Infectious disease Flashcards
Threadworm
Background:
AKA pin worm or enterobiasis
Most common parasitic infection in the UK, very widespread.
Normally affects children
Aetiology:
Nematode infection - enterobius vermicularis, typically white in colour and roughly 1cm in length
Risk factors:
Prevalence highest in ages 5-9 YO
Presentation:
Pruritus of the anus or vulva (tend to lay eggs around the vulva)
Typically worse at night (when worms lay their eggs)
Vaginal discharge
Urinary tract infections
Bed wetting that is not usual for them
May see worms around the anus or vulva region at night/during bathing
Asymptomatic
Threadworm Ix, Mx and prevention
Investigation/diagnosis:
Safeguarding if abuse is suspected
Clinical diagnosis if diagnosis is obvious
If uncertain - adhesive tape test to look for eggs can be done (place tape around perianal skin to look for eggs under microscope)
Stool examination is not recommended as is only positive in 5% of cases
Management:
General hygiene advice, shower everyday, regular bed linen and towel changes, regular hand washing
Advice for all family members to be treated if one member has an infection
Mebendazole 100 mg (can buy OTC) in those ages 6 months + (specialist advice for those under age 6 months)
Typically a single dose, should be repeated 2 weeks after initial dose to ensure infection is gone as it does not kill eggs.
2nd line - albendazole or pyrantel pamoate
Prevention:
General hygiene advice, shower everyday, regular bed linen and towel changes, regular hand washing
Hookworm
Background:
Typically infected in more tropical locations as they like to live in more humid climates.
Second most common helminthic infection in the world, affecting one in four of the world’s population
Not that common in the UK
Pathology:
Typically live in the small intestines of hosts
Infection spread by walking on, handling or laying on infected ground or soil
Eggs are passed through the stool, typically hatch within 1-2 days after being passed.
On contact with human host they penetrate the skin and are carried through the bloodstream to the heart and lungs
Penetrate alveoli and bronchial tree to the pharynx where they are swallowed
Work into the small intestines where they mature into adults, attach to the intestinal wall and lay eggs
Irritation occurs mostly due to GIT inflammation
Aetiology:
Parasitic nematodes.
Two types known to infect humans - ancylostoma duodenale and necator americanus
Risk factors:
Warmer climates
Hookworm presentation and investigation
Presentation: Asymptomatic mostly Nausea Abdominal pain Diarrhoea Iron deficiency anaemia Local skin irritation and pruritus Respiratory symptoms (dyspnoea) Anaemia and malnutrition can cause developmental delay in children/poor growth
Investigation/diagnosis:
Bloods - FBC (eosinophilia)
Stool microscopy for worms and eggs (diagnostic usually)
CXR - alveolar infiltration in migration stage
Hookworm management and prevention
Management:
Albendazole - most effective, may need multiple doses
Mebendazole 2nd line
Iron and vitamin supplementation B12, folate
If in cutaneous phase - local cryotherapy
More severe cases - surgical endoscopic removal to reduce the amount of parasites
Rapid reinfection is common in endemic areas
Prevention:
Do not walk barefoot on soil/outdoors
Don’t defecate outdoors
Don’t use human faeces or raw sewage as fertiliser
Community control is difficult in less developed countries due to lack of sanitation and resources
Malaria
Background:
Mortality is 0.2% and each year 500 million are affected
In endemic areas mortality is mainly in infants and those who survive to adulthood acquire significant immunodeficiency
Transmitted by bite of infected female anopheline mosquitoes; can also be vertically transmitted mother to baby
Types:
Plasmodium falciparum - most fatal; symptoms of mild infection which rapidly progress to fever with rigors, severe multiorgan failure, coma and death
Non-falciparum malaria - P. vivax, P. ovale, P.malariae which cause more benign illness but may relapse after treatments
Aetiology:
Protozoan parasite
Malaria pathology
Pathology:
Insect bite; sporozoites pass through skin and via bloodstream to the liver
Multiple inside hepatocytes as merozoites
After a few days the infected hepatocytes rupture releasing merozoites into the blood
Enter erythrocytes and cause subsequent rupture
Causes anaemia and release pyrogens causing rigors and fever
The sequence of entering and rupturing RBCs occurs harmoniously every day causing rigor, fever then severe sweating in constant cycle throughout infection
Infected RBCs with P. falciform adhere to the endothelium of small vessels causing vascular occlusion, severe organ damage to multiple organs
RBCs destroyed more causing jaundice, also invades the liver causing malfunction (jaundice)
P. ovale and P. vivax remain latent in the liver and this is responsible for relapses that may occur after treatment
Tests will show gametocytes of the mosquito in the blood
When more than 1% RBCs are infected it may cause cerebral malaria or blackwater fever
Malaria presentation and complications
Presentation:
Incubation period 10-14 days in P. vivax, P. ovale and P. falciform infection
18 days to 6 weeks incubation in P. malariae infection
Abrupt onset of rigors, fever (>40 degrees)
Tachycardia
Followed by profuse sweating for some hours later
May show anaemia and hepatosplenomegaly and jaundice
Nausea and vomiting, dry cough, headache, fatigue, pain
Hypoglycaemia is severe complication of malaria presents similarly to cerebral malaria so must be ruled out
Cerebral malaria: altered consciousness, confusion, convulsions, coma and eventually death.
