ACUTE EPIGLOTTITIS 5.

Serial monitoring and fibreoptic Management

Rare but serious infection.
Aetiology
Haemophilus Influenzae type B

 Other pathogens --> Strep Pneumoniae,
group A streptococci, Staph Aureus,
fungal and viral infections
 Non-infective causes --> thermal injury
Epidemiology
 Historically > in children (2-7 year old).
With the use of HiB vaccine, now it’s more
common in adults.
 F=M
 Incidence : 2.00 cases per 100000
person-years
Features
 Rapid onset
 Severe sore throat and odynophagia
 Muffled voice or “hot potato” voice
 High fever (generally in bacterial infections)
 Stridor --> high-pitched inspiratory noise
(indicative of airway obstruction)
 Drooling of saliva
'Tripod' position --> easier to breath if

leaning forward & extending their neck in
a seated position
Prompt recognition needed as can cause
 travels up spinal cord to brain.
airway obstruction
Diagnosis
1. Direct visualization
2. Xray
Lateral view --> THUMB SIGN (swelling of
 Features
the epiglottis)
PA view --> STEEPLE SIGN (shows
 
subglottic narrowing in croup )
laryngoscopy to track progress 1. Cleanse wound.
2. Puncture wounds should not be sutured
closed unless cosmesis is at risk
3. Abx of choice --> Co-amoxiclav
4. if penicillin-allergic then doxycycline +
ASPERGILLOMA metronidazole is recommended
A mycetoma (mass-like fungus ball)
Often colonises an existing lung cavity (ex :
secondary to TB / Lung Ca / CF)
Features RABIES
 Usually asymptomatic
 Cough RNA Rhabdovirus (specifically a lyssavirus)
 Haemoptysis (may be severe) Viral disease that causes acute encephalitis.
Has a bullet-shaped capsid.
Investigations
 CXR --> rounded opacity, crescent sign Epidemiology
may be present Mortality --> 25000-50000 people across the
 High titres of Aspergillus precipitins world each year
Generally in Africa & Asia
Pathogenesis
Vast majority of cases are caused by dog bites
but it may also be transmitted by bat, raccoon
and skunk bites.
1. Virus enters via animal bite
2. Virus replicates in muscle at site of bite
3. Virus infects nerve in the peripheral nerve
AMOEBIASIS
system. Moves by retrograde transport.
4. Virus replicated in dorsal root ganglion &
Entamoeba histolytica (amoeboid protozoan)
5. Brain infected
Spread --> faecal-oral route
6. Virus travels from brain via nerves to other
~10% chronically infected.
tissues such as kidney, eyes, salivary
gland.
Features
 Asymptomatic
 Mild diarrhoea / severe amoebic dysentery
 Prodrome --> headache, fever, agitation
 Liver & colonic abscesses.
Hydrophobia --> fear of water (water-
provoking muscle spasms, unable to
Amoebic dysentery
swallow water)
 Profuse, bloody diarrhoea
 Aerophobia --> fear of air / wind
 Long incubation period
 Hypersalivation
 Stool microscopy --> show trophozoites if
examined within 15 mins or kept warm
Investigations
('hot stool')
Rabies PCR --> urine, saliva, serum, CSF
 Rx --> Metronidazole
Nuchal skin biopsy
 Taken from nape of neck
Amoebic liver abscess
 Most reliable test of rabies infection in the
 Usually a single mass in the right lobe
first week
(may be multiple).
 Negri bodies --> cytoplasmic inclusion
 Contents described as 'anchovy sauce'
bodies found in infected neurons
 Features --> fever, RUQ pain, malaise,
hepatomegaly
 Investigations --> USG HBS, serology +ve
in > 95%

Management
3. Flexible fibreoptic laryngoscopy 1. Invasive stage --> Metronidazole &
 Can directly visualize epiglottis but can Tinidazole
trigger laryngospasm 2. Cystic stage --> Luminal amoebicide (ex :
4. Blood culture and throat swabs diloxanide furoate) Management
 Cystic stage is resistant to metronidazole 1. Wash wound
Management & tinidazole 2. If already immunised, then 2 further doses
1. Intubation may be needed to protect of vaccine should be given
airway 3. If not previously immunised, then human
 If suspected do NOT examine the throat rabies immunoglobulin (HRIG) should be
due to the risk of acute airway obstruction ANIMAL BITES given along with a full course of
--> should only be done by senior staff vaccination.
who are able to intubate if necessary Generally polymicrobial but Pasteurella 4. If possible, the dose should be
2. Empirical broad spectrum antibiotics (ex multocida is MC administered locally around the wound
3rd gen cephalosporins) 5. If untreated the disease is nearly always
3. Supportive care Mainly due to cats & dogs fatal.
4. Vaccination
  May result from eating contaminated food
(e.g. tinned) or IVDU Trichomonas vaginalis --> Highly motile,
HUMAN BITES  Neurotoxin often affects bulbar muscles & flagellated protozoan parasite.
ANS
Features
Multimicrobial infection --> both aerobic & Features  Vaginal discharge --> offensive,
anaerobic bacteria.  Usually fully conscious yellow/green, frothy
 No sensory disturbance  Vulvovaginitis
Common organisms  Flaccid paralysis  Strawberry cervix
 Streptococci spp.  Diplopia  pH > 4.5
 Staphylococcus aureus  Ataxia  Usually asymptomatic in men but may
 Eikenella  Bulbar palsy cause urethritis
 Fusobacterium
 Prevotella Treatment Investigation
1. Botulism antitoxin & supportive care Microscopy of a wet mount --> motile
Management 2. Antitoxin is only effective if given early -- trophozoites
1. Abx of choice --> Co-amoxiclav > once toxin has bound its actions, cannot
2. Screen for viral infections --> HIV & Hep C be reversed Management
Oral Metronidazole for 5-7 days OR STAT dose
of 2g Metronidazole

CAT SCRATCH DISEASE BACTERIAL VAGINOSIS

Bartonella henselae (Gram negative rod) Gardenella Vaginalis
Features Pathogenesis
 Fever  Overgrowth of predominately anaerobic
 History of cat scratch organisms such as Gardnerella vaginalis.
 Regional lymphadenopathy  This leads to fall in lactic acid producing
 Headache aerobic lactobacilli resulting in a raised
 Malaise vaginal pH.
 Whilst BV is not a STI, it is seen almost
exclusively in sexually active women.

ANTHRAX @ Woolsorter’s d/s Features

Vaginal discharge --> 'fishy', offensive
CHLAMYDIA

Bacillus anthracis (Gram positive rod)  Asymptomatic in 50%

Pathogenesis Amsel's criteria (for dx) Sexually transmitted infection

 Spread by infected carcasses 3/4 points should be present
 Bacillus anthracis produces a tripartite 1. Thin, white homogenous discharge Chlamydia Trachomatis (obligate intracellular
protein toxin 2. Clue cells on microscopy --> stippled pathogen)
o protective antigen vaginal epithelial cells
o oedema factor --> a bacterial 3. Vaginal pH > 4.5 1/10 young women in UK
adenylate cyclase which 4. Positive whiff test (addition of potassium Incubation period --> 7-21 days
increases cAMP hydroxide results in fishy odour)
o lethal factor --> toxic to Features
macrophages Management  Asymptomatic in ~70% of F & ~ 50% of M
1. Asymptomatic  F --> cervicitis (discharge, bleeding),
Features  Treatment is usually not required dysuria
 Painless & non-tender black eschar 2. Symptomatic  M --> urethral discharge, dysuria
(cutaneous 'malignant pustule', but no pus)  Oral Metronidazole for 5-7 days
 Marked oedema  Single oral dose 2g Metronidazole (if Complications
 Can cause GI bleeding adherence is an issue) 1. Epididymitis
 70-80% initial cure rate 2. PID
Management  Relapse rate > 50% within 3 months 3. Endometritis
1. Cutaneous anthrax --> Ciprofloxacin  Alternatives --> topical metronidazole 4. Increased risk of ectopic pregnancy
2. Further Rx is based on microbiological Ix or topical clindamycin 5. Infertility
& expert advice 6. Reactive arthritis
Bacterial vaginosis in pregnancy 7. Perihepatitis (Fitz-Hugh-Curtis syndrome)
 Increased risk of preterm labour, low birth
weight, chorioamnionitis and late Investigation
miscarriage. Nuclear acid amplification tests (NAATs)
BOTULISM  Ix of choice
 Oral metronidazole 5-7 days / topical
metronidazole.  Urine (first void urine sample),
Clostridium botulinum (Gram positive vulvovaginal swab or cervical swab may
anaerobic bacillus)  The STAT dose of 2g metronidazole is not
recommended be tested using the NAAT technique
 For women --> the vulvovaginal swab 1st
Pathogenesis line
 7 serotypes A-G  For men --> urine test 1st line
 Produces botulinum toxin, a neurotoxin Chlamydia testing should be carried out two
which irreversibly blocks the release of
TRICHOMONAS VAGINALIS weeks after a possible exposure
acetylcholine.
Sexually tansmitted infection (STI) Screening
in England the National Chlamydia Screening
Programme is open to all men and women aged
15-24 years
the 2009 SIGN guidelines support this approach,
suggesting screening all sexually active patients
aged 15-24 years
relies heavily on opportunistic testing
Management
 Ist line --> Doxycycline (7 day course)
 Doxycycline is now preferred to
azithromycin due to concerns about
Mycoplasma genitalium. This
infection is often coexistant in
patients with Chlamydia and there
is evidence of rising levels of
macrolide resistance, hence why
doxycycline is preferred
 If Doxycycline contraindicated / not
tolerated --> Azithromycin 1g OD for one
day or 500mg OD for 2 days.
 If pregnant --> Azithromycin /
Erythromycin / Amoxicillin
Partner notification
 For men with urethral symptoms --> all
contacts since & 4 weeks prior to, the
onset of sx.
 For women & asymptomatic men --> all
partners from the last 6m or the most
recent sexual partner should be contacted.
 Contacts of confirmed Chlamydia cases
should be treated prior to results being
known (treat then test).
GENITAL WARTS @Condolymata
Accuminata
HPV 6 & 11
(HPV 16, 18 & 33 cause cervical Ca)
Features
 Small (2 - 5 mm) fleshy protuberances
 slightly pigmented
 may bleed or itch
 Often resistant to Rx & recurrence is
common
Management
1. Multiple, non-keratinised warts -->
topical podophyllum
2. Solitary, keratinised warts --> cryotherapy
3. 2nd line --> Imiquimod (topical cream)
4. Majority of anogenital infections with HPV
clear without intervention within 1-2 years
GONORRHOEA
Neisseria Gonorrhea (Gram-negative
diplococcus)
Incubation period --> 2-5 days
Features
 Acute infection can occur on any mucous
membrane surface, typically genitourinary
but also rectum and pharynx.
M --> urethral discharge, dysuria

 F --> cervicitis e.g. leading to vaginal
GENITAL HERPES
discharge
HSV-1 and HSV-2
 Rectal and pharyngeal infection is usually
asymptomatic
Features
 Painful genital ulceration & blisters
Microbiology
 Associated with dysuria & pruritus
Immunisation is not possible & reinfection is
 Primary infection is often more severe
common due to antigen variation of type IV Pili
than recurrent episodes
(proteins which adhere to surfaces) and Opa
 Systemic features --> headache, fever &
proteins (surface proteins which bind to
malaise are more common in primary
receptors on immune cells)
episodes
 Tender inguinal lymphadenopathy
Complications
 Urinary retention
1. Urethral strictures
2. Epididymitis
3. Salpingitis (may lead to infertility)
4. Disseminated infection
5. Gonococcal arthritis / Septic arthritis
Management
1. 1st line --> IM Ceftriaxone 1g (single dose)
 Ciprofloxacin used to be the Rx of choice
but cephalosporins are more widely used Investigations
now due to inreased resistance to 1. Ix of choice --> Nucleic acid amplification
Ciprofloxacin tests (NAAT)
2. If needle phobic --> T Cefixime 400mg 2. HSV serology --> useful in recurrent
(single dose) + T Azithromycin 2g (single genital ulceration of unknown cause
dose)
3. If sensitive to Ciprofloxacin --> T Management
Ciprofloxacin 500mg (single dose) 1. Saline bathing
2. Analgesia
Disseminated gonococcal infection (DGI) 3. Topical anaesthetic agents e.g. lidocaine
 Haematogenous spread from mucosal 4. Oral aciclovir
infection (e.g. Asymptomatic genital 5. If frequent exacerbations --> longer-term
aciclovir
infection).
 Initially there may be a classic triad of
symptoms: tenosynovitis, migratory Pregnancy
polyarthritis and dermatitis. ELLSCS at term is advised if a primary attack
 Later complications include septic arthritis, occurs at >28 weeks gestation
endocarditis and perihepatitis (Fitz-Hugh- Women with recurrent herpes who are pregnant
Curtis syndrome) --> suppressive tx, & should be advised that the
 Features of DGI risk of transmission to baby is low
 tenosynovitis
 migratory polyarthritis
 dermatitis (maculopapular or
vesicular) CHANCROID
Haemophilus Ducreyi
Tropical disease
NON-GONOCOCCAL URETHRITIS Features
 Painful genital ulcers --> typically have
sharply defined, ragged, undermined
Presence of urethritis when gonococcal bacteria
not identifiable on the initial swab. border.
 Microscopy --> neutrophils but no gram  Unilateral, painful inguinal lymph node
neg diplococci (no evidence of gonorrhea) enlargement.
 Immediate Rx has to be initiated while
waiting for chlamydia test is pending -->
therefore initial dx of NGU is made
Possible causative organisms
 Chlamydia trachomatis (MC cause)
 Mycoplasma genitalium
 Ureaplasma Urealyticum
 Trichomonas vaginalis
 E Coli
SYPHILIS
Management
Contact tracing
Oral Azithromycin / Doxycycline Sexually transmitted infection
Spirochaete Treponema pallidum. 1. Rose Bengal plate test --> used for
Incubation period 9-90 days Possible result Interpretation screening but other tests are required to
Non treponemal Test : +ve Active syphilis confirm the dx.
Transmission Treponemal Test : +ve infection 2. Brucella serology --> best test for dx
 Sexual contact Non treponemal Test : +ve False positive 3. Blood & bone marrow cultures may be
 Vertical transmission Treponemal Test : -ve result suitable in certain pts, but these tests are
 Blood transfusion often negative
Non treponemal Test : -ve Successfully
Treponemal Test : +ve treated syphilis
Primary Features Management
 Incubation period --> 9-90 days Doxycycline & streptomycin
 Chancre --> painless ulcer at the site of Management
sexual contact  1st line --> IM Benzathine penicillin 2.4
 Regional non-tender lymphadenopathy mega units once weekly x3 weeks
Often not seen in F (lesion may be on  Alternative --> Doxycycline

