occur after several months but
symptoms usually occur within the first 7 days after exposure.

Approximately 80% of patients develop generalised tetanus. The commonest presenting feature of
generalised tetanus is trismus (lockjaw), occurring in approximately 75% of affected individuals. Other
clinical features include:

 Facial spasms (risus sardonicus)

  Opisthotonus (characteristic body shape during spasms)
 Neck stiffness
 Dysphagia
 Calf and pectoral muscle rigidity
 Fever
 Hypertension
 Tachycardia 

Spasms can occur frequently and last for several minutes, they can continue to occur for up to 4 weeks.
Current mortality rates are between 10 and 15%.

Tetanic spasms are caused by the exotoxin tetanospasmin. The effects of tetanolysin are not fully
understood but it is not believed to have clinical significance.

Localised tetanus is a rare form of the disease, occurring in around 1% of affected individuals. Patients
have persistent contraction of muscles in the same anatomic area as the injury. It may precede
generalised tetanus.

Clostridium perfringens is a Gram-positive, rod-shaped, anaerobic, spore-forming pathogenic

bacterium.

It is the organism most commonly associated with gas gangrene (85-90% of cases), but other species,
such as C. septicum and C. novyi can also be implicated. It is capsulate and produces a range of toxins, of
which lecithinase C (alpha-toxin) is the most important and is the cause of gas gangrene.

Gas gangrene typically develops when a devitalized wound becomes contaminated with spores from the
environment. The spores germinate and organisms multiply in the ischaemic conditions, releasing
toxins, which can further damage tissues. 60% of all cases are post-traumatic and the majority of these
cases follow road traffic accidents.

The clinical features of gas gangrene usually appear within 24 hours of the injury. Initially there is
oedema and reddening and then blackening of the muscles. The overlying skin has a marbled
appearance before turning black and sloughing off. There is usually a foul smelling serous exudate.
Crepitus can often be detected under the skin due to gas production by the clostridia. Progression to
toxaemia and shock is often very rapid.

Treatment with antibiotics alone is ineffective as they do not penetrate into the ischaemic tissues
effectively. Treatment is by debridement and excision of infected, necrotic tissues with adjuvant
antibiotic therapy.  Hyperbaric oxygen may also be helpful. The condition can be prevented by good
management of potentially infected devitalized wounds.

Clostridium perfringens spores survive cooking and during slow cooling and unrefrigerated storage
germinate to form vegetative cells. It is the third commonest cause of food poisoning in the UK.

Clostridium difficile is a Gram-positive, anaerobic, spore forming bacteria. It is present in the gut of
approximately 3% of healthy adults. (2012 UK HPA estimates).

Clostridium difficile associated diarrhoea (CDAD) often follows the use of broad-spectrum antibiotics,
which alter the normal bacteria flora of the bowel and allow Clostridium difficile to proliferate. The
mucosa of the large intestine becomes inflamed and bleeds, taking on the characteristic
‘pseudomembranous appearance’. Over 80% of Clostridium difficile infections are reported in people
over the age of 65.

They found the risk for CDI to be increased nearly sevenfold after antibiotic treatment (OR, 6.91). Risk
was greatest with clindamycin (OR, 20.43), followed by fluoroquinolones (OR, 5.65), cephalosporins (OR,
4.47), penicillins (OR, 3.25), macrolides (OR, 2.55), and trimethoprim/sulfonamides (OR, 1.84). 

The main clinical features of CDAD are:

 Abdominal cramps,
 Severe bloody and/or watery diarrhoea
 Diarrhoea often offensive smelling
 Fever 

The current gold standard for the diagnosis of Clostridium difficile colitis is cytotoxin assay. This test does
have its disadvantages, however, as it is difficult to perform and results can take up to 48 hours to
become available. The most common laboratory test for the diagnosis of Clostridium difficile colitis is an
enzyme-mediated immunoassay that detects toxins A and B. This test has a specificity of 93-100% and a
sensitivity of 63-99%.