Blackwater fever: severe haemolysis, haemoglobinuria (dark brown/black urine)
Complications - anaemia, liver failure, kidney failure, ARDS
malaria investigation and prevention
Investigation:
Blood testing: FBC (anaemia), blood smear (thick and thin with Giemsa stain GOLD STANDARD FOR DIAGNOSIS), creatinine and urine output, clotting screen, LFTs, U+Es, glucose, BM, ABG/lactate, urinalysis
Microscopy of thick (diagnosis of malaria) and thin (percentage of infected RBCS and species identification) blood smear
CXR
Rapid diagnostic test detects parasite antigen
Prevention:
Aware of risks
Bite avoidance: repellants, permethrin impregnated clothing, sleeping under impregnated bednets
Chemoprophylaxis: mefloquine, doxycycline, chloroquine, malarone: start drug at least 1 week before departure and continue for 4 weeks without interruption after return
Malaria management
Management:
Notifiable disease (public health)
P. falciform infection is a medical emergency due to fast degeneration of patient
Always immediate referral to specialists for management
Uncomplicated: symptomatic but no severe signs, vital organ dysfunction and parasitic count <2%
Non-falciparum gives chloroquine (0, 6, 24, 48 hours) + Primaquine for 2 weeks (to eradicate P. vivax and P. ovale from liver)
Uncomplicated P. falciparum gives ACT + Primaquine single dose
Falciparum malaria - quinine sulphate + doxycycline for 7 days
Severe falciparum malaria: presence of impaired conscious/seizures, AKI, shock, hypoglycaemia, pulmonary oedema, Hb <80g/L, spontaneous bleeding, acidosis, haemoglobinuria, parasitaemia >10%
Artesunate IV first line
Quinine IV with DW5% second line
Toxoplasmosis
Background:
Widespread global infection
Pathology:
Main host is cats, eggs are excreted in cat faeces then mature in the environment
Potentially ingested by secondary hosts
Can transmit to pregnant mothers, especially during the 1st trimester, incidence increases from 14% to 59%
Primary infection is usually subclinical but can lead to chorioretinitis or may damage foetal in pregnancy
Reactivation of latent infection in immunocompromised patients may cause life-threatening encephalitis
Aetiology:
Toxoplasma gondii, an intracellular protozoan parasite
toxoplasmosis presentation, Ix and Mx and prevention
Presentation:
Mostly asymptomatic in healthy non-pregnant individuals
Ocular toxoplasmosis - visual symptoms, floaters, uveitis, reduced auticity
Immunocompromised - encephalitis, pneumonitis, multiorgan failure and shock
Congenital infections
Neonates - convulsions, microcephaly, hepatosplenomegaly, jaundice, hydrocephalus, mental retardation, defective vision
Investigation/diagnosis:
Serological screening in pregnancy (IgG and IgM)
MRI or CT for brain lesions
Foetal USS if suspected maternal infection
Management:
Healthy non-pregnant people - no treatment unless symptoms are severe, persistent or incurred through blood products or lab transmission
Treated with pyrimethamine, sulfadiazine and folinic acid for 4-6 weeks
If positive during pregnancy - given spiramycin ASAP then treatment as above until term or until foetal infection documented
Immunocompromised - trimethoprim/sulfamethoxazole is effective
Prevention:
Avoid cleaning cat litter
Good hygiene around cats/cat faeces
Amoebiasis
Background:
Infection of the GIT with entamoeba species
Infects approx. 50 million people worldwide, of which 100,000 die annually
Pathology:
Transmitted by contaminated water, ingestion of mature cysts in food/water or contamination with faeces.