cervix)  Jarisch-Herxheimer reaction is sometimes GASTROENTERITIS
 Can heal spontaneously withour Rx, 25% seen following treatment
disseminate causing secondary / late  fever, rash, tachycardia after the 1st E Coli Common amongst travellers
syphilis dose of abx within few hours Watery stools
 No wheeze or hypotension in Abdominal cramps and nausea
Secondary features contrast to anaphylaxis Giardiasis Prolonged, non-bloody
 6-10 wks after primary infection  Due to release of endotoxins diarrhoea
 Systemic sx --> fevers, lymphadenopathy following bacterial death Cholera Profuse, watery diarrhoea
 rash on trunk, palms & soles  PCM, no other Rx needed. Severe dehydration resulting in
 Buccal 'snail track' ulcers (30%) weight loss
 Condylomata lata (painless, warty lesions Not common amongst travellers
on genitalia ) Shigella Bloody diarrhoea
Vomiting & abdo pain
Tertiary features LYMPHOGRANULOMA VENEREUM
Staph Severe vomiting
 Gummas (granulomatous lesions of the aureus Short incubation period
skin & bones) Chlamydia trachomatis serovars L1, L2 &L3
Campylo- A flu-like prodrome is usually
 Ascending aortic aneurysms bacter followed by crampy abdominal
 General paralysis of the insane Risk factors
MSM pains, fever & diarrhoea (may
 Tabes dorsalis 
be bloody)
 Argyll-Robertson pupil  HIV
May mimic appendicitis
Stages Complications include GBS
Congenital syphilis
Bacillus 2 types of illness are seen :
 Blunted upper incisor teeth (Hutchinson's 1 Small painless pustule which later forms an Cereus vomiting within 6 hours,
teeth), 'mulberry' molars ulcer 
stereotypically due to rice
 Rhagades (linear scars at the angle of the 2 Painful inguinal lymphadenopathy  diarrhoeal illness
mouth) may occasionally form fistulating buboes
occurring after 6 hours
 Keratitis 3 Proctocolitis
 Saber shins Ameobiasis Gradual onset bloody diarrhoea,
 Saddle nose abdo pain & tenderness which
Management may last for several weeks
 Deafness
Doxycycline.
Diagnosis Incubation period
Treponema pallidum is a very sens organism & 1-6 hrs Staph Aureus
cannot be grown on artificial media. Bacillus Cereus
Dx is therefore usually based on clinical features, BRUCELLOSIS 12-48 hrs Salmonella
serology & microscopic examination. E Coli
Zoonosis more common in the Middle East & in 48-72 hrs Shigella
Investigations farmers, vets & abattoir workers. Campylobacter
Non-treponemal tests Treponemal Incubation period 2 - 6 weeks. >7 days Giardiasis
tests Amoebiasis
(i) RPR (i) TP-EIA Four major species cause infection in humans
(ii) VDRL (ii) TPHA 1. B melitensis (sheep) Traveller’s diarrhoea --> at least 3 loose stools in
2. B abortus (cattle) 24 hours with or without 1 of the following ; abdo
Not spec for syphilis, More complex 3. B canis (pigs) cramps, fever, nausea, vomiting, blood in stool.
therefore may result in false & expensive 4. B suis (pigs) MC cause is E Coli.
+ve but spec for
Causes of false +ve : syphilis Features Acute food poisoning --> sudden onset vomiting,
 Pregnancy Qualitative  Non-specific --> fever, malaise nausea and diarrhoea after ingestion of toxin
 SLE, APLS only & are  Hepatosplenomegaly (MC cause is Staph Aureus, Bacillus Cereus,
 TB reported as  Sacroiliitis --> spinal tenderness Clostridium Perfringens).
 Leprosy 'reactive' or
 Malaria 'non-reactive' Complications
 HIV  Osteomyelitis CAMPYLOBACTER
Based upon the reactivity of  IE
serum from infected patients  Meningoencephalitis Most common bacterial cause of infectious
to a cardiolipin-cholesterol-  Orchitis intestinal disease in the UK.
lecithin antigen.  Leukopenia Majority caused by Campylobacter Jejuni
Assesses the quantity of (Gram negative bacillus)
antibodies being produced. Diagnosis
Becomes -ve after Rx
Spread by the faecal-oral route SHIGELLA  Headache
Incubation period 1-6 days.  Rhinitis
Types  Sore throat
Features 1. S Sonnei (from UK)  Cough
 Prodrome --> headache malaise 2. S Flexneri  Diarrhoea & vomiting
 Diarrhoea --> often bloody 3. S Dysenteriae  ARDS
 Abdominal pain --> may mimic
appendicitis Features Treatment
 Diarrhoea (may be bloody) 1. Oseltamivir (Tamiflu) - Oral
Management  Abdominal pain  MOA --> neuraminidase inhibitor
1. Usually self-limiting  Severity depends on type: S sonnei may which prevents new viral particles
2. Treat if severe / immunocompromised be mild, S. flexneri or S. dysenteriae may from being released by infected
3. First line abx --> Clarithromycin be severe. cells
4. Alternative --> Ciprofloxacin  Common SE --> Nausea,Vomiting,
Management diarrhoea & headaches
Complications Usually self-limiting & does not require abx 2. Zanamivir (Relenza) - Inhaled
 Guillain-Barre syndrome Abx (e.g. ciprofloxacin) are indicated for  IV prep available for those acutely
 Reactive arthritis severe disease / immunocompromised / bloody unwell
 Septicaemia diarrhoea  MOA --> neuraminidase inhibitor
 Endocarditis  SE --> may induce bronchospasm
 Arthritis in asthmatics

E COLI
CHOLERA Facultative anaerobic, lactose-fermenting, Gram CLOSTRIDIA
negative rod which is a normal gut commensal.
Vibro cholerae - Gram negative bacteria Gram-positive, obligate anaerobic bacilli.
Lead to a variety of d/s :
Features  diarrhoeal illnesses Clostridium Produces α-toxin, a lecithinase,
 Profuse 'rice water' diarrhoea  UTIs Perfringens which causes gas gangrene
 Dehydration  neonatal meningitis (myonecrosis) & haemolysis
 Hypoglycaemia Features --> tender,
E Coli O157:H7 oedematous skin with
Management  Particular strain associated with severe, haemorrhagic blebs & bullae.
Oral rehydration tx haemorrhagic, watery diarrhoea. Crepitus may present on
Abx --> Doxycycline, Ciprofloxacin  High mortality rate palpation
 Can be complicated by haemolytic Clostridium Typically seen in canned foods
uraemic syndrome. Botulinum & honey
 Often spread by contaminated ground Prevents acetylcholine (ACh)
GIARDIASIS beef. release leading to flaccid
paralysis
Giardia Lamblia (Flagellate protozoan) Serotypes Clostridium Causes pseudomembranous
 Antigen O - origin from Difficile colitis, typically seen after the
Spread by faecal-oral route. Lipopolysaccharide layer use of broad-spectrum abx
 Antigen K - origin from capsule Produces both exotoxin &
Risk factors  Neonatal meningitis secondary to E. cytotoxin
 Foreign travel coli is usually caused by a serotype Clostridium Produces an exotoxin
 Swimming/drinking water from a river or that contains the capsular antigen Tetani (tetanospasmin) that prevents
lake K-1 the release of glycine from
 MSM  Antigen H - origin from Flagellin Renshaw cells in the spinal cord
causing a spastic paralysis
Features
 Often asymptomatic
 Lethargy, bloating, abdo pain H1N1 INFLUENZA
Flatulence

Non-bloody diarrhoea
DIPHTHERIA
 Subtype of Influenza A virus
 Steatorrhoea
Corynebacterium diphtheriae (Gram positive)
 Chronic diarrhoea, malabsorption & The 2009 H1N1 influenza (swine flu) outbreak
lactose intolerance can occur was first observed in Mexico in early 2009. In Pathophysiology
June 2009, the WHO declared the outbreak to  Releases an exotoxin encoded by a β-
Investigations be a pandemic. prophage
1. Stool microscopy for trophozoite & cysts --
 Exotoxin inhibits protein synthesis by
> ~65% sens Risk factors catalyzing ADP-ribosylation of elongation
2. Stool antigen detection assay --> greater 1. Pts with chronic illness factor EF-2
sens & faster turn-around time than 2. Immunosuppressants
conventional stool microscopy methods 3. Pregnant Features
3. PCR assays are also being developed 4. Young <5y/o  Systemic features --> necrosis of
myocardial, neural & renal tissue
Treatment Features  Sore throat with a 'diphtheric membrane' -
Metronidazole. Flu-like illness
 grey, pseudomembrane on the posterior
 Fever >38 ºC pharyngeal wal lcaused by necrotic
 Myalgia mucosal membrane
 Lethargy
 Bulky cervical lymphadenopathy --> 'bull infecting immune cells. <50 CMV retinitis --> ~30-40%
neck' Maraviroc --> binds to CCR5, Mycobacterium avium-intracellulare
 Neuritis e.g. cranial nerves preventing an interaction with infection
 Heart block gp41
Enfuvirtide --> binds to gp41, Neurocomplications
Investigations also known as a 'fusion Toxoplasmosis ~50% of cerebral lesions in
Throat swab C&S --> uses tellurite agar or inhibitor' HIV
Loeffler's media Features --> constitutional
NRTI Zidovudine (AZT), Abacavir, symptoms, headache,
Management (Nucleoside Emtricitabine, Didanosine, confusion, drowsiness
1. IM Penicillin analogue Lamivudine, Stavudine, CT --> single/multiple ring
2. Diphtheria antitoxin reverse Zalcitabine, Tenofovir enhancing lesions, mass
transcriptase effect may be seen
inhibitors) General SE --> peripheral
neuropathy
HIV Tenofovir SE --> renal
impairment & osteoporosis
RNA retrovirus of the lentivirus genus  Tenofovir is used in
(lentiviruses are characterized by a long BHIVAs two-
incubation period) reccommended regime
NRTI
2 variants - HIV-1 & HIV-2 Zidovudine SE --> Anaemia,
HIV-2 --> more common in West Africa, lower myopathy, black nails
transmission rate, less pathogenic, slower Didanosine SE --> Pancreatitis Mx --> Sulfadiazine &
progression to AIDS Pyrimethamine
NNRTI Evirapine, Efavirenz Thallium SPECT negative
Basic structure (Non-
 Spherical with 2 copies of single-stranded nucloside SE --> P450 enzyme Primary CNS ~30% of cerebral lesions in
RNA enclosed by a capsid of the viral reverse interaction (nevirapine lymphoma HIV
protein p24. transcriptase induces), rashes Associated with EBV
 Matrix composed of viral protein p17 inhibitors) CT --> single/multiple
surrounds the capsid. Protease Indinavir, Nelfinavir, homogenous enhancing
 Envelope proteins --> gp120 & gp41 inhibitors Ritonavir, Saquinavir lesions
 Pol gene encodes for viral enzymes
reverse transcriptase, integrase & HIV General SE --> DM,
protease dyslipidemia, buffalo hump,
central obesity, P450 enzyme
Cell entry inhibition
HIV can infect CD4 T cells, macrophages & Indinavir SE --> renal stones,
dendritic cells asymptomatic
gp120 binds to CD4 & CXCR4 on T cells and hyperbilirubinaemia
CD4 & CCR5 on macrophages Ritonavir --> a potent inhibitor
Management :
Mutations in CCR5 can give immunity to HIV of the P450 system
 Steroids (reduce
tumour size)
Replication Integrase Raltegravir, Elvitegravir,  Chemotherapy (e.g.
After entering a cell, the enzyme reverse inhibitors Dolutegravir methotrexate) +/-
transcriptase creates dsDNA from the RNA for whole brain
integration into the host cell's genome MOA --> block the action of irradiation.
integrase, a viral enzyme that  Surgery may be
Investigations inserts the viral genome into considered for lower
1. HIV antibody test the DNA of the host cell grade tumours
 MC & accurate test Thallium SPECT positive
 Consists of both screening ELISA test &
confirmatory Western Blot Assay Complications TB Rare
 Most people develop antibodies to HIV at CD4 Opportunistic Infections CT --> single enhancing
4-6 wks but 99% do by 3 months 200 - Oral thrush --> Candida albicans lesion
2. p24 antigen test 500 Shingles --> Herpes Zoster
 usually +ve from about 1 wk to 3 - 4 wks Hairy leukoplakia --> EBV Encephalitis May be due to CMV or HIV
after infection with HIV Kaposi sarcoma --> HHV 8 itself
 sometimes used as an additional
100 - Cryptosporidiosis --> usually self- HSV encephalitis but is
screening test in blood banks
200 limiting & similar to immunocompetent relatively rare in the context
hosts of HIV
Management
Cerebral toxoplasmosis CT --> oedematous brain
ART involves a combination of at least 3 drugs,
typically two NRTI & either a PI or NNRTI. Progressive multifocal
This combination both decreases viral replication leukoencephalopathy --> JC Virus Cryptococcus MC fungal infection of CNS
but also reduces the risk of viral resistance Pneumocystis jirovecii pneumonia Features --> headache,
emerging. HIV dementia fever, malaise, N/V,
Start ART as soon as dx is made 50 - Aspergillosis --> Aspergillus fumigatus seizures, focal neuro deficit,
100 Oesophageal candidiasis --> Candida meningitis, SOL
albicans CSF --> high opening
Entry Maraviroc, Enfuvirtide
Cryptococcal meningitis pressure, India ink test +ve,
inhibitors
Primary CNS lymphoma --> EBV elevated protein, reduced
Prevents HIV-1 from entering &
glucose, normally a
 lymphocyte predominance  Complications  Fundoscopy --> retinal haemorrhages and
but in HIV, WCC may be  Pneumothorax (common) necrosis ('pizza' retina)
normal.  Extrapulmonary manifestations (~1-  Mx --> Iv Ganciclovir, may be
CT --> meningeal 2%) discontinued once CD4 > 150 after
enhancement, cerebral  Hepatosplenomegaly HAART
oedema  Lymphadenopathy  Alternative Mx --> IV Foscarnet or
 Choroid lesions Cidofovir
 Investigations
 CXR --> bilateral interstitial HIV - oesophageal candidiasis
pulmonary infiltrates / lobar  Generally when CD4 <100
consolidation / normal  Features --> odynophagia, dysphagia
 Exercise-induced desaturation  Rx --> itraconazole / fluconazole
 Sputum --> often fails to show PCP
 BAL often needed to show PCP HIV - Immunisation
(silver stain --> characteristic cysts) Can be used in Can be Contraindicated
AIDS Dementia Caused by HIV virus itself Management
 all HIV-infected used if in HIV-infected
Complex Features --> behavioural Co-trimoxazole
 adults CD4 > adults
changes, motor impairment IV Pentamidine in severe cases
 200
CT --> cortical & subcortical  Aerosolized pentamidine --> less
atrophy Hepatitis A MMR Cholera
effective with a risk of Hepatitis B Varicella CVD103-HgR
Progressive Widespread demyelination pneumothorax H influenzae B Yellow Influenza-
multifocal due to infection of  Steroids if hypoxic (reduce risk of Influenza- Fever intranasal
encephalopathy oligodendrocytes by JC respiratory failure by 50% & death parenteral Poliomyelitis-oral
(PML) virus (a polyoma DNA by a third if pO2 <9.3kPa) Japanese (OPV)
virus)
encephalitis TB (BCG)
Features --> subacute
Meningococcus-
onset, behavioural
MenC
changes, speech, motor,
Meningococcus-
visual impairment
ACWY I
CT --> single/multiple
Pneumococcus-
lesions, no mass effect,
PPV23
don't usually enhance.
Poliomyelitis-
MRI is better --> high-signal
parenteral (IPV)
demyelinating white matter
Rabies
lesions seen
Tetanus-
HIV - Kaposi’s Sarcoma Diphtheria (Td)
Mycobacterium Avium Complex
 Atypical mycobacterial infection seen in  Caused by HHV-8
Features HIV - Seroconversion
HIV when CD4 <50 
 Purple papules / plaques on skin or  Symptomatic in 60-80% & typically
 Caused by both Mycobacterium avium &
mucosa (e.g. gastrointestinal and presents as a glandular fever type illness.
Mycobacterium intracellulare, and is often
respiratory tract)  Increased symptomatic severity is assoc
referred to as Mycobacterium avium-
 Skin lesions may later ulcerate with poorer long term prognosis.
intracellulare (MAI).
 Massive haemoptysis  Typically occurs 3-12 wks after infection
 >95% caused by Mycobacterium avium.
 Pleural effusion  Features
 Features
Management  Sore throat
 fever, sweats 
 Radiotherapy + resection  Lymphadenopathy
 Abdo pain, diarrhoea
 Malaise, myalgia, arthralgia
 Dyspnoea, cough
HIV - Diarrhoea  Diarrhoea
 Anaemia
Due to the effects of HIV itself or OI  Maculopapular rash
 Lymphadenopathy 
Possible causes  Mouth ulcers
 Hepatomegaly/deranged LFTs 
 Cryptosporidium + other protozoa  Rarely meningoencephalitis
 Diagnosis
(MC)  Diagnosis
 Blood C&S
 CMV  Antibodies to HIV may not be
 BMAT
 Mycobacterium avium intracellulare present
 Prophylaxis
 Giardia  HIV PCR and p24 antigen tests can
 Clarithromycin / Azithromycin when
Cryptosporidium confirm diagnosis
CD4 is <100 