Hand washing is an effective way to prevent the spread of C. difficile

Patients can go on to develop toxic megacolon and the condition can be fatal, especially in frail or
elderly patients. 

Oral metronidazole is the current first line treatment of choice in cases of CDAD. Oral vancomycin is the
second line agent.

Chickenpox (varicella zoster) has an incubation period of between 7-21 days. It is highly contagious
and air-borne spread. There is often a prodromal phase when there is a fever, aches and headaches. Dry
cough and sore throat may also occur. The rash appears as crops of spots that are itchy and vesicular.
They can occur anywhere and several crops may appear over several days.

Recognized complications include:

 Infected spots
 Otitis media
 Pneumonia
 Encephalitis
 Myocarditis
 Glomerulonephritis
 Appendicitis
 Hepatitis
 Pancreatitis
 Orchitis

Treatment is mainly symptomatic and includes managing any fevers with paracetamol. Ibuprofen should
not be used as there is a (rare) link between this and necrotizing fasciitis when used in patients with
chickenpox. An emollient and antihistamine may be used to help ease the itchy rash.

There are several groups of children that are at higher risk of developing complications. Aciclovir is more
likely to be given in these cases. These include:

 Children less than one month of age

 Children with immunosuppression (leukaemia/ HIV or on steroids)
 Children with severe skin problems
 Children with severe cardiorespiratory problems
Prophylactic VZIG is recommended for high-risk patients with no known immunity (i.e. no known
previous chickenpox) who have had a significant exposure to varicella zoster (considered > 4 hours close
contact).

High-risk groups include:

 Neonates
 Pregnant women
 The immunocompromised
 Those on high dose steroids (children on more than 2 mg/kg/day for more than 14 days, or
adults on 40 mg/day for more than a week)

She is at high risk of adrenal insufficiency and needs a temporary increase in her steroid dose during
times of infection or stress. It would be inappropriate to stop or wean down her dose of prednisolone. 

She is at risk of developing severe varicella infection, with complications including pneumonia, hepatitis
and DIC. In addition, varicella infection may present atypically or insidiously and the typical varicella rash
may not be a prominent feature.

A patient on high dose steroids who develops varicella infection requires admission, specialist review
and intravenous aciclovir.
Measles belongs to the paramyxoviridae group of viruses. The incubation period is 7-18 days (average
10) and it is spread by airborne or droplet transmission. The classical presentation is of a high fever with
coryzal symptoms and photophobia with conjunctivitis often being present. The rash that is associated is
a widespread erythematous maculopapular rash. Koplik spots are pathognomonic for measles, and are
the presence of white lesions on the buccal mucosa.

Differential diagnoses would include:

 Rubella
 Roseola infantum (exanthem subitom)
 Scarlet fever
 Kawasaki disease
 Erythema infectiosum (5th disease)
 Enterovirus
 Infectious mononucleosis
Diagnosis can be confirmed by the following means:

 Salivary swab for measles specific IgM

 Serum sample for measles specific IgM
 Salivary swab for RNA detection

Possible complications include:

 Otitis media
 Febrile convulsions
 Pneumonia
 Bronchiectasis
 Diarrhoea
 Meningitis
 Encephalitis
 Immunosuppression
 Subacute sclerosing panencephalitis
 Death

Legionella pneumophila is a Gram negative bacterium that is found in natural water supplies and in
the soil. It is the cause of Legionnaires’ disease. Outbreaks of Legionnaires’ disease have been linked to
poorly maintained air conditioning systems, whirlpool spas and hot tubs.

The clinical features of the pneumonic form of Legionnaires’ disease include:

 Mild flu-like prodrome for 1-3 days
 Cough (usually non-productive and occurs in approximately 90%)
 Pleuritic chest pain
 Haemoptysis
 Headache
 Nausea, vomiting and diarrhoea
 Anorexia

Legionella pneumophila  infections can be successfully treated with macrolide antibiotics, such as
erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur with Legionnaires’
disease and will result in hyponatraemia as is seen in this case.