Cysts enter small intestines and release active amoebic parasites which invade the epithelial cells of the large intestines, causing flask shaped ulcers. Infection can then spread from intestines to other organs (lungs, liver, brain etc.) via the venous system.
Causes amoebic dysentery
Asymptomatic carriers pass cysts in faeces and carriage state can persist indefinitely
Cysts remain viable for up to 2 months
Incubation may be between 7 days - 4 months
Aetiology:
Protozoan entamoeba histolytica
Risk factors:
Common in south and central america, west africa and southeast asia
Travellers and immigrants
Residents of institutions
Amoebiasis presentation, Ix and Mx
Presentation:
Often asymptomatic
Abdominal pain and diarrhoea, later developing dysentery
Rectal bleeding
Abdominal mass (usually in RIF)
Hepatic amoebiasis - sweating, pyrexia, painful liver/diaphragm, weight loss, fever, hepatomegaly
Investigation/diagnosis:
Stool sample
Bloods - FBC (leukocytosis), ESR, LFTs, parasite serology
PCR test
USS, CT, MRI
Proctoscopy, sigmoidoscopy, colonoscopy for mucosal scrapings and biopsy
Management:
Metronidazole antibiotic for acute invasive amoebic dysentery
Diloxanide furoate for asymptomatic patients (10 day course)
Fluid and electrolyte replacement
Gastric suction
Blood transfusion PRN
Candidiasis
Background:
Infection ranges from local to disseminated
Most severe/common in immunocompromised patients
Most common fungal infection within hospitals
Pathology:
Types: Oral Oesophageal Vulvovaginal Skin Invasive
Aetiology:
Combination or various different candida infections, most commonly candida albicans
Best like fungi which can be part of the normal flora of the human body
Candidiasis risk factors
Immunocompromised patients (including diabetics) Antibiotics use Poor oral hygiene Intensive care patients Pregnancy Radiotherapy Steroid inhalers (oral thrush) Oral steroids
oral thrush overview
Very common
Typically presents with sore mouth, coated tongue, bad breath
Coating is easily removed showing red mucosa
Can bleed easily on contact
Take swabs to confirm species but is clinical diagnosis
If recurrent may swab, history (oral or inhaled steroid use) or take bloods, urinalysis to investigate cause (diabetes, HIV)
Mx with topical agents: daktarin gel or nystatin solution (antifungal mouthwashes) used for a week or longer
If not responding swab for resistance
oesophageal candidiasis overview
Normally progresses from oral thrush
Oral symptoms along with dysphagia, retrosternal pain and odynophagia
Normally associated with treatment of malignancy (chemo or radiotherapy)
If HIV positive then need urgent admission to hospital as is an AIDS defining illness
Refer to secondary care as it can become a severe infection
Treated with oral fluconazole 200-400 mg BD for 2-3 weeks
Urgent admission to hospital for any signs of systemic illness.
vulvovaginal thrush overview
Very common
Often caused by fluctuation of oestrogen, vaginal flora and pH
70% of women will likely have thrush at some point
One of the most common causes of vaginitis
Symptoms include pruritus, vulval soreness, discharge, dyspareunia, dysuria.