 Management  MC infective cause of diarrhoea in

 Rifampicin + Ethambutol +
Clarithromycin
Pneumocystis Jirovecii Pneumonia
 Pneumocystis carinii @ Pneumocystis
jiroveci (unicellular eukaryote, generally
classified as a fungus but some authorities
consider it a protozoa)
 Most common OI in AIDS
 All pts with CD4 < 200 should receive
PCP prophylaxis
 Features
 Dyspnoea
 Dry cough
 Fever
 Very few chest signs
HIV
 Intracellular protozoa
 Incubation period --> 7 days.
 Features --> variable (mild to
severe)
 Ix --> Modified Ziehl-Neelsen stain
(acid-fast stain) of stool -->
characteristic red cysts of
Cryptosporidium.
 Rx --> supportive tx, nitazoxanide is
licensed in the US for
immunocompetent patients
HIV - CMV Retinitis
~30-40% of pts with CD4 < 50.

Clinical dx

 Features --> visual impairment
HIV -pregnancy
 HIV screening should be done for all
pregnant women
 Aim of treating --> minimise harm to
both mother & fetus, & to reduce the
chance of vertical transmission.
 Factors which reduce vertical transmission
(from 25-30% to 2%)
 maternal antiretroviral therapy
 mode of delivery (caesarean
section)
 neonatal antiretroviral therapy
 infant feeding (bottle feeding)
 Antiretroviral therapy should be offered
regardless of whether they were taking it
previously
 Mode of delivery 8. Increased incidence of appendicitis  Purpuric skin lesions
 SVD is recommended if viral load is 9. Myocarditis  'Salt and pepper' chorioretinitis
< 50 at 36 wks, otherwise LSCS.  Microphthalmia
 Zidovudine infusion should be Management of contacts  Cerebral palsy
started 4 hours before LSCS. If a child that is immunized is in contact with
 Neonatal antiretroviral therapy measles, then MMR should be offered (given Diagnosis
 Zidovudine is usually administered within 72 hours) --> vaccine-induced measles IgM antibodies -->raised in women recently
orally to the neonate if maternal antibody develops more rapidly than that exposed to the virus
viral load is <50. following natural infection Very difficult to distinguish Rubella from
 Otherwise triple ART should be Parvovirus B19 clinically. It is therefore important
used. to also check parvovirus B19 serology as there
 Tx should be continued for 4-6 is a 30% risk of transplacental infection, with a 5-
weeks. MUMPS 10% risk of fetal loss
 Infant feeding
 Advised not to breast feed Management
RNA paramyxovirus  Since 2016, Rubella immunity is no longer
Immune reconstitution inflammatory Tends to occur in winter and spring routinely checked during booking visit
syndrome (IRIS)  If not immune --> MMR vaccine after
Generally associated with HIV / Spread delivery
immunosuppression, in which the immune  by droplets  MMR vaccines should not be given to
system begins to recover, but then responds to a  respiratory tract epithelial cells → parotid pregnant / women attempting to be
previously acquired opportunistic infection with glands → other tissues pregnant
an overwhelming inflammatory response that  Infective 7 days before and 9 days after
paradoxically makes the symptoms of infection parotid swelling starts
worse.  Incubation period = 14-21 days
Typically, IRIS occurs within 2-12 wks after ORF
initiation of ART, but may present later. Features
The most frequently occurring IRIS events are  Fever
 Malaise Parapox virus
associated with mycobacterial disease (TB/MAC Found in sheeps & goats but can be spread to
infection) & cryptococcal disease.  Myalgia
 Parotitis ('earache', 'pain on eating'): humans.
unilateral initially then becomes bilateral in
70% Features
MEASLES  'scabby' lesions around the mouth & nose
Prevention  Generally affects the hands and arms
RNA paramyxovirus MMR vaccine: the efficacy is around 80%  Initially small, raised, red-blue papules
Spread by droplets (aerosol transmission)  Later may increase in size to 2-3 cm &
Infective from prodrome until 4 days after rash Management become flat-topped + haemorrhagic
starts Pest
Incubation period 10-14 days paracetamol for high fever/discomfort
Notifiable disease
Features
Prodromal phase
JAPANESE ENCEPHALITIS
 Complications
 Irritable 1. Orchitis - uncommon in pre-pubertal
 Conjunctivitis Flavivirus
males but occurs in ~25-35% of post- Transmitted by culex mosquitos which breeds in
 Fever pubertal males. Typically occurs four or
Koplik spots --> typically develop before rice paddy fields.
 five days after the start of parotitis Reservoir hosts are aquatic birds, but pigs are
the rash, white spots ('grain of salt') on the 2. Hearing loss - usually unilateral &
buccal mucosa an amplification host and therefore close
transient domestic contact with pigs is a risk factor.
 Rash --> starts behind ears then to the 3. Meningoencephalitis
whole body, discrete maculopapular rash 4. Pancreatitis
becoming blotchy & confluent Most common cause of viral encephalitis in SE
 Desquamation that typically spares the Asia, China the Western Pacific & India (~
palms & soles may occur after a week 50,000 cases annually)
 Diarrhoea ~10%
Features
RUBELLA @ German Measles  Majority asymptomatic
Investigations
IgM antibodies --> detected within a few days of  Headache
Togavirus  Fever
rash onset Rare after MMR vaccine  Seizures & confusion.
Incubation period : 14-21 days  Parkinsonian features --> indicate basal
Management Infectious from 7 days before symptoms appear
Supportive ganglia involvement.
to 4 days after the onset of the rash.  Acute flaccid paralysis.
Admit if immunosuppressed / pregnant
Notifiable disease → inform public health Risk in pregnancy Diagnosis
In first 8-10 weeks risk of damage to fetus is as Serology or PCR.
Complications high as 90%
1. Otitis media (most common) Damage is rare after 16 wks
2. Pneumonia (most common COD) Management
3. Encephalitis --> 1-2 wks after onset of Supportive.
Congenital Rubella Syndrome Prevention with vaccine
illness)  Sensorineural deafness
4. Subacute sclerosing panencephalitis -->  Congenital cataracts
very rare, may present 5-10 yrs later  Congenital heart d/s (ex PDA)
5. Febrile convulsions  Growth retardation
6. Keratoconjunctivitis, corneal ulceration  Hepatosplenomegaly LEMIERRE’S SYNDROME
7. Diarrhoea
Infectious thrombophlebitis of the internal jugular 3. Give reassurance that there is no link to CSF --> pleocytosis, often lymphocytes
vein. disease in cattle (nontuberculous bacteria usually cause a rise in
4. HPA recommends that children who are neutrophils), raised protein, reduced glucose
Pathogenesis unwell should be kept off scholl until they
 Often secondary to a bacterial sore throat feel better. Management
caused by Fusobacterium necrophorum Sensitive to amoxicillin/ampicillin
leading to a peritonsillar abscess. (cephalosporins usually inadequate)
 A combination of spread of the infection Listeria meningitis --> IV Amoxicillin/Ampicillin +
laterally from the abscess and LEPTOSPIROSIS Gentamicin
compression lead to thrombosis of the IJV.
Spirochaete Leptospira interrogans Pregnant women
Features (serogroup L. icterohaemorrhagiae)  20x more likely to develop listeriosis
 H/O bacterial sore throat Classically spread by infected rat urine. compared with the rest of the population
 Followed by neck pain, stiffness & due to changes in the immune system.
tenderness (may be mistaken for Risk factors  Fetal/neonatal infection can occur both
meningitis) Vets transplacentally & vertically during child
 Systemic involvement (fevers, rigors) Farmers birth
 Septic pulmonary emboli may also occur. Sewage workers  Complications --> miscarriage, premature
People who work in an abattoir labour, stillbirth & chorioamnionitis
Returning traveller  Dx --> Blood C&S
 Rx --> Amoxicillin
LEPROSY Features
Early phase
Mycobacterium Leprae  Due to bacteraemia & lasts for ~1wk
Granulomatous disease primarily affecting the  May be mild / subclinical LEISHMANIASIS
peripheral nerves & skin  Fever
 Flu-like symptoms Leishmania (intracellular protozoa)
Features  Subconjunctival suffusion Spread by the bites of sandflies.
 Patches of hypopigmented skin typically (redness)/haemorrhage
affecting the buttocks, face & extensor Second immune phase Types
surfaces of limbs  May lead to more severe d/s (Weil's 1. Cutaneous
 Sensory loss d/s) 2. Mucocutaneous
 AKI in ~50% 3. Visceral
Types  Hepatitis --> jaundice, hepatomegaly
The degree of cell mediated immunity  Aseptic meningitis Cutaneous leishmaniasis
determines the type of leprosy a patient will  Weil's d/s should always be  Leishmania Tropica or Leishmania
develop. considered in high-risk pts with Mexicana
1. Lepromatous Leprosy ('multibacillary') hepatorenal failure  Crusted lesion at site of bite
 Low degree of cell mediated immunity  May be underlying ulcer
extensive skin involvement Investigation  If acquired in Africa or India --> can be mx
 symmetrical nerve involvement 1. Serology --> antibodies to Leptospira conservatively
2. Tuberculoid leprosy ('paucibacillary') develop after about 7 days  If acquired in South or Central America -->
 High degree of cell mediated 2. PCR Rx because risk of mucocutaneous
immunity 3. Culture --> growth may take several Leishmaniasis
 Limited skin disease weeks so limits usefulness in dx
 Asymmetric nerve involvement → 4. Blood & CSF samples are generally Mucocutaneous leishmaniasis
hypesthesia positive for the first 10 days  Leishmania Braziliensis
 Hair loss 5. Urine cultures become +ve during the 2nd  Skin lesions may spread to involve
week of illness mucosae of nose, pharynx etc
Management
Triple therapy --> Rifampicin + Dapsone + Management Visceral leishmaniasis (kala-azar)
Clofazimine High-dose Benzylpenicillin or Doxycycline  Leishmania Donovani
 occurs in the Mediterranean, Asia, South
America, Africa
 Features
LISTERIA  fever, sweats, rigors
HAND FOOT & MOUTH DISEASE  massive splenomegaly.
Listeria monocytogenes (Gram-positive hepatomegaly
Picornaviridae family (most commonly  poor appetite, weight loss
coxsackie A16 and enterovirus 71) bacillus)
Spread via contaminated food, typically  grey skin --> 'kala-azar' means
Self-limiting condition affecting children. black sickness
Very contagious unpasteurised dairy products.
Able to multiply at low temperatures  pancytopaenia secondary to
Typically have outbreaks in nursery hypersplenism
Features  Gold std for dx --> Bone marrow or splenic
Features aspirate
 Mild systemic upset --> sore throat, fever,  Diarrhoea
oral ulcers  Flu-like illness
 Followed later by vesicles on the palms &  Pneumonia
soles of the feet  Meningoencephalitis
 Ataxia MALARIA
Management  Seizures
1. Symptomatic Rx Falciparum Malaria
2. Advice regarding hydration & analgesia Investigations  Most common & most severe type of
Blood C&S -->’tumbling motility’ on wet mounts malaria
 Features of severe malaria  Plasmodium vivax/ovale --> cyclical  Proguanil --> folate
 schizonts on a blood film fever every 48 hours. supplementation (5mg od) should
 parasitaemia > 2%  Plasmodium malariae -->cyclical be given
 hypoglycaemia fever every 72 hours, assoc with  Malarone (atovaquone + proguanil)
 acidosis nephrotic syndrome --> avoid these drugs unless
 temperature > 39 °C  Ovale & vivax malaria have a essential. If taken then folate
 severe anaemia hypnozoite stage & can relapse supplementation should be given
 Complications after Rx .  Mefloquine --> caution advised
 Cerebral malaria --> seizures, coma  Treatment  Doxycycline is CI
 Acute renal failure --> blackwater  In chloroquine-sensitive areas -->
fever, secondary to intravascular ACT or chloroquine
haemolysis, mechanism unknown  In chloroquine-resistant areas -->
 ARDS ACT MELIOIDOSIS @Whitmore’s disease
 Hypoglycaemia  Avoid ACTs in pregnant women
 DIC  Patients with ovale / vivax malaria Burkholderia pseudomallei (Gram negative
should be given primaquine bacterium) --> Widely distributed environmental