Legionella longbeachae is another less commonly encountered species that has also been implicated in
outbreaks. It is predominantly found in soil and potting compost, and has caused outbreaks of Pontiac
fever, the non-respiratory and less severe variant of Legionnaires’ disease.

Bacillus cereus  is a Gram-positive, rod-shaped, beta-haemolytic bacterium. It is the cause of ‘fried rice
syndrome’.
Hardy spores in rice can survive boiling and then leaving the rice at room temperature for long periods
prior to frying allows these spores to germinate. Emetic enterotoxin-producing strains cause nausea and
vomiting, usually between 1 and 6 hours after consumption. The vomiting can be severe and typically
lasts between 6 and 24 hours.

There are also diarrhoegenic enterotoxin-producing strains also exist. These predominantly cause
abdominal pain and vomiting, which starts 8-12 hours after ingestion and usually resolves within 12 to
24 hours. This is more commonly associated with ingestion of meat, vegetables and dairy products.

The clinical history and examination in this case is highly suggestive of a Pneumocystis
jirovecii pneumonia.

Pneumocystis jirovecii is a yeast-like fungus that causes opportunistic infection in

immunocompromised individuals and remains a leading AIDS-defining infection in HIV-infected
individuals. It tends to cause infection in HIV positive patients who have a CD4 count less than 200
cells/mm3.

This patient has a past history of intravenous drug abuse, which makes him at high risk for HIV infection.
The examination findings of oral thrush and widespread lymphadenopathy would also support this as an
underlying diagnosis.

The clinical features of Pneumocystis jirovecii pneumonia include:

 Cough (usually non-productive)

 Exertional dyspnoea
 Fever
 Tachypnoea
 Chest pain
 Crackles and wheeze

Although focal chest signs can be present the chest examination is often entirely normal, particularly in
mild-moderate cases.

Chest X-ray can be normal, or can show perihilar fluffy shadowing, as is present in the chest X-ray in this
case. Patients with Pneumocystis jirovecii pneumonia are also at an increased risk of developing a
pneumothorax.

Desaturation on exertion is recognized as being a very sensitive sign of Pneumocystis

jirovecii pneumonia.

High-dose co-trimoxazole (trimethoprim-sulfamethoxazole) is the drug treatment of choice. Alternatives

include atovaquobe and dapsone with trimethoprim. Treatment is usually required for 2-3 weeks.

Tuberculosis is the most common contagious infection in HIV-immunocompromised patients leading to

death.
Mycobacteria tuberculosis is an obligate pathogenic bacteria, of the Mycobacteriaceae family. It
contains a lipid-rich cell wall that renders it impervious to Gram-staining and decolourisation with acid
(acid-fast).

The primary infection is usually asymptomatic and only around 5-10% of patients go on to develop

post-primary tuberculosis. These patients usually have some form of impaired immunity.

Patients with post-primary tuberculosis are often asymptomatic or have only minor symptoms, such as a
chronic dry cough. In symptomatic patients, constitutional symptoms are prominent with fever, malaise
and weight loss common. A productive cough and/or haemoptysis may also be present.

The Ghon focus is a primary lesion caused by tuberculosis that develops in the lung of previously
unaffected individuals. It represents a calcified caseating granuloma. It typically appears in the middle-
third of the lung (the lower part of the upper lobe or upper part of the lower lobe).

Pott’s disease is extrapulmonary tuberculosis that affects the spine. It primarily affects the lower
thoracic and upper lumbar vertebrae.

Scrofula refers to cervical tuberculous lymphadenopathy. Scrofula is also referred to as a cold abscess

due to the absence of erythema and warmth.

Miliary tuberculosis (disseminated tuberculosis) refers to tuberculosis that has widely disseminated to

other organs via blood or lymphatics.

For diagnosis specimens are stained using the Ziehl-Neelson stain and then cultured using
the Lowenstein-Jenson medium to suppress other organisms. Culture on the Lowenstein-Jenson
medium typically takes 4-6 weeks. It can be more rapidly identified using nucleic acid amplification
testing (NAAT).