Take swabs of discharge to rule out STIs
Emollients for itching or excoriated, avoid irritants like perfumed soaps or bubble baths
Intravaginal or topical clotrimazole and oral fluconazole one off treatment
If symptoms persist after 7-14 days then follow up is needed to investigate underlying causes
Skin infections (candidiasis) overview
Typically on the hands, feet or moist skin folds
Areas are sore, itchy, erythematous
Skin can slough off or can be white like discharge
Intertrigo is a common form
Typically only investigate for recurrent or non-responsive treatment
Topical antifungals normally treat this well
Miconazole cream topically 2-3 x daily for a week
Daktacort (hydrocortisone + miconazole) helps with itching and infection
Invasive candidate infection overview
Variety of severe disease caused by candida infection, most commonly candidemia
Normally has underlying immunocompromise or critical illness, abdominal surgery, implants or catheters
Low index of suspicion for those with spiking fever, neutropenic and have risk factors
Take blood cultures, swab any catheter lines, culture of bodily fluids, serology testing for fungal disease beta D glucan
Mx IV antifungal agents (caspofungin, fluconazole, voriconazole)
Always discuss with infectious disease specialist for best management
Crytococcus
Background:
Invasive budding yeast fungus
Major cause of mortality in HIV +ve patients worldwide despite antiviral therapy
Pathology:
Abundant in soil contaminated with pigeon droppings
Once infected, can affect several organs but mostly causes meningitis or meningoencephalitis
Aetiology:
Cryptococcus yeast species
Two serotypes - type A (majority of cases) and type D
Risk factors:
Immunocompromised patients are most at risk (HIV +ve, diabetes, hepatic cirrhosis, steroids, sarcoidosis, connective tissue disorders)
Solid organ transplant recipients
Cryptococcus presentation, investigation, management and prevention
Presentation: Cough Pleuritic chest pain SOB Headache N+V Confusion and behavioural changes Brain abscess Meningitis (neck stiffness, photophobia)
Investigation/diagnosis: Bloods - cultures, FBC, LFTs Urinalysis and cultures LP - CSF analysis for fungal meningitis CXR MRI
Management:
Fluconazole if mild for minimum of 8 weeks
Amphotericin B if severe
Maintenance therapy low dose of oral fluconazole for 6-12 months
Prevention:
Prophylaxis with fluconazole in HIV+ve patients with CD4 count <100cell/mm3 (not always effective)
Histoplasmosis
Background:
Systemic fungus found in soil, widespread
Common in the USA
Pathology:
Found in bat/bird droppings and soils.
Transmitted via inhalation and usually occurs as an atypical pneumonia
Affects organs and can cause organ failure in severe cases
Aetiology:
Histoplasmosis fungal infection
Risk factors:
Immunocompromised patients
Histoplasmosis presentation, Ix, Mx and prevention
Presentation: Fever, chills, headache Dry cough Muscle aches Chest discomfort Joint pain Rash Immunocompromised patients - disseminated infection, fever, dyspnoea, cough, loss of weight, prostration with hepatosplenomegaly, usually fatal within 6 weeks.
Investigation/diagnosis:
Clinical history and presentation
Swab cultures
Management:
Antifungal - itraconazole for mild-moderate cases
Amphotericin in severe cases if itraconazole fails
Prevention:
Face masks in high risk environment e.g. poultry workers
Prevent exposure
Pneumocystis infection
Background:
Atypical fungi that causes pneumonia in humans and occasionally extrapulmonary disease
Widespread globally
Major cause of morbidity and mortality among immunocompromised people
Leading AIDS-defining opportunistic infection in HIV +ve people
Pathology:
Causes fungal pneumonia
Aetiology:
Pneumocystis jirovecii
Risk factors:
Immunocompromised patients are most at risk (HIV +ve, steroids, chemotherapy, organ transplant patients, severe malnutrition etc.)