 Uncomplicated falciparum malaria following acute Rx with chloroquine saprophyte in soil & fresh surface water.
 Strains resistant to chloroquine are to destroy liver hypnozoites & Endemic in tropics & subtropics climates, mainly
prevalent in certain areas of Asia & prevent relapse in SE Asia (e.g Thailand, Malaysia) & Northern
Africa America.
 1st line Tx --> Artemisinin-based Investigations 150,000 case/year worldwide, with most cases
combination therapies (ACTs)  Gold std --> Blood film occurring in wet seasons.
 In Malaysia, commonly given  Thick --> more sensitive Incubation period: 1-21 days
Artemeter + Lumefantrine (RIAMET)  Thin --> determine species
--> 6 doses over 3 days --> STAT  FBC Spread
dose followed by a dose at 8 hours,  thrombocythaemia is characteristic  Percutaneous inoculation --> contact with
24 hours, 36 hours, 48 hours and  NCNC anaemia contaminated soil / water (MC)
60 hours after first dose.  normal WCC  Inhalation, aspiration, or ingestion of
 Other examples od ACTs:  Reticulocytosis contaminated dust or water
 Artesunate + Amodiaquine  Rapid diagnostic tests (detecting  Person-to-person transmission is rare
 Artesunate + Mefloquine plasmodial histidine-rich protein 2) are
 Artesunate + Sulfadoxine- currently being trialled and have shown Risk factors
pyrimethamine sensitivities from 77-99% and specificities 1. DM (the strongest RF)
 Dihydroartemisinin + from 83-98% for falciparum malaria 2. Chronic renal, liver, or lung d/s
Piperaquine 3. Immunocompromised states
Prophylaxis 4. Occupational exposure --> agricultural
 Severe falciparum malaria Drug SE Time Time work
 Parasite counts >2% will need to to
parenteral Rx irrespective of clinical begin end Features
state before after  Acute /chronic (>2 months) / reactivations
 IV Artesunate is now recommended travel travel of latent infection.
by in preference to IV Quinine Atovaquone GI Upset 1-2 7  Wide range of presentation (mild - severe)
 If parasite count > 10%, consider + Proguanil days days  Acute pulmonary infection (MC)
exchange transfusion (Malarone)  Localized infection --> skin ulcer, nodule,
 shock may indicate coexistent Chloroquine Headache 1 wk 4 wks or abscess.
bacterial septicaemia - malaria CI in epilepsy  Visceral abscesses: esp in prostate,
rarely causes haemodynamic Taken spleen, kidney & liver.
collapse weekly  Disseminated infection in ~55% with 20%
Doxycycline Photo- 1-2 4 wks mortality rate.
Non-falciparum Malaria sensitivity days
 Types Oeso- Diagnosis
 Plasmodium Vivax (most common) phagitis  Culture
- Central America & Indian Gram stain of sputum or abscess pus
Mefloquine Dizziness 2-3 4 wks 
Subcontinent CXR : may show acute pneumonia
(Lariam) Neuro- wks 
 Plasmodium ovale - Africa
psychiatric
 Plasmodium malariae Treatment
disturbance
 Plasmodium knowlesi - SE Asia Initial intensive tx --> IV Ceftazidime, Imipenem,
CI in epilepsy
 Features or Meropenem for 10–14 days
Taken
 fever, headache, splenomegaly Followed by eradication tx --> oral TMP/SMX
weekly
0m - 3m Group B Strep (MC in neonates) (plus doxycycline) for 3–6 months
Proguanil 1 wk 4 wks
E. coli Adjunct tx --> abscess drainage.
(Paludrine)
Listeria monocytogenes
Proguanil + See above 1 wk 4 wks
3m - 6y Neisseria meningitidis Prevention
chloroquine
Streptococcus pneumoniae Avoid contact with soil & standing water
Haemophilus influenzae Wear boots / masks / gloves / gowns
Pregnant women
6y - 60y Neisseria meningitidis No vaccination available
 Should avoid travelling malaria endemic
Streptococcus pneumoniae regions
> 60y Streptococcus pneumoniae  Dx can be difficult as parasites may not be
Neisseria meningitidis detectable in the blood film due to
Listeria monocytogenes placental sequestration. MENINGITIS
Immunosup Listeria monocytogenes  If travel cannot be avoided
pressed  Chloroquine can be taken Causes
CSF Analysis as it is widely available & only requires
 Ziehl-Neelsen stain is only 20% sensitive one dose PUBIC LICE @ Peducularis pubis /
in the detection of tuberculous meningitis  Risk is highest in the first 7 days but Phthiriasis pubis
& therefore PCR is sometimes used persists for at least 4 wks
(sensitivity = 75%)  Meningococcal vaccination should be
Sexually transmitted infestation
 Mumps is unusual in being associated offered to close contacts when serotype
Phthirus pubis @ 'crab louse'
with a low glucose level in a proportion of results are available, including booster
M>F
cases. doses to those who had the vaccine in
15-40 y/o
 A low glucose may also be seen in herpes infancy.
Incubation minimum 5 days but a longer
encephalitis  No prophylaxis is generally needed for
asymptomatic period is possible
pneumococcal meningitis.
APPEARANCE Features
Bacterial Cloudy Meningococcal septicaemia
 Itching/pruritus --> worse at night
Viral Clear/Cloudy  High morbidity and mortality unless
 localised to the pubic region or rarely
Tuberculous Slight cloudy / Fibrin Web treated early. Presentation of
eyelashes and & head
meningococcal disease:
Fungal Cloudy  'black/rust-coloured powder' on underwear.
 15% - meningitis
 Excoriation marks due to pruritus.
 25% - septicaemia
GLUCOSE  Blue macules (maculae ceruleae) --> due
 60% - meningitis & septicaemia
Bacterial Low (<1/2 Plasma) to anticoagulant saliva injected by the lice
 Investigations
during their feeding.
Viral 60-80% of plasma  Blood C&S & PCR
Tuberculous Low (<1/2 of plasma)  LP is usually CI
Investigations
Fungal Low  FBC & clotting to assess for DIC
Dx is clinical
Microscopic/dermascopic evaluation of hair
PROTEIN Full sexual health screen.
Bacterial High (>1g/L)
Viral Normal/Raised VIRAL MENINGITIS Management
Tuberculous High (>1g/L) 1. Decontaminate clothing & bed linen
Fungal High Inflammation of the leptomeninges & CSF of  Wash at >50ºC or place in a sealed plastic
subarachnoid space. bag for >7 days.
More benign & common compared to bacterial 2. Creams / Lotions
WHITE CELLS
meningitis.  malathion 0.5%, permethrin 1%,
Bacterial 10-5000 polymorphs/mm3 phenothrin 0.2% or carbaryl 0.5%
~3000/year
Viral 15-1000 lymphocytes/mm3  Should be re-applied after 3-7 days -->
Tuberculous 30-300 lymphocytes/mm3 Causes due to the presence of lice & eggs being
Fungal 20-200 lymphocytes/mm3 1. Non-polio enteroviruses (ex : coxsackie at different stages of their life cycle.
virus, echovirus) 3. Mechanical removal with nit-combs
Management 2. Mumps 4. Shaving not recommended
Initial empirical tx IV Cefotaxime + 3. HSV 5. Re-examine in 1wk to ensure response
<3m Amoxicillin (or ampicillin) 4. CMV 6. Contact tracing --> sexual partners in the
Initial empirical tx IV Cefotaxime / 5. HZV last 3m should be examined & Rx
3m - 50 yrs Ceftriaxone 6. HIV
Initial empirical IV Cefotaxime (or 7. Measles
tx >50 yrs Ceftriaxone) +
Amoxicillin (or Ampicillin) Risk factors
Meningococcal IV Benzylpenicillin or Extremes of age (< 5 yrs & elderly) ENTERIC FEVER (TYPHOID &
meningitis Cefotaxime (or Immunocompromised PARATYPHOID)
Ceftriaxone) IVDU
Pneumococcal IV Cefotaxime (or Salmonella Typhi & Salmonella paratyphi
Features
meningitis Ceftriaxone) (types A, B & C) - aerobic, Gram-negative rods,
 Headache
Meningitis caused IV Cefotaxime (or not normally present as commensals in the gut
 Neck stiffness
by Haemophilus Ceftriaxone)
 Photophobia (milder than bacterial
influenzae Spread
meningitis)
Meningitis caused IV Amoxicillin (or Faecal-oral route (contaminated food & water)
 Confusion
by Listeria Ampicillin) + Gentamicin  Fevers
Features
 focal neurological deficits
IV Dexamethasone should also be given  Systemic upset
  Seizures --> suggests
to reduce the risk of neurological sequelae,  Relative bradycardia
meningoencephalitis
but withhold if:  Abdo pain, distension
 septic shock  Constipation --> constipation is more
Investigation
 meningococcal septicaemia common than diarrhoea in typhoid
1. LP
 immunocompromised  Rose spots --> on trunk in ~40%, more
2. Viral PCR
 meningitis following surgery common in paratyphoid.
 Use chloramphenicol if has H/O Management
immediate hypersensitivity reaction to Complications
Supportive Rx while awaiting result of LP 1. Osteomyelitis (especially in sickle cell d/s
penicillin or to cephalosporins Broad spectrum abx with CNS penetration (IV
where Salmonella is one of the most
Ceftriaxone & Aciclovir)
Management of contacts common pathogens)
Generally, viral meningitis is self-limiting --> sx
Should be offered to household / close 2. GI bleed/perforation
 improve within 7-14 days & complications are
contacts/ those exposed to respiratory 3. Meningitis
rare in immunocompetent pts.
secretion 4. Cholecystitis
 Oral Ciprofloxacin or Rifampicin or may be 5. Chronic carriage (1%, more likely if adult
used. Ciprofloxacin is the drug of choice females)
 Spread by caves/bats & primates.
Zoonotic infection --> spread by Aedes
mosquitos
Incubation period 2 - 14 days
MYCOBACTERIUM MARINUM @ Fish DENGUE FEVER
Tank Granuloma Features
RNA virus of the genus Flavivirus  Mild flu-like illness lasting <1 wk
 Typically presents in patients who have Trasmitted by Aedes Aegyptii / Aedes Albopictus  Sudden onset of high fever, rigors, nausea
had an exposure to, or frequently work Four serotypes (DENV 1-4) & vomiting.
with fish. Incubation period of 3-4 wks Each episode of infection induces life-long  Bradycardia may develop.
 Lesions can be painful / painless. protective immunity to the homologous  A brief remission is followed by jaundice,
serotypes but confers only partial & transient haematemesis, oliguria
Spread protection against other serotypes.  If severe jaundice, haematemesis may
A cut or break in the skin can be enough for the Secondary infection is a major risk factor for occur
organism to enter the blood stream & track up severe dengue due to antibody-dependent
the lymphatic system (sporotrichoid spread). enhancement. Investigations
Incubation period 4-7 days Councilman bodies (inclusion bodies) may be
Treatment seen in the hepatocytes
Tetracyclines, Fluoroquinolones, Sulfonamides & Classification
Macrolides. 1. Without warning signs
2. With warning signs
3. Severe dengue (dengue haemorrhagic ZIKA VIRUS
fever)
VIRAL HAEMORRHAGIC FEVER Flavivirus
Features
Group of viral infections ranging from a flu-like  fever Transmission
illness to multisystem failure.  headache (often retro-orbital) 1. Bite of an infected Aedes mosquito
 myalgia, bone pain & arthralgia ('break- 2. Sexual transmission (small number of
Examples bone fever') cases)
1. Flaviviridae --> Dengue, Yellow fever  pleuritic pain 3. Via placenta from mother to fetus.
2. Arenaviridae --> Lassa fever  facial flushing (dengue)
3. Filoviridae --> Ebola virus, Marburg virus  maculopapular rash First isolated from a monkey in the Zika forest in
4. Bunyaviridae --> Hantaviruses, Crimean-  haemorrhagic manifestations ( ex: positive Uganda in 1947.
Congo haemorrhagic fever, Rift Valley tourniquet test, petechiae,
fever purpura/ecchymosis, epistaxis) Features
 Warning signs  Asymptomatic in majority
Features  abdo pain  Mild, short-lived febrile d/s (2-7 days)
 Flu-like sx  hepatomegaly  Rash
 Abdo pain  persistent vomiting  Arthralgia/arthritis
 Haemorrhage  clinical fluid accumulation (ascites,  Conjunctivitis
 Petechiae/bruising pleural effusion)  Myalgia
 Haematochezia  Headache
 Haematemesis Phases  Retro-orbital pain
 Haemoptysis 1. Febrile phase  Pruritus
 DIC High grade fever, lasts 2-7 days
 Multiorgan failure Progressive decrease in TWC, followed by Complications
reductioni n pletelet count Guillain-Barre syndrome
Management 2. Critical phase Microcephaly & other congenital abnormalities
Generally supportive Rx Often occurs on D3 of fever.
Lassa Fever --> Ribavirin
Dengue haemorrhagic fever
Prevention Form of DIC resulting in :
 thrombocytopenia
CHIKUNGUNYA
 Yellow fever vaccine is available
Dengue and Ebola vaccine have been  spontaneous bleeding