The only vaccine currently available is the Bacillus Calmete-Guerin (BCG).

On microscopy Mycobacteria tuberculosis is characterised by caseating

granulomas containing Langhans giant cells, which have a ‘horseshoe’ pattern of nuclei. The organisms
can be recognised by their red colour on acid-fast staining.

Mycobacteria tuberculosis can be typed by a restriction fragment length polymorphism (RFLP) method.

The investigation for suspected pulmonary TB is as follows:

 Send at least three spontaneous sputum samples for culture and microscopy
 If this is not possible consider bronchoscopy and lavage
  The samples should be taken before treatment is started

Mycobacterium tuberculosis fluoresces with auramine staining

Any type of immunosuppressant such as corticosteroids may be important risk factors for developing
tuberculosis.

Cavitation most commonly occurs at the lung apices

Salmonella gastroenteritis is an infection caused by Salmonella spp. Salmonella spp. are Gram-

negative, rod-shaped, non-spore forming bacteria. They are predominantly motile organisms and are
also facultative anaerobes, capable of surviving with or without oxygen.

Numerous subtypes of Salmonella spp. exist. Serotypes B, C, and D are the ones that usually cause
disease in humans and Salmonella enteritidis is serotype D and is the most common cause of salmonella
gastroenteritis.

Salmonella typhi and Salmonella paratyphi cause Typhoid and Paratyphoid fever respectively.

Salmonellosis is a zoonotic infection and can be transmitted from animal vectors to humans. The
incubation period is approximately 12-72 hours after ingestion of an infectious dose.

Common symptoms include diarrhoea, abdominal cramping, vomiting and fever. The diarrhoea can be
bloody. Salmonella infection is usually self-limiting, and is most commonly managed conservatively with
rehydration alone. The illness tends to last 4-7 days and there is usually a full recovery. Antibiotics are
only required in severe cases.

Central venous catheters are a common source of infection and should be suspected as a source of
sepsis in any patient that has had a line in situ for a prolonged period (usually longer than a week).

Diagnosis can be difficult and it is important to note that only 50% of patients with line sepsis have
evidence of infection at the insertion site.

The following features are indicative of the vascular catheter as the source of infection:

 Bacteraemia (or fungaemia) in an immunocompetent patient without any underlying disease

 Absence of another identifiable source of infection

 Presence of a vascular catheter (or alternative intravascular device) or the onset of fever
  Inflammation or purulence at the catheter insertion site or along the tunnel

The current recommendation by NICE and the BNF on the treatment of septicaemia related to vascular
catheter is to use vancomycin first-line. If Gram-negative sepsis is suspected, especially in the
immunocompromised, then a broad-spectrum antipseudomonal beta-lactam antibiotic should be
added.

Norwalk virus (norovirus), also known as the winter vomiting bug, is the most common cause of
infective vomiting and diarrhoea across all age groups. It is an RNA vrus in the family Calciciviridae. It is
highly infectious and also causes vomiting, diarrhoea, abdominal pain and fever. The Norwalk virus has
been linked to outbreaks in institutions such as nurseries, retirement homes, schools and hospitals.

Cryptosporidia diarrhoea is caused by Cryptosporidium, a protozoan parasite with acid-fast walls. It is

spread by the faeco-oral route. In healthy individuals with intact immune systems it causes self-limiting
diarrhoea. In immuno-compromised individuals it causes a much more severe variant of the disease that
can be fatal. Cryptosporidia are resistant to chlorine treatment and conventional filtering methods and
there is no effective antibiotic treatment for it.

E.Coli strain 0157 causes enterohaemorrhagic diarrhoea and can be followed by haemolytic uraemic
syndrome (renal failure, haemolytic anaemia and thrombocytopenia)

Giardia lamblia is a flagellated protozoan parasite that is transmitted by the faeco-oral route. It is also
resistant to standard chlorination. It is a common cause of traveller’s diarrhoea and can cause chronic
symptoms and malabsorption in some patients. It does, however, not cause bloody diarrhoea. Giardiasis
can be successfully treated with metronidazole and tinidazole.
Rotavirus is the most common cause of severe diarrhoea among infants and young children. It is an RNA
virus in the family Reoviridae. Infection is characterised by vomiting, watery diarrhoea, abdominal pain
and a low-grade fever. The infection normally lasts between 4 and 8 days. Transmission of rotavirus is
primarily via the faeco-oral route but can also be via airborne spread in some cases. Children in the UK
are now immunised with the Rotarix vaccine at 2-months.

Infective causes of bloody diarrhoea include:

 Campylobacter spp
 Shigella spp
 Salmonella spp
 Clostridium difficile
 Enteroinvasive Escherichia coli
 Yersinia spp
 Shistosomiasis
 Amoebiasis (Entamoeba histolytica)

Acute mastoiditis is a rare complication of acute otitis media (AOM). Rates have fallen since the
advent of antibiotic usage. The commonest causative organism is Streptococcus pneumoniae.

Acute mastoiditis generally presents with the following clinical features:

 Recent history of AOM

 Pyrexia
 Otorrhoea and perforation of tympanic membrane
 Otalgia
 Post-auricular pain
 Mastoid swelling and erythema
 Ear may protrude forwards 

Acute mastoiditis with numerous complications including:

 Permanent hearing loss

 Osteomyelitis
 Zygomatic extension
 Subperiosteal abscess
 Cranial nerve palsies (e.g. CN V, VI and VII)
 Intracranial abscess formation
 Meningitis
 Venous sinus thrombosis
 Bezold’s abscess (spread to neck muscles)
 Gradenigo’s syndrome (Petrositis causing CN VI palsy, deep trigeminal facial pain and
suppurative otitis media)
 Carotid artery spasm or arteritis
  Carotid artery occlusion
 Carotid artery rupture

This child should be referred as an emergency for immediate in-hospital management with IV antibiotics
and occasionally surgical intervention is required.

Neisseria meningitidis is a Gram-negative diplococcus that can cause meningococcal meningitis.

Carriage of Neisseria meningitidis is very common and it exists in the normal flora in the nasopharynx in
5 - 15% of adults. Actual disease only develops in a very small percentage of individuals. Infection is
most common in the winter months and epidemics tend to occur about once every 10 years.

Most invasive infections are caused by serotypes A, B or C. In the UK, most cases of meningococcal
septicaemia are caused by Neisseria meningitidis group B. The vaccination programme for Neisseria
meningitidis group C has made this type much less common. A vaccine for group B disease has now been
initiated in children.

The main determinant of the pathogenicity of Neisseria meningitidis is the antiphagocytic

polysaccharide capsule. Meningococci cross mucosal epithelium by endocytosis and the capsule allows
survival in the bloodstream. Lipo-oligosaccharide activates complement activation and cytokine release,
resulting in shock and disseminated intravascular coagulation (DIC).

The clinical features of meningococcal meningitis include:

 Non-blanching rash
 Neck stiffness
 Headache
 Photophobia
 Altered mental state (drowsiness, confusion)
 Focal neurological deficits
 Seizures
 Septic shock

Rapid antigen detection or nucleic acid amplification testing (NAAT) on blood and CSF are both sensitive
and reliable.

 Antibiotics should be started immediately. In the hospital setting IV ceftriaxone (2 g adult; 80 mg/kg
child) or IV cefotaxime (2 g adult; 80 mg/kg child) are the preferred agents. IM benzylpenicillin can be
given as an alternative in the pre-hospital setting and chloramphenicol is a suitable alternative if there is
a history of anaphylaxis to cephalosporins. Treatment does not eradicate carriage and the patient
should be given ‘prophylaxis’ following recovery.