 ~20-30% of these pts go on to develop Alphavirus
developed but are not widely used at the Mosquito-borne
current time DSS
African, Asian & Indian subcontinent
 No vaccines are available for the other Tanzania had the first reported case
VHFs Investigations
1. Leukopenia
2. Thrombocytopenia Features
3. raised aminotransferases  Severe joint pain
LASSA FEVER 4. Serology (IgG & IgM)  Abrupt onset of high fever
5. NAATs for viral RNA  General flu-like illness of muscle ache,
Arenaviridae 6. NS1 antigen test headache, & fatigue
Spread by excreta of infected African rats  Rash
(Mastomys rodent) or by person-to-person. Treatment  Similar symptoms as dengue but tends to
Symptomatic e.g. fluid resuscitation, blood have more joint pain which can be
transfusion etc debilitating.
no antivirals are currently available
Management
MARBURG VIRUS Symptomatic Rx
Filoviridae
Very similar to Ebola. YELLOW FEVER
CUTANEOUS LARVA MIGRANS STRONGYLOIDIASIS
Toxoplasma gondii (obligate intracellular
Ancyclostoma braziliense (Dog hookworm) Strongyloides stercoralis (parasitic nematode protozoan)
worm)
Dermatological condition The larvae are present in soil and gain access to Pathogenesis
Prevalent in tropical & subtropical regions the body by penetrating the skin. Infects the body via the GI tract, lung or broken
Cutaneous penetration & migration of nematode skin. It's oocysts release trophozoites which
larvae (Ancyclostoma Braziliense) Features migrate widely around the body including to the
 Diarrhoea eye, brain & muscle.
Features  Abdo pain/bloating Usual animal reservoir is the cat, although other
Very itchy creeping serpinginous rash that  Papulovesicular lesions --> skin has been animals such as rats carry the disease.
worsens over time penetrated by infective larvae (ex soles of
Can lead to secondary bacterial infection due to feet / buttocks) Immunocompetent patients
excessive scratching  Larva currens --> pruritic, linear, urticarial  Mostly asymptomatic.
rash  Symptomatic pts usually have a self-
Management  Pneumonitis similar to Loeffler’s syndrome limiting infection, often having features
Albendazole or Ivermectin may be triggered if the larvae migrate to resembling infectious mononucleosis
the lungs (fever, malaise, lymphadenopathy).
 Other less common manifestations include
Treatment meningoencephalitis & myocarditis.
Ivermectin & Albendazole Ix of choice --> serology
WUCHERERIA BANCROFTI

 No rx required unless severe infection /
immunosuppressed
Parasitic filarial nematode
~90% of cases of filariasis HIV / Immunosuppressed patients
Transmitted by mosquitoes TRYPANOSOMIASIS  Cerebral toxoplasmosis is ~50% of
Dx --> Blood smears cerebral lesions in HIV pts
Mx --> Diethylcarbamazine African trypanosomiasis (sleeping sickness)  Features --> constitutional sx, headache,
 Trypanosoma Gambiense in West Africa confusion, drowsiness
 Trypanosoma Rhodesiense in East  CT --> single or multiple ring-enhancing
Africa lesions, mass effect may be seen
MUCORMYCOSIS  Spread by Tsetse fly  Mx --> Pyrimethamine plus Sulphadiazine
 Trypanosoma Rhodesiense tends to for at least 6 wks
Fungal infection seen in poorly controlled follow a more acute course.  May also develop a chorioretinitis
diabetes.  Features secondary to toxoplasmosis.
Typically infects the sinuses, lungs & brain.  Trypanosoma chancre --> painless
subcutaneous nodule at site of Congenital toxoplasmosis
infection  Due to transplacental spread from the
 intermittent fever mother.
 enlargement of posterior cervical Effects
CRYPTOSPORIDIOSIS LN

 Neurological damage
 Later --> CNS nvolvement e.g.  cerebral calcification
Cyptosporidium Parvum & Cyptosporidium somnolence, headaches, mood  hydrocephalus
Hominis changes, meningoencephalitis  chorioretinitis
MC protozoal cause of diarrhoea in UK  Management  Ophthalmic damage
 Early d/s --> IV Pentamidine or  retinopathy
Risk factors Suramin  Cataracts
Immunocompromised (HIV)  Later d/s or CNS involvement --> IV
Young pts Melarsoprol

Features American trypanosomiasis, (Chagas' disease)

 watery diarrhoea  Protozoan Trypanosoma Cruzi SCHISTOSOMIASIS @ Bilharzia
 abdominal cramps  Features
 fever  ~95% asymptomatic in the acute Parasitic flatworm infection
 In immunocompromised pts, the entire GI phase S. Mansoni, S. Japonicum, S. Haematobium.
tract may be affected causing  Chagoma (an erythematous nodule
complications such as sclerosing at site of infection) & periorbital Acute infections
cholangitis & pancreatitis oedema sometimes seen.  In those who travel to endemic areas,
 Chronic Chagas' d/s --> mainly as they don't have any immunity to the
Diagnosis affects heart & GI tract worms.
Modified Ziehl-Neelsen stain (acid-fast stain) of  Myocarditis --> dilated CM (with  Acute manifestations
the stool --> characteristic red cysts of apical atophy) & arrhythmias  Swimmers' itch
Cryptosporidium  GI features --> megaoesophagus &  Acute schistosomiasis syndrome
megacolon causing dysphagia & (Katayama fever)
Management constipation  Fever
Supportive Rx for immunocompetent patients  Management  Urticaria/angioedema
If HIV pt & not on ART, ART should be started &  Azole or nitroderivatives such as  Arthralgia/myalgia
this will often be enough to resolve the infection. Benznidazole or Nifurtimox  Cough
Nitazoxanide may be used for  Chronic d/s --> Rx complications  Diarrhoea
immunocompromised pts / pts with severe such as HF  Eosinophilia
disease
Chronic infections
1. Schistosoma haematobium
TOXOPLASMOSIS
 These worms deposit egg clusters 1. Perihepatitis (Fitz-Hugh Curtis Syndrome)
(pseudopapillomas) in the bladder, --> ~10%, RUQ pain, may be confused Classification
causing inflammation. with According to the causative organism
 Xray --> calcification of the egg clusters 2. Infertility --> 10-20% Type 1 Caused by mixed anaerobes &
seen, not the bladder itself. 3. Chronic pelvic pain aerobes (often occurs post-surgery in
 Depending on the site of these 4. Ectopic pregnancy diabetics). MC type.
pseudopapillomas in the bladder, they can Type 2 Strep Pyogenes
cause obstructive uropathy & kidney
damage. Risk factors
 Typically presents as 'swimmer's itch' in CELLULITIS  Skin factors --> recent trauma, burns / soft
pts who have recently returned from Africa. tissue infections
 RF for squamous cell bladder cancer. DM --> esp if being Rx with SGLT-2
Features Strep pyogenes / Staph Aureus 

Inflammation of the skin & S/C tissues inhibitors
 frequency  IVDU
 haematuria Immunosuppression
 bladder calcification Features 

Management  commonly occurs on the shins


 Erythema Features
 Single oral dose of praziquantel MC site --> Perineum (Fournier’s
2. Schistosoma mansoni & Schistosoma  Pain 
 Swelling gangrene)
japonicum Acute onset
Mature in the liver and then travel through  Systemic sx --> fever 

 Pain out of proportion
the portal system to inhabit the distal Swelling, erythema
colon. Diagnosis 
Clinical dx  Rapidly worsening cellulitis
 Their presence in the portal system can Hypoaesthesia to light touch
lead to progressive hepatomegaly & Blood Ix may be needed if septicaemia 
suspected  Skin necrosis & crepitus/gas gangrene-->
splenomegaly due to portal vein late signs
congestion. Fever & tachycardia --> may be absent or
Lead to complications of liver cirrhosis, Eron Classification 

Class Features occur late
variceal disease & cor pulmonale. ~20% mortality rate
I No

3. Schistosoma intercalatum and Schistosoma signs of systemic toxicity & no
mekongi uncontrolled co-morbidities
Management
 Less prevalent than the other 3 forms, but
are both attributed to intestinal
II Either systemically unwell or
systemically well but with a co-
Urgent surgical debridement
IV antibiotics
schistosomiasis. morbidity (Ex --> PAD, chronic
venous insufficiency, or morbid obesity)
which may complicate or delay
resolution of infection
SPINAL EPIDURAL ABSCESS
PELVIC INFLAMMATORY DISEASE III Significant systemic upset such as
acute confusion, tachycardia,
tachypnoea, hypotension, or unstable Collection of pus that is superficial to the dura
Infection & inflammation of the female pelvic
co-morbidities that may interfere with a mater (of the meninges) that cover the spinal
organs including the uterus, fallopian tubes,
response to Rx, or a limb-threatening cord.
ovaries and the surrounding peritoneum.
infection due to vascular compromize Typically bacterial, MC is Staph Aureus
Usually result of ascending infection from the
endocervix.
Pathophysiology
IV Sepsis syndrome or a severe life-
threatening infection such as Bacteria enters the spinal epidural space by
Causes
necrotizing fasciitis contiguous spread from adjacent structures (e.g.
1. Chlamydia trachomatis (MC)
discitis), haematogenous spread from
2. Neisseria gonorrhoeae
3. Mycoplasma genitalium concomitant infection (e.g. bacteraemia from
Indications for admission + IV abx IVDU), or by direct infection (e.g. spinal surgery).
4. Mycoplasma hominis
1. Eron Class III or IV
2. Severe / rapidly deteriorating cellulitis Features
Features
3. <1 y/o / frail  Fever
 Lower abdominal pain
 Fever 4. Immunocompromised  Back pain
5. Significant lymphoedema.  Focal neurological deficits according to
 Deep dyspareunia
6. Facial cellulitis (unless very mild) / the segment of the cord affected.
 Dysuria
 Menstrual irregularities periorbital cellulitis.
Investigations
 Vaginal / Cervical discharge
Management  Routine bloods
 Cervical excitation
1. 1st line for mild / moderate -->  Blood cultures
Flucloxacillin  Infection screen
Investigation
2. Preganancy --> Clarithromycin,  MRI whole spine (the entire spine is
Preganancy test TRO ectopic
erythromycin imaged since skip lesions may be present)
High vaginal swab --> often -ve
3. Allergic to penicillin --> Doxycyline  If the primary source of infection is not
Screen for Chlamydia & Gonorrhoea
4. Severe cellulitis --> co-amoxiclav, clear, a wide search for sources requires
cefuroxime, clindamycin or ceftriaxone. further Ix like echo & dental x-rays.
Management
1. Oral Ofloxacin + Oral Metronidazole OR
2. IM Ceftriaxone + Oral Doxycycline + Oral Management
Metronidazole Long-term course of abx
Surgical evacuation of the abscess.
3. Removal of the IUD should be considered
--> assoc with better short term clinical NECROTIZING FASCIITIS
outcomes
Medical emergency that is difficult to recognise
Complications in the early stages.
ERYTHEMA INFECTIOSUM @ FIFTH  Haemolytic anaemia secondary to cold 1. Significant exposure to chickenpox or
DISEASE @ SLAPPED CHEEK agglutins (IgM) herpes zoster (ex : exposure to limited,
Maculopapular, pruritic rash in ~99% who covered-up shingles may not warrant
SYNDROME

take ampicillin/amoxicillin whilst they have post-exposure prophylaxis)
infectious mononucleosis 2. Clinical condition that increases the risk of
Parvovirus B19, DNA virus severe varicella (ex : immunosuppressed
Spread by the respiratory route Diagnosis pts, neonates & pregnant women, long-
Person is infectious 3 to 5 days before the Heterophil antibody test (Monospot test) & FBC term steroids, MTX & other common
appearance of the rash. in the 2nd wk of illness. immunosuppressants)
Children no longer infective once rash appears 3. No antibodies to the varicella virus--> all
Management at-risk exposed pts should have a blood
Features 1. Supportive test for varicella antibodies. However, thsi
 Mild feverish illness 2. Sx usually resolve within 2-4wks should not delay PEP >7days after last
 Rose-red rash 3. Drink plenty of fluid contact.
 Bright red over cheeks 4. Avoid alcohol
 May spread to rest of the body 5. Avoid contact sports for 4wks to reduce Chickenpox in pregnancy
 Rarely involves the palms and soles. risk of splenic rupture  In pregnancy, there is a risk to both
 Child begins to feel better once rash 6. Simple analgesia for any aches or pains mother & fetus --> fetal varicella syndrome
appears Peaks after a week and  5 times greater risk of pneumonitis for the
then fades. mother
 Warm bath, sunlight, heat or fever  Fetal varicella syndrome (FVS)
can trigger a recurrence of the rash <20wk gestation : ~1% risk
CHICKENPOX 
itself even months later  20-28 wks : very small risk
 Can be asymptomatic  >28 wks : None
Varicella Zoster virus
 Pancytopaenia in immunosuppressed pts  Features
 Aplastic crises (ex : in sickle-cell disease)  Skin scarring
Primary infection --> Chickenpox
 Suppresses erythropoiesis for ~1wk  Eye defects (Microphthalmia)
Reactivation of the dormant virus in the dorsal
so aplastic anaemia is rare unless  Limb hypoplasia
root ganglion --> Shingles
there is a chronic haemolytic  Microcephaly
Highly infectious
anaemia  Learning disabilities
Spread via the respiratory route
 Hydrops fetalis Shingles in infancy
Can be spread from someone with shingles 
 Can cross the placenta in pregnant  1-2% risk if maternal exposure in
Infectivity = 4 days before rash, until 5 days after
women. 2nd or 3rd trimester
the rash first appeared
 Causes severe anaemia due to viral Severe neonatal varicella
Incubation period = 10-21 days 
suppression of fetal erythropoiesis  If mother develops rash between 5
→ heart failure secondary to days before and 2 days after birth --
Features
severe anaemia → the > risk of neonatal varicella
 Fever initially
accumulation of fluid in fetal serous  Fatal to the newborn in ~20%
 Itchy rash --> starting from head/trunk
cavities (e.g. ascites, pleural &
before spreading
pericardial effusions) Post-exposure prohylaxis in preganancy
 Initially macular then papular then
 Rx with intrauterine blood Maternal blood should be checked
vesicular 
transfusions urgently for varicella antibodies
 Mild systemic upset
 Acute arthritis in adults  If </=20wks & not immune to varicella
Management  Give VZIG asap.
Management  Effective upto 10 days post
1. Supportive
No specific Rx exposure
2. Trim nails
Most children recover If >20wks & not immune to varicella
3. Calamine lotion 
School exclusion not needed as the child is not  Give either VZIG or antivirals
4. School exclusion
infectious once the rash emerges. (aciclovir or valaciclovir) on day 7-
5. Immunocompromised pts & newborns
with peripartum exposure should receive 14 after exposure
varicella zoster immunoglobulin (VZIG).
6. If chickenpox develops then IV Aciclovir Management of chickenpox in pregnancy
INFECTIOUS MONONUCLEOSIS @ should be considered 1. Oral aciclovir if ≥ 20 wks and she
GLANDULAR FEVER presents within 24 hours of onset of the
Complications rash
1. Secondary bacterial infection 2. If < 20 wks, the aciclovir should be
Epstein-Barr virus @ HHV-4 in 90%
NSAIDs may increase this risk 'considered with caution'
Less common --> CMV & HHV-6 
In adolescents & young adults.  Can manifest as a single infected
lesion/small area of cellulitis, but
Features rarely invasive group A strep soft
 Classic Triad --> sore throat, pyrexia & tissue infections may occur SPLENECTOMY
lymphadenopathy in ~98% resulting in NF
 Lymphadenopathy --> in anterior & 2. Pneumonia Post splenectomy, pts are at risk from
posterior triangles of the neck, in contrast 3. Encephalitis (cerebellar involvement may pneumococcus, Haemophilus, meningococcus &
to tonsillitis which typically only results in be seen) Capnocytophaga canimorsus infections
the upper anterior cervical chain being 4. Disseminated haemorrhagic chickenpox
enlarged 5. Arthritis Vaccination
 Malaise, anorexia, headache 6. Nephritis If elective, should be done 2 wks prior to
 Palatal petechiae 7. Pancreatitis operation or 2 wks following splenectomy
 Splenomegaly --> in ~50% & may rarely  Hib, meningitis A & C
cause splenic rupture Post-exposure prophylaxis  Annual influenza vaccination
 Hepatitis, transient rise in ALT VZIG should be given if fulfill the following  Pneumococcal vaccine every 5 years
 Lymphocytosis --> 50% lymphocytes with criteria :
at least 10% atypical lymphocytes
Antibiotic prophylaxis have both pharmacological and Full course of If tetanus prone wound -->
Penicillin V / Macrolide mechanical protection. vaccine with reinforcing dose of vaccine
 No clear guidelines on how long abx last dose >10 If high-risk wounds (ex :
should be continued. yrs ago compound fractures, delayed
 Generally accepted that should be surgical intervention,
continued for at least 2 yrs & until pt is 16 TETANUS significant degree of
y/o. devitalised tissue) -->
 Majority of pts are put on prophylactic abx Clostridium Tetani reinforcing dose of vaccine +
lifelong tetanus immunoglobulin
 Penicillin V 500mg BD or Amoxicillin Pathophysiology Incomplete or Reinforcing dose of vaccine,
250mg BD  Tetanospasmin exotoxin released from unknown regardless of the wound
Clostridium tetani which prevents release vaccination hx severity
Indications for splenectomy of GABA. For tetanus prone & high-risk
1. Trauma --> 1/4 are iatrogenic  Tetanus spores are present in soil & may wounds --> reinforcing dose
2. Spontaneous rupture --> EBV be introduced into the body from a wound, of vaccine + tetanus
3. Hypersplenism --> hereditary which is often unnoticed. immunoglobulin
spherocytosis or elliptocytosis etc
4. Malignancy --> lymphoma or leukaemia Features
5. Splenic cysts / hydatid cysts / splenic  Prodrome --> fever, lethargy, headache
abscesses  Trismus (lockjaw)
 Risus sardonicus SCARLET FEVER
Elective splenectomy  Opisthotonus (arched back,
 Spleen is often large (sometimes massive) hyperextended neck)
Most cases can be performed Reaction to erythrogenic toxins produced by

 Spasms (ex--> dysphagia) Group A haemolytic streptococci (usually
laparoscopically. The spleen will often be
macerated inside a specimen bag to Streptococcus pyogenes).
Management More common in children 2-6 y/o
facilitate extraction. 1. Supportive tx Peak incidence at 4 y/o
2. Ventilatory support Spread via the respiratory route by inhaling or
Complications 3. Muscle relaxants
1. Haemorrhage (may be early & either from ingesting respiratory droplets or by direct contact
4. IM Human Tetanus immunoglobulin for with nose and throat discharges, (especially
short gastrics or splenic hilar vessels) high risk wounds (ex --> compound
2. Pancreatic fistula (from iatrogenic damage during sneezing and coughing).
fractures, delayed surgical intervention, Incubation period of 2-4 days
to pancreatic tail) significant degree of devitalized tissue)
3. Thrombocytosis --> prophylactic aspirin 5. Metronidazole is now preferred to
4. Encapsulated bacteria infection e.g. Strep. Features
Benzylpenicillin as the abx of choice. Fever --> typically lasts 24-48 hours
pneumoniae, Haemophilus influenzae & 

Neisseria meningitidis  Malaise

Tetanus vaccine  Headache
 Cell-free purified toxin that is normally N/V
Post-splenectomy changes given as part of a combined vaccine.


Platelets will rise first (therefore in ITP should be  Sore throat

 Part of the routine immunisation schedule 'Strawberry' tongue
given after splenic artery clamped) at 2m, 3m, 4m, 3-5yrs & 13-18 yrs


Blood film will change over following  Rash


 5 doses of tetanus containing vaccine -->  Fine punctate erythema ('pinhead')
weeks, Howell-Jolly bodies will appear considered to provide adequate long-term
Target cells  Appears first on the torso

protection against tetanus.  Spares the palms and soles
 Pappenheimer bodies
Increased risk of post-splenectomy sepsis,  Flushed appearance with
Management of wounds circumoral pallor.
therefore prophylactic antibiotics &
Clean Wounds less than 6 hours old, non-  Rash is more obvious in flexures
pneumococcal vaccine should be given.
wound penetrating with negligible tissue  Rough 'sandpaper' texture
damage Desquamination occurs later esp around
Post-splenectomy sepsis 

 Hyposplenism may complicate certain fingers & toes

medical conditions where splenic atrophy Tetanus Puncture-type injuries acquired in a
occurs or may be the result of medical prone contaminated environment (Ex : Diagnosis
intervention such as splenic artery wound gardening injuries) Throat swab
embolization and splenectomy for trauma. Wounds containing foreign bodies  Abx should be started immediately prior to
 Dx of hyposplenism is difficult & whilst Compound fractures results
there may be peripheral markers of the Wounds / burns with systemic
splenectomised state (e.g. Howell-Jolly sepsis Management
bodies) these are neither 100% sens or Certain animal bites & scratches Oral Penicillin V for 10 days
spec. Penicillin allergy --> Azithromycin
 The most sens test is a radionucleotide High- Heavy contamination with material Can return to school 24 hrs after abx
labelled red cell scan. risk likely to contain tetanus spores Notifiable disease
 Hyposplenism, by whatever mechanism it tetanus (soil, manure)
occurs dramatically increases the risk of prone Wounds / burns that show Complications
post-splenectomy sepsis, particularly with extensive devitalised tissue 1. Otitis media (MC)
encapsulated organisms. Wounds / burns that require 2. Rheumatic fever --> ~20days after
 Since these organisms may be opsonised, surgical intervention infection
but this then goes undetected at an 3. Acute GN --> ~10days after infection
immunological level due to loss of the 4. Rare invasive complications (ex :
spleen. For this reason, individuals are Full course of no vaccine nor tetanus bacteraemia, meningitis, necrotizing
recommended to be vaccinated and have vaccines with immunoglobulin is required, fasciitis)
antibiotic prophylaxis last dose regardless of the wound
 Asplenic individuals travelling to malaria <10yrs ago severity
endemic areas are at high risk and should
STAPHYLOCOCCI  No rash but causes atypical lopathy
pneumonia
Often found normal commensal organisms but  Typical prodrome --> fever, malaise CMV
may also cause invasive disease.  Causes pyrexia of unknown origin pneumonitis
Gram-positive cocci  Transaminitis
Facultative anaerobes  Endocarditis (culture-negative) CMV colitis
Produce catalase  Mx --> Doxycycline