Neisseria gonorrhoeae is a Gram-negative diplococcus that causes the sexually transmitted infection

gonorrhoea.
Infection is most common between 15 and 35 years of age and it is almost exclusively spread by sexual
contact. Antigenic variation of the gonococcal pili means that recovery from infection does not provide
immunity and re-infection is possible.

Neisseria gonorrhoeae adheres to the genitourinary epithelium via pili. It then invades the epithelial
layer and provokes a local acute inflammatory response.

The clinical features of gonorrhoea in men include:

 Urethritis (in around 80%)
 Dysuria (in around 50%)
 Mucopurulent discharge
 Rectal infection (usually asymptomatic but can cause anal discharge)
 Pharyngitis (usually asymptomatic)

The clinical features of gonorrhoea in women include:

 Vaginal discharge (in around 50%)
 Lower abdominal pain (in around 25%)
 Dysuria (in 10-15%)
 Pelvic/lower abdominal tenderness (< 5%)
 Endocervical discharge and/or bleeding
 Rectal infection (usually asymptomatic but can cause anal discharge)
 Pharyngitis (usually asymptomatic)

The complications of Neisseria gonorrhoeae infection include:

 Pelvic inflammatory disease (PID) in women
 Epididymo-orchitis or prostatitis in men
 Arthritis
 Dermatitis
 Pericarditis and/or myocarditis
 Hepatitis

For diagnosis pus from the urethra, cervix, rectum or throat should be plated directly or transported
rapidly to the laboratory in specialised transport medium. Traditionally diagnosis has been made with
Gram-stain and culture but new PCR testing methods are becoming more commonly used.

Treatment should be given before sensitivity results are available. Currently ceftriaxone is one of the
few effective antibiotics and this is usually given in combination with azithromycin or doxycycline.
Resistance is becoming an increasingly troublesome problem.

 
Ocular toxoplasmosis

Toxoplasmosis is caused by the protozoan organism Toxoplasma gondii.

Infections in healthy adults usually cause no symptoms but occasionally can cause a flu-like illness and
lymphadenopathy. It is usually spread via ingestion of poorly cooked food containing cysts
of  Toxoplasma gondii or due to exposure to infected cat faeces.

Toxoplasmosis is one of the commonest causes of infectious chorioretinitis. This most commonly occurs
as a congenital infection but can also occur in patients with a weakened immune system, as has
occurred in this case.

The commonest presenting features of ocular toxoplasmosis are unilateral reduced visual acuity and
floaters. The condition is usually painless.

The diagnosis can often be made clinically on the basis of the appearance if the characteristic features
on fundoscopy:

 Exudative ‘cotton balls’ (focal white atrophic areas)

 Overlying inflammation of the vitreous humour

 Old dark chorioretinal scarring often also present

Because of the high prevalence of positive toxoplasma titres in many populations, serology is generally
only useful to ‘rule out’ the diagnosis. Completely negative IgG titres can rule out the diagnosis in an
immunocompetent individual. The development of PCR testing for toxoplasmosis has proved to be
useful in assisting diagnosis in atypical or difficult cases. Detection of Toxoplasma gondii DNA by PCR in
both the aqueous and vitreous fluid is both sensitive and specific.

Sight-threatening lesions are treated for 4-6 weeks with classic triple therapy consisting of
pyrimethamine, sulfadiazine and folinic acid.

A 41-year-old man presents with dysuria, fevers, rigors and right-sided loin pain. On examination he is
tender over the right renal angle and he has a temperature of 38.8°

Acute pyelonephritis. He also has signs of sepsis and it would therefore be prudent to admit him for
inpatient treatment with intravenous antibiotics.

NICE recommend admission for patients with pyelonephritis who:

 Are significantly dehydrated or who are unable to take oral fluids and medications.

 Have signs of sepsis, including:

o A temperature greater than 38°C or less than 36°C, and

o Marked signs of illness (such as impaired level of consciousness, perfuse sweating,

rigors, pallor, significantly reduced mobility), or

o Significant tachycardia, hypotension, or breathlessness.