2 main types Endemic typhus

Staphylococcus aureus Staphylococcus  Caused by Rickettsia typhi
epidermidis  Vector --> Flea
 Transmitted between hosts by arthropods LYME DISEASE
 Features
Coagulase-positive Coagulase- Borrelia burgdorferi (Sprirochaete)
 Rash (maculopapular) starts
Causes skin infections negative Spread by ticks
centrally then spreads to the
(ex: cellulitis), abscesses, Cause of central
peripheries
osteomyelitis, toxic shock line infections & IE Features
 Widespread vasculitis
syndrom Early (<30 days) Late (>30 days)
 Fever, headache
 Black eschar at site of original Erythema migrans Heart block
Staphylococcal toxic shock syndrome
inoculation  typically small Peri/myocarditis
 Severe systemic rxn to staphylococcal
 Complications papule often at site Facial nerve palsy
exotoxins, the TSST-1 superantigen toxin.
 Deranged clotting of the tick bite Radicular pain
 Became prominent in early 1980s
 Renal failure which develops into Meningitis
following a series of cases related to
 DIC a larger annular Polyarthritis
infected tampons.
lesion with central
 Centers for Disease Control & Prevention
Tick typhus clearing, 'bulls-eye'.
Diagnostic Criteria  Caused by R conorii  In ~70% of pts
i. Fever --> T > 38.9ºC  Rash initially in axilla then spreads  develops 1-4 wks
ii. HypoTN --> SBP < 90 mmHg after the initial bite
iii. Diffuse erythematous rash Epidemic typhus but may present
iv. Desquamation of rash, esp palms & sooner
 Caused by Rickettsia prowazekii
soles  Vector --> Human body louse  usually painless,
v. Involvement of >/=3 organ systems more than 5 cm in
(Ex : GI, mucous membrane
Ehrlichliosis diameter & slowlly
erythema, renal failure, hepatitis, increases in size
 Caused by Ehrlichia
thrombocytopenia, CNS
 Vector --> Tick
involvement
 Management
Headache
 Removal of infection focus
Lethargy
(ex :retained tampon)
CYTOMEGALOVIRUS Fever
 IV Fuids Arthralgia
 IV Abx
One of the herpes viruses.
~50% of people have been exposed to CMV but
it only causes d/s in immunocompromised. Investigation
1. Dx clinically if erythema migrans is
RICKETTSIAE Pathophysiology present.
Infected cells --> 'Owl's eye' appearance due 2. Erythema migrans is therefore an
Gram-negative obligate intracellular indication to start antibiotics
to intranuclear inclusion bodies
parasites. 3. 1st line Ix --> ELISA antibodies to Borrelia
Typical features --> fever, headache & rash Burgdorferi.
Patterns of disease
Q fever is an exception --> causes pneumonia 4. If 1st test is -ve & Lyme d/s is still
Congenital Features --> growth
but no rash suspected --> repeat test in 4-6 wks
CMV retardation, pinpoint petechial
Weil-Felix reaction is positive except in Q fever. 5. If still suspected in people who have had
infection 'blueberry muffin' skin lesions,
Rickettsial diseases are all Rx with tetracyclines. sx for >12wks --> Immunoblot test
microcephaly, sensorineural
deafness, encephalitiis 6. If ELISA +ve or equivocal -->
Rocky Mountain spotted fever immunoblot test
(seizures) &
 Caused by Rickettsia ricketsii
hepatosplenomegaly
 Vector --> Tick Management of asymptomatic tick bites
 Features 1. If the tick is still present, remove it is using
 Headache and fever are common CMV mono- Infectious mononucelosis-like
fine-tipped tweezers
 Macular rash starts on the nucleosis illness may develop in
2. Area should be washed after that
peripheries (wrist, ankles) before immunocompetent individuals
3. NICE guidance does not recommend
spreading centrally. routine antibiotic treatment to patients
 Initially maculopapular before CMV retinitis Common in HIV pts with a low who've suffered a tick bite
becoming vasculitic CD4 count (< 50)
 Endemic to east coast of US Presents with visual Management of Lyme disease
impairment. Fundoscopy --> 1. Early d/s --> Doxycycline
Q fever retinal haemorrhages & 2. Alternative --> Amoxicillin
 Caused by Coxiella burnetti necrosis, often called 'pizza' 3. Disseminated d/s --> Ceftriaxone
 No vector retina 4. People with erythema migrans should be
 Source of infection is typically an abattoir, Rx of choice --> IV Ganciclovir commenced on abx without further tests
cattle/sheep or it may be inhaled from 5. Jarisch-Herxheimer reaction
infected dust CMV Seen in pts with HIV who have  Sometimes seen after initiating tx
 Features encepha- low CD4 counts
 Fever, rash, tachycardia after first dose of tigecycline have activity against MRSA but  People travelling to or going to
abx should be reserved for resistant cases reside in areas of high or
 More commonly seen in syphilis, another intermediate prevalence, if aged > 1
spirochaetal d/s y/o.
 People with chronic liver d/s
UTI  Pts with haemophilia
 Men who have MSM
STREPTOCOCCI  IVDUs
Non-pregnant women  Those with occupational risk -->
 Trimethoprim or Nitrofurantoin for 3 days laboratory worker, staff of large
Gram-positive cocci.  Send Urine C&S if :
Divided into alpha & beta haemolytic types residential institutions, sewage
 >65 years old workers, people who work with
 Visible or non-visible haematuria primates
Alpha haemolytic streptococci (partial
haemolysis) Pregnant women
 Examples  Urine C&S should be sent for all
 Streptococcus pneumoniae  Mx
 Streptococcus viridans  1st line : Nitrofurantoin (should be HEPATITIS B
 Common cause of pneumonia, meningitis avoided near term)
& otitis media.  2nd line : Amoxicillin or Cefalexin Double-stranded DNA Hepadnavirus
 Trimethoprim is teratogenic in 1st Incubation period 6-20 wks
Beta haemolytic streptococci (complete trimester & should be avoided Spread by infected blood or body fluids, sexual
haemolysis) during pregnancy contact, vertical transmission from mother to
 Subdivided into groups A-H.  Asymptomatic bacteriuria in pregnant child.
 Only groups A, B & D are important in women:
humans.  Urine C&S at first antenatal visit Features
 Group A  Nitrofurantoin (should be avoided  Fever
 Most important organism is near term), amoxicillin or cefalexin  Jaundice
Streptococcus pyogenes for 7 days  Elevated liver transaminases.
 Responsible for erysipelas,  Should be treated due to significant
impetigo, cellulitis, Type 2 risk of progression to acute Complications
necrotizing fasciitis & pharyngitis / pyelonephritis 1. Chronic hepatitis (5-10%) : 'Ground-glass'
tonsillitis.  Urine C&S should be sent again hepatocytes may be seen on light
 Immunological reactions can cause after Rx as a test of cure microscopy
rheumatic fever or post- 2. Fulminant liver failure (1%)
streptococcal glomerulonephritis Men 3. HCC
 Erythrogenic toxins cause scarlet  Abx for 7 days 4. GN
fever  1st line : Trimethoprim or Nitrofurantoin 5. PAN
 Group B  Urine C&S should be sent 6. Cryoglobulinaemia
 Streptococcus agalactiae
 May lead to neonatal meningitis & Catherised patients Immunisation
septicaemia  Asymptomatic --> no need to Rx  Part of the routine immunisation schedule
 Group D  Symptomatic --> Abx for 7 days given at 2, 3 & 4 m.
 Enterococcus  Remove / Change catheter if it has been  Contains HBsAg adsorbed onto aluminium
there for >7days hydroxide adjuvant & is prepared from
yeast cells using recombinant DNA
technology.
MRSA  ~10-15% of adults fail to respond or
HEPATITIS A respond poorly to 3 doses of the vaccine.
Suppression of MRSA from a carrier once  Risk factors for poor response --> age >
identified RNA Picornavirus 40 , obesity, smoking, alcohol excess &
 Nose: mupirocin 2% in white soft paraffin, Incubation period 2-4 wks immunosuppression
tds for 5 days Spread by fecal-oral  Testing for anti-HBs is only recommended
 Skin: chlorhexidine gluconate, od for 5 Benign, self-limiting disease for those at risk of occupational exposure
days. Apply all over but particularly to the Doesnt cause chronic d/s & pts with CKD.
axilla, groin and perineum Serious outcomes are rare  In these pts anti-HBs levels should be
checked 1-4 m after primary immunisation
The following antibiotics are commonly used in Features
the treatment of MRSA infections:  Flu-like prodrome Anti- Response
 Vancomycin  Abdominal pain --> typically RUQ HBs
 Teicoplanin  Tender hepatomegaly level
 Linezolid  Jaundice > 100 Adequate response
 Cholestatic LFTs No further testing required.
Some strains may be sensitive to the antibiotics Should still receive booster at 5
listed below but they should not generally be Complications years
used alone because resistance may develop: Rare 10 - 100 Suboptimal response
 Rifampicin No increased risk of HCC One additional vaccine dose should
 Macrolides be given.
 Tetracyclines Immunisation If immunocompetent no further
 Aminoglycosides  Effective vaccine is available testing is required
 Clindamycin  After the initial dose, a booster dose < 10 Non-responder.
should be given 6-12m later Test for current or past infection.
Relatively new antibiotics such as linezolid,  Who should be vaccinated? Give further vaccine course (i.e. 3
quinupristin/dalfopristin combinations and doses again) with testing following.
 If still fails to respond --> give HBIG
Management
1. Pegylated interferon-alpha
 1st line
 Used to be the only Rx available.
 Reduces viral replication in up to 30% of
chronic carriers.
 Better response in F <50y/o, low HBV
DNA levels, non-Asian, HIV negative, high
degree of inflammation on liver biopsy
2. Other antivirals --> Tenofovir, Entecavir &
Telbivudine (a synthetic thymidine
nucleoside analogue)
Hepatitis B Serology
HBsAg First marker to appear & causes the
production of anti-HBs
HBsAg normally implies acute
disease (present for 1-6 months)
If HBsAg is present for > 6 months
then this implies chronic disease (i.e.
Infective)
Anti- Implies immunity (either exposure or
HBs immunisation). It is negative in
chronic disease
Anti- Implies previous / current infection.
HBc  IgM anti-HBc appears during
acute or recent hepatitis B
infection and is present for
about 6 months.
 IgG anti-HBc persists
HbeAg Results from breakdown of core
antigen from infected liver cells as is,
therefore, a marker of infectivity.
Marker of HBV replication and
infectivity
Example results
 Previous immunisation -->anti-HBs
positive, all others negative
 Previous hepatitis B (> 6 months ago), not
a carrier --> anti-HBc positive, HBsAg
negative
 Previous hepatitis B, now a carrier -->
anti-HBc positive, HBsAg positive
HEPATITIS C
RNA Flavivirus
Incubation period 6-9 wks
Spread by blood & body fluids, vertical
transmission (6%), needlestick injury (2%)
No vaccine available for Hepatitis C
Breastfeeding is not contraindicated
Risk factors
IVDU
Blood tx prior to 1991 (haemophiliacs)
Features
 Transient rise in serum aminotransferases
 Jaundice
 Fatigue
 Arthralgia
Investigations
HCV RNA --> Ix of choice for acute infection
Outcome
~15-45% --> clear acute infection
~55-85% --> develop chronic hepatitis C
Chronic hepatitis C
 Persistence of HCV RNA for 6m.
 Potential complications
 Rheumato--> arthralgia, arthritis
 Eye problems --> Sjogren's
syndrome
 Cirrhosis --> 5-20%
 HCC
 Cryoglobulinaemia--> Type II
(mixed monoclonal & polyclonal)
 Porphyria cutanea tarda (PCT)-->
esp if there are other factors such
as alcohol abuse
 Membranoproliferative GN
 Management of chronic infection
 Rx depends on the viral genotype
 Combination of protease inhibitors
(e.g. daclatasvir + sofosbuvir or
sofosbuvir + simeprevir) with or
without ribavirin are used
 Interferon based treatments are no
longer recommended
 Aim of Rx is sustained virological
response (SVR), defined as
undetectable serum HCV RNA 6m
after tx
 Complications of Rx
 Ribavirin SE --> haemolytic
anaemia, cough, cannot get
pregnant for 6m as it is teratogenic
 Interferon alpha SE --> flu-like sx,
depression, fatigue, leukopenia,
thrombocytopenia
Hepatitis C & pregnancy
 Trasmission rate from mother to child is
about 6%. Risk is higher if there is a high
viral load or coexistent HIV.
 Management
 Standard drug tx cannot be used in
pregnancy due to concerns about
teratogenicity
 HCV-positive pregnant women should be
monitored throughout pregnancy
 HCV RNA and LFTs should be done as
early as possible into prenatal care to
assess the risk of transmission and
degree of liver disease
if pruritic or they develop jaundice,

suspect intrahepatic cholestasis of
pregnancy and perform LFTs.
 Invasive procedures should be minimised
in mother and fetus to prevent vertical
transmission.
 The evidence base surrounding the use of
caesarean section vs vaginal delivery is
inconclusive, but it is not currently routine
practice to offer a caesarean section.
 Breastfeeding is not contraindicated in
mothers with hepatitis C
HEPATITIS D
Single stranded RNA Deltaviridae
Incomplete RNA virus that requires hepatitis B
surface antigen to complete its replication &
transmission cycle.
Spread in a similar fashion to hepatitis B
(exchange of bodily fluids)
Pts may be infected with hepatitis B & hepatitis
D at the same time.
Terminology
1. Co-infection --> Hepatitis B & Hepatitis D
infection at the same time.
2. Superinfection --> Hepatitis B surface
antigen positive patient subsequently
develops a hepatitis D infection.
Superinfection
Associated with high risk of fulminant hepatitis,
chronic hepatitis status & cirrhosis.
Diagnosis
Reverse PCR of hepatitis D RNA.
Management
Interferon is currently used, but with a poor
evidence base.
HEPATITIS E
RNA hepevirus
Spread by faecal-oral route
Incubation period 3-8 wks
Common in Central & SE Asia, North & West
Africa, Mexico
Causes a similar d/s to Hepatitis A, but carries a
significant mortality (~20%) during pregnancy
Does not cause chronic d/s
No increased risk of HCC
Vaccine is currently in development, but is not
yet in widespread use
EBV ASSOCIATED CONDITIONS
Malignancies associated with EBV infection
3. Burkitt's lymphoma (both African and
sporadic Burkitts)
4. Hodgkin's lymphoma
5. Nasopharyngeal carcinoma
6. HIV-associated CNS lymphomas
The non-malignant condition hairy leukoplakia is
also associated with EBV infection.
ENTEROVIRUSES
 Positive-sense single stranded RNA
viruses.
 The family contains the Coxsackievirus,
echovirus and rhinovirus as well as others.
 MC cause of viral meningitis in the adult
population but can cause a range of
different diseases, in both adults and
children esp HFM d/s, herpangina &
pericarditis
HERPES SIMPLEX VIRUS
2 strains --> HSV-1 and HSV-2.
Whilst it was previously thought HSV-1
accounted for oral lesions (cold sores) and HSV-
2 for genital herpes it is now known there is
considerable overlap
  Infection is often arrested at this stage and infection or
Features bacteria may remain dormant for years. BCG
 primary infection: may present with a  The peripheral lung lesion and the nodes >15mm Strongly positive Suggests
severe gingivostomatitis heal and may calcify. - strongly tuberculosis
 cold sores  The entire process if often asymptomatic. hypersensitive to infection.
 painful genital ulceration However, specific immunity develops and tuberculin protein
tuberculin skin tests become positive.
Management  In immunocompetent people, the initial 2. Heaf Test
1. Gingivostomatitis --> oral aciclovir, lesion usually heals by fibrosis.  Previously used in the UK but has been
chlorhexidine mouthwash  Those who are immunocompromised may since been discontinued.
2. Cold sores --> topical aciclovir although develop disseminated disease (miliary  Injection of PPD equivalent to 100,000
the evidence base for this is modest tuberculosis). units per ml to the skin over the flexor
3. Genital herpes --> oral aciclovir. Some surface of the left forearm.
patients with frequent exacerbations may Secondary (post-primary) TB  Read 3-10 days later.
benefit from longer term aciclovir  If the host becomes immunocompromised 3. Interferon gamma test
the initial infection may become  Used if :
Pregnancy reactivated.  Mantoux test is positive/equivocal
ELLSCS at term is advised if a primary attack of  Reactivation generally occurs in the apex  When Tuberculin test may be
herpes occurs during pregnancy >28 of the lungs and may spread locally or to falsely negative
Recurrent herpes during pregnancy --> more distant sites.
suppressive tx & should be advised that the risk  Possible causes of immunocompromise Investigations
of transmission to their baby is low include: 1. Sputum smear
 Immunosuppressive drugs including  3 specimens are needed
steroids  rapid and inexpensive test
 HIV  stained for the presence of AFB (Ziehl-
TUBERCULOSIS  Malnutrition Neelsen stain)
 The lungs remain the most common site  All mycobacteria will stain positive (i.e.
for secondary TB nontuberculous mycobacteria)
Mycobacterium tuberculosis
 Extra-pulmonary infection may occur in  Sensitivity 50-80%, decreased in
Rarely, it may be due to Mycobacterium bovis or
the following areas: individuals with HIV to ~20-30%
Mycobacterium africanum.
 CNS (TB meningitis - the most 2. Sputum culture
9th leading cause of death worldwide
serious complication)  Gold std investigation
In many cases, TB may remain dormant before it
 Vertebral bodies (Pott's d/s)  More sens than sputum smear & NAATs
progresses to its active form.
 Cervical lymph nodes  Can assess drug sensitivities
Notifiable disease.
(scrofuloderma)  Can take 1-3 wks (if using liquid media,
 Renal longer if solid media)
Epidemiology
 GI Tract 3. CXR
Mostly affects adults in their most productive
 Reactivation may be precipitated by  Upper lobe cavitation --> classical finding
years.
reduced immunity (ex malignancy, of reactivated TB
>95% deaths are in developing countries
immunosuppressive drugs like steroids)  Bilateral hilar lymphadenopathy
4. Nucleic acid amplification tests (NAAT)
Risk factors
Latent TB  Allows rapid dx (within 24-48 hours)
Strong Weak More sensitive than smear but less
 A state of persistent immune response to 
Having lived in Asia, Latin Malignancy stimulation of M.tuberculosis antigen sensitive than culture
America, Eastern Europe, or ESRF without clinical evidence of active TB. 5. Lateral Flow Urine Lipoarabinomannan Assay
Africa for years IVDU  ~30% of individuals exposed to M.  New method to dx TB
Exposure to infectious TB Malnutrition tuberculosis will develop latent TB and, if  It detects lipoarabinomannan, a
case Alcoholism untreated, ~5-10% will progress to active component of the mycobacterial cell wall,
HIV (20-30x higher risk) Congested TB within one hour.
Immunocompromised residence  Easier to perform and without the risk of
individuals (DM / on (nursing homes, Screening for latent TB laboratory
immunosuppressive tx, homeless 1. Mantoux test  More sensitive to diagnose TB in HIV
malnourished, haemato shelters)  Main technique used to screen for latent positive adults
malignancies) Smoking TB
Silicosis  0.1 ml of 1:1,000 purified protein Management
Apical fibrosis derivative (PPD) injected intradermally  PTB: 2EHRZ/4HR
 Result read 2-3 days later  Pyridoxine 10 mg/day should be
 False negative tests may be caused by: given to patients on isoniazid.
Most commonly affects the lungs.  Miliary TB  Those with high risk of neuropathy
 Sarcoidosis (pregnant women / PLHIV / elderly /
Primary TB  HIV DM / alcoholism / malnutrition /
 A non-immune host who is exposed to M.  Lymphoma chronic renal failure) should be
tuberculosis may develop a primary  Very young age (< 6m) given pyridoxine 30 mg/day.
infection of the lungs. Diameter Positivity Interpretation  TB Meningitis: 2EHRZ/10HR
 A small lung lesion known as Ghon focus <6mm Negative - no Previously  Bone and joint TB: 2EHRZ/4-7HR
develops in the mid/lower zone of the lungs. significant unvaccinated  Other EPTB: 2EHRZ/4HR
 The Ghon focus is composed of tubercle- hypersensitivity individuals may  Latent TB
laden macrophages. The combination of a to tuberculin be given the  3 months of Isoniazid (+ Pyridoxine)
Ghon focus and hilar lymph nodes is protein BCG and Rifampicin in <35years old
known as a Ghon complex 6-15mm Positive - Should not be  6 months of Isoniazid (+ Pyridoxine)
 Bacilli are transported through the hypersensitive to given BCG. in immunocompromised patients
lymphatics to the draining LN, which tuberculin protein May be due to
enlarge considerably and undergo previous TB Complications of treatment
caseation. 1. Immune reconstitution disease
 Typically 3-6 wks after starting Rx
 Often presents with enlarging lymph
nodes
Rifampicin Potent liver enzyme inducer
(R) Hepatitis
Orange secretions
Flu-like symptoms
Dose : 10mg/kg/day
Max dose : 600mg/day
Isoniazide Peripheral neuropathy: prevent
(H) with pyridoxine (Vit B6)
Hepatitis
Agranulocytosis
Liver enzyme inhibitor
Dose : 5-8mg/kg/day
Max dose : 300mg/day
Pyrazinamide Hyperuricaemia causing gout
(Z) Arthralgia, Myalgia
Hepatitis
Dose : 25mg/kg/day
Max dose : 1500mg/day
Dose adjustment if renal
impairment
Ethambutol Optic neuritis : check visual
(E) acuity before and during Rx
Dose : 15-25mg/kg/day
Max dose : 1200mg/day
Dose adjustment if renal
impairment
Streptomycin Avoided in renal impairment
Dose : 15mg/kg/day
Max dose : 1500mg/day
Akurit-4 H : 75mg
R : 150mg
E : 275mg
Z : 400mg
30-39kg : 2 tabs
40-54kg : 3 tabs
55-70kg : 4 tabs
>70kg : 5 tabs
LOIASIS
Filarial infection caused by Loa Loa.
Transmitted by the Chrysops deerfly
Rainforest regions of Western and Central Africa.
Features
 Pruritus
 Urticaria
 Calabar swellings --> transient, non-
erythematous, hot swelling of soft-tissue
around joints
 'Eye worm'--> the dramatic presentation of
subconjunctival migration of the adult
worm.
Treatment
Ivermectin / DEC
 High loa loa microfilaraemia is associated
with encephalopathy following Rx with
either Ivermectin or DEC.
 This occurs due to the death of vast
numbers of blood microfilaria.
 Both of these drugs are contraindicated if  Responds only to voice or pain/
loa loa microfilaraemia exceeds 2500 unresponsive
mf/ml.  Acute confusional state
 SBP <= 90 mmHg (or drop >40 from
normal)
 HR > 130/min
SEPSIS  RR >= 25/min
 Needs oxygen to keep SpO2 >=92%
Sepsis --> life-threatening organ dysfunction  Non-blanching rash, mottled/ ashen/
caused by a dysregulated host response to an cyanotic
infection.  Not passed urine in last 18 h/ UO < 0.5
Septic shock --> a more severe form sepsis, ml/kg/hr
technically defined as 'in which circulatory,  Lactate >=2 mmol/l
cellular, and metabolic abnormalities are  Recent chemotherapy
associated with a greater risk of mortality than
with sepsis alone' Amber flag criteria
 Relatives concerned about mental status
The term 'systemic inflammatory response  Acute deterioration in functional ability
syndrome (SIRS)' has fallen out of favour.  Immunosuppressed
 Trauma/ surgery/ procedure in last 6 wks
quickSOFA (qSOFA) score  RR 21-24
>= 2 of the following criteria  SBP 91-100 mmHg
 RR>20/min  HR 91-130 OR new dysrhythmia
 SBP </= 100mmHg  Not passed urine in last 12-18 hours
 Altered mentation  Temperature < 36ºC
 Clinical signs of wound, device or skin
SOFA score infection
A SOFA score >/= 2 reflects 10% overall
mortality risk Sepsis Six
1. Give Oxygen --> Aim SPO2 >94% (88-92% if
0
PaO2/FiO2 >400
at risk of CO2 retention e.g. COPD)
Platelets >150
2. Give broad spectrum abx
Bilirubin 20
3. Give IV Fluid challenges (NICE recommends
BP MAP >70
blous 500ml crystalloid over <15mins)
GCS 15
4. Take blood C&S
Creat <110
5. Take serum lactate
Urine output >500
6. Measure hourly urine output
1
PaO2/FiO2 <400
Platelets <150
Bilirubin 20-32
BP MAP 70 ACTINOMYCES ISRAELII
GCS 13-14
Creat 110-170 Gram-positive rods that form fungus-like
Urine Output >500 branched networks of hyphae-like filaments.
Commensal bacteria that become pathogenic
2
PaO2/FiO2 <300 when a mucosal barrier is breached.
Platelets <100
Bilirubin 33-101 Chronic, progressive granulomatous d/s caused
BP Dopamine <5 or dobutamine (any by filamentous Gram-positive anaerobic bacteria
dose) from the Actinomycetaceae family.
GCS 10-12
Creat 171-299 Features
Urine output <500  Usually occurs in the head & neck,
3
PaO2/FiO2 <200 although it may also occur in the
Platelets <50 abdominal cavity & in the thorax.
Bilirubin 102-204  Typically causes oral/facial abscesses
BP Dopamine 5.1-15 or epinephrine 0.1 with sulphur granules in sinus tracts.
or norepinephrine 0.1  May also cause an abdominal mass e.g.
GCS 6-9 in the RIF
Creat 300-440  The mass will often enlarge across tissue
Urine output <500 planes with the formation of multiple sinus
tracts.
Abdominopelvic actinomycosis occurs
4
PaO2/FiO2 <100 
Platelets <20 most frequently in individuals that have
Bilirubin >204 had appendicitis (65%).
BP Dopamine >15 or epinephrine >0.1
or norepinephrine >0.1 Pathology
GCS <6  On histological examination Gram-positive
Creat >440 organisms and evidence of sulphur
Urine output <200 granules.
 Sulphur granules are colonies of
organisms that appear as round or oval
Red flag criteria basophilic masses.
 They are also seen in other conditions
such as nocardiosis
Treatment
 Long-term abx tx, usually with penicillin
 Surgical resection is indicated for
extensive necrotic tissue, non-healing
sinus tracts, abscesses or where biopsy is
needed to exclude malignancy.
CROUP
Emergency Mx --> High flow O2, Neb Adrenaline
Single dose of oral Dexamethasone (0.15mg/kg)
to all children regardless of severity
Prednisolone is an alternative if dexamethasone
is not available
BUBONIC PLAGUE
MC form of plague in humans
Yersinia Pestis

Form of URTI seen in infants & toddlers Transmission

Parainfluenza virus --> majority of cases
Epidemiology
Peak incidence at 6 months - 3 years
More common in autumn
Features
 Stridor
 Laryngeal oedema & secretions
 Barking cough (worse at night)
 Fever
 Coryzal symptoms
MILD Occasional barking cough
No audible stridor at rest
No or mild suprasternal and/or
intercostal recession
The child is happy & is
prepared to eat, drink & play
MODERATE Frequent barking cough
Easily audible stridor at rest
Suprasternal and sternal wall
retraction at rest
No or little distress or agitation
The child can be placated and
is interested in its surroundings
SEVERE Frequent barking cough
Prominent inspiratory (and
occasionally, expiratory) stridor
at rest
Marked sternal wall retractions
Significant distress and
agitation, or lethargy or
restlessness (a sign of
hypoxaemia)
Tachycardia occurs with more
severe obstructive symptoms
and hypoxaemia
 Fleas transmit the bacteria from rodents to
humans via their bite.
 The bacteria can also be spread from one
infected human to another if it develops
into pneumonic plague (in the lungs) via
aerosolized particles.
Features
 Flu-like sx (3-7 days after exposure)
 Fever
 Headache
 Weakness
 Inflamed, tense & painful lymph nodes
Treatment
Typically abx such as streptomycin
BED BUGS
Cimex Hemipteru
Features
 Itchy skin rash / bites
 Allergic symptoms
Management
Topical hydrocortisone
Pest management
 House fumigation, washing bed linen &
using mattress covers

Admission Criteria
1. Moderate / Severe croup
2. < 6m of age
3. Known upper airway abnormalities (ex :
Laryngomalacia, Down's syndrome)
4. Uncertainty about dx (important ddx
include acute epiglottitis, bacterial
tracheitis, peritonsillar abscess & foreign
body inhalation)

Investigations
Clinical dx
CXR
 PA view will show subglottic narrowing -->
'steeple sign'
 Lateral view will show swelling of the
epiglottis --> 'thumb sign'

Management