 Are pregnant and pyrexial

 Are frail, elderly residents in care homes who have recently been hospitalized or who have had
recurrent urinary tract infection

 Fail to improve significantly within 24 hours of starting antibiotics

The current recommendations by NICE and the BNF on the treatment of acute pyelonephritis are:

 A broad spectrum cephalosporin (e.g. cefuroxime) or a quiniolone (e.g. ciprofloxacin)

 Suggested duration of treatment 10-14 days (but longer treatment may be necessary in
complicated pyelonephritis)
Helicobacter pylori is a Gram-negative, helix shaped (curved rod), microaerophilic bacterium. It
typically has 4-6 lophotrichous flagellae and is therefore highly motile. It has an outer membrane
consisting of phospholipids and lipopolysaccharide.

Helicobacter pylori Is found in the upper gastrointestinal tract of approximately 50% of the population.

There is a strong association between mucosa-associated lymphoid tissue (MALT) lymphoma

and Helicobacter pylori colonization.

The most reliable method for testing for colonization with Helicobacter pylori is by biopsy during
endoscopy and histological examination.

Colonization with  Helicobacter pylori  confers a 10-20% lifetime risk of developing peptic ulcers and a 1-
2% lifetime risk of developing gastric cancer.

Typically eradication requires a 14-day course of triple therapy with amoxicillin, clarithromycin and a
proton pump inhibitor. Metronidazole is also often used as an alternative antibiotic in a triple therapy
regime.

Serum antibody levels fall slowly and therefore cannot be used to accurately assess eradication. Either
of the 13C-urea breath test or the stool antigen test are viable options for assessing successful
eradication.

Needle stick injuries:

The risk of contracting HIV from an HIV positive source patient is 0.2-0.5%.
 The risk of contracting Hepatitis C from a Hepatitis C positive source patient is between 3-10%.

Post exposure prophylaxis for HIV is only effective up to 72 hours after the needle-stick injury and should
be given as soon as possible after. (Please refer to the DOH guidelines on PEP).

There is no post exposure prophylaxis for hepatitis C however if seroconversion is proven via follow-up
PCR testing then interferon and/or ribavirin should be administered.

The estimated seroconversion rates are outlined below:

 30% for percutaneous exposure of a non-immune person to an HBeAg positive

contact.
 0.5-1.8% for percutaneous exposure to HCV-infected blood with detectable RNA.
 0.1% for mucocutaneous exposure to HIV-infected blood.
 0.3% for percutaneous exposure to HIV-infected blood.

Osteomyelitis:

In the majority of patients the commonest causative organism for osteomyelitis is Staphylococcus
aureus. Salmonella spp. are the commonest cause in patients with sickle cell disease.

Other bacteria that can cause osteomyelitis include:

 Enterobacter spp.
 Group A and B Streptococcus spp.
 Haemophilus influenzae

The current recommendations by NICE and the BNF on the treatment of osteomyelitis are:

 Flucloxacillin first-line
 Consider adding fusidic acid or rifampicin for initial 2 weeks
 If penicillin allergic use clindamycin
 If MRSA is suspected use vancomycin
 Suggested duration of treatment is 6 weeks for acute infection

Septic arthritis, which is the purulent invasion of a joint by an infectious agent. In this patient the
history of recent travel to Bangkok, the presence of a vesicular rash on his trunk and the finding of
Gram-negative diplococci on the joint aspirate clinch a diagnosis of a gonococcal septic arthritis.

The clinical features of septic arthritis include:

 Pain in affected joint

 Joint redness, warmth and swelling
 Inability to move joint common
 Fever and systemic upset
The commonest causative organism for septic arthritis is Staphylococcus aureus. Other bacteria that can
cause septic arthritis include:

 Streptococcus spp.
 Haemophilus influenzae
 Neisseria gonorrhoea  (typically sexually active young adults, macules or vesicles frequently
seen on the trunk)
 Escherichia coli (seen in IVDUs, the elderly and seriously ill)

The current recommendations by NICE and the BNF on the treatment of septic arthritis are:

 Flucloxacillin first-line
 If penicillin allergic use clindamycin
 If MRSA is suspected use vancomycin
 If gonoccal arthritis or Gram-negative infection is suspected use cefotaxime
 Suggested duration of treatment is 4-6 weeks (longer if infection complicated)

The current UK childhood immunisation schedule is as follows:

2 months:
 DTaP/IPV(polio)/Hib (diptheria, tetanus, pertussis, polio and Haemophilus influenza type b)
– all-in-one inejection (Pediacel)
 PCV (pneumococcal conjugate vaccine) – Prevenar 13
 Rotarix (rotavirus gastroenteritis) – oral route
 Men B (meningitis B)

3 months:
 DTaP/IPV(polio)/Hib – 2nd dose: Pediacel plus
 Rotarix (2nd dose) – oral route

4 months:
 DTaP/IPV(polio)/Hib – 3rd dose: Pediacel plus
 PCV – 2nd dose: Prevenar 13
 Men B (meningitis B 2nd dose)

Between 12 and 13 months:

 Hib/Men C (combined as one injection) – 4 th dose of Hib and 1st dose of Men C
  MMR (measles, mumps and rubella) – Priorix or MMR II
 PCV – 3rd dose: Prevenar 13
 Men B (meningitis B 3rd dose)

2,3 and 4 years plus school years 1 and 2:

 Children’s flu vaccine (annual)

Between 3 years 4 months and 5 years:

 Pre-school booster of DTaP/IPV(polio) – Repevax or Infanrix-IPV
 MMR – 2nd dose: Priorix or MMR II

Between 12 and 13 years:

 HPV (human papilloma virus types 6, 11, 16 and 18) – three injections of Gardasil given. Second
injection 1-2 months after first and third injection 6 months after first.

Between 13 and 18 years:

 Td/IPV (polio) booster – Revaxis
 Men C – booster dose: NeisVac or Meningitec

The BCG vaccination is only offered to neonates in high-risk areas or with high-risk backgrounds.
Typhoid fever is a bacterial infection caused by Salmonella typhi. Paratyphoid fever is a similar illness
caused by Salmonella paratyphi, and together these are collectively referred to as the enteric fevers.

Typhoid fever is endemic in India and many other parts of Asia, Africa, Central America and South
America. It is most often acquired through the ingestion of food or water that has been contaminated by
the faeces of an acutely infected or convalescent person or a chronic, asymptomatic carrier.
Approximately 1-6% of people infected with S. typhi  become chronic carriers. The incubation period is
between 7 and 21 days.

In the first week of the illness, patients become weak and lethargic and a steadily rising fever develops.
The onset of the illness tends to be insidious and constipation is more common than diarrhoea in the
early stages of the illness. Other early symptoms include headache, abdominal pain and epistaxis. The
fever of typhoid fever can occur with a relative bradycardia, as is seen in this case. When present this is
referred to as Faget’s sign.

As the illness progresses into the second week, patients often become so tired that they cannot get up.
Diarrhoea becomes prominent, the fever increases in intensity and patients can become agitated and
delirious. The abdomen often becomes tender and distended and 75% of patients develop
splenomegaly. Crops of red macules (Rose spots) appear in up to a third of patients, and these can be
seen on the chest of the patient in this case.

 
The illness progresses further in the third week with a number of potential complications occurring.
Intestinal haemorrhage can occur due to bleeding in congested Peyer’s patches. Intestinal perforation,
secondary pneumonia, encephalitis, myocarditis, metastatic abscesses and septic shock can all also
develop.

After the third week the patients that survive start to improve with the fever and symptoms slowly
resolving over the course of the next 7-14 days. Death occurs in 15-30% of untreated patients.
Traditionally drugs such as ampicillin and trimethoprim have been used. However, due to the advent of
multi-drug resistant cases, azithromycin or fluoroquinolones are now the mainstay of treatment.

All of the other options in this question can cause a febrile illness but this exact clinical presentation is
most likely to be caused by typhoid fever.