Pneumocystis presentation, Ix, Mx and prevention
Presentation: Cough - usually non-productive Exertional dyspnoea Fever Tachypnoea Chest pain Underlying conditions (AIDS, immunocompromised) Scattered crackles and/or wheezes may be present Hepatosplenomegaly Lymphadenopathy Ocular disease
Investigation/diagnosis: Bloods - LDH elevated, ABG PCR test CXR/CT Sputum sample Lung biopsy Spirometry
Management:
High dose co-trimoxazole
Prevention:
High dose co-trimoxazole
Gram staining morphology
Differential stain based on cell wall structure (cellular morphology)
Cocci - round
Rods - bacilli
Clusters - cocci in clusters
Most food poisoning bacteria are gram negative bacillus
Lyme disease
Background:
Quite rare but incidences are rising
In the UK is most common in Exmore, new forest, south downs etc. where deer are present
Peak age of incidence are 24-44 and 45-65 YO
Pathology:
Disease is caused by infection and body immune response to the infection
Different strains cause different clinical manifestations
Transmitted from host to host by ixodes ticks or deer ticks
Ixodes ticks emerge from larval form in summer and feeds on one animal host, then becomes nymph and feeds only once again on another host (humans can be victims in this stage)
In autumn the adult tick emerges to feed on deer again once. Humans can also be host at this stage. The tick must be significantly infected to pass on spirochaete infection
Often the host clears the infection and remains asymptomatic but seropositive OR elicits immune response causing clinical presentation
Aetiology:
Caused by spirochaete bacterium borrelia burgdorferi
Lyme disease risk factors and presentation
Risk factors:
Areas with high prevalence
Presentation:
Early/stage 1/localised disease: circular rash at site of infestation within 3-36 days. Rash is round/oval, pink/red or purple. Often central erythema with sparing around it gives a target-like appearance. Eventually resolves after some weeks
later/stage 2 disease/disseminated: flu like symptoms; malaise, muscle and joint pains, fever, tiredness, nausea or vomiting
Neurological disorders can occur in 10% untreated cases: uni/bilateral facial nerve palsies, meningism, meningitis, mild encephalitis, peripheral mononeuritis
Cardiovascular problems
Lymphocytomas - bluish red nodular lesions typically on earlobe or nipple
Late/stage 3 disease: arthritis, acrodermatitis chronica, late neurological disorders (polyneuropathy, chronic encephalomyelitis, vertigo and psychosis), chronic lyme disease
Acrodermatitis chronica atrophicans - blue discolouration on top of feet and hands
Lyme disease investigation and management
Investigation:
Clinical diagnosis of classical target rash or with erythema migrans and tick bite history
Bloods - antibody testing for B. Burgdorferi
PCR testing for new onset arthritis and symptoms of lyme disease
Management:
Remove tick with fine tipped tweezers pull upwards without twisting
Clean site after with antiseptic
Rash: Treat oral antibiotics for 2-3 weeks doxycycline or amoxicillin
Erythema migrans - doxycycline 100 mg BD for 3 weeks or amoxicillin 500 mg TDS for 3 weeks if allergic to doxycycline
Seek advice from infectious diseases for any other symptoms with likely history of tick bite
Flu-like symptoms, facial palsy or neurological symptoms after tick bite - speak with infectious disease specialists and consider serology testing. If there is a high suspicion of Lyme disease, treat while awaiting results.
Salmonellosis
Background:
Salmonella gastroenteritis
One of the most common forms of food poisoning worldwide
Pathology:
Found in foods such as chicken and other poultry
Typically invade intestinal mucosa and produce toxins causing GIT symptoms from inflammation
Incubation between 6-72 hours
Aetiology:
Salmonella Spp. bacteria toxins
Risk factors:
Contaminated foods
Undercooked foods
International travel to regions with poor hygiene and sanitation or lack of farm vaccination
Salmonellosis presentation, Ix, Mx and prevention
Presentation: Most symptoms are mild and self-limiting Diarrhoea (can be bloody) Fever Abdominal cramping N+V Symptoms tend to last 4-7 days
Investigation/diagnosis:
>7 days diarrhoea - send off stool microscopy
Dehydration status
Bloods for ongoing symptoms - U+Es (electrolyte disturbance)
Management:
Good fluid intake, eating little and often stick to bland foods
Rest, avoid public areas like schools/work until 48 hours after last bout of diarrhoea/vomiting
Loperamide (CI for IBD, dysentery, shigella, E. coli, pseudomembranous colitis)
Antibiotics only in >50 YOs, immunocompromised or under 6 months old
Prevention:
UK vaccinate livestock such as hens
Shigellosis
Background:
Highly contagious
Human and apes seem to be only natural hosts
Rare in the UK
Pathology:
Spread by contaminated water, swimming pools and foods
Causes bacterial dysentery due to bacteria causing damage and inflammation to the colon
Incubation period of 1-3 days
Aetiology:
Gram negative bacilli shigella
Risk factors:
Recent travel abroad
Shigellosis presentation, Ix, Mx and prevention
Presentation: Normally very watery diarrhoea, can be bloody, mucus and pus Abdominal pain Tenesmus Fever and malaise Self limiting normally
Investigation/diagnosis:
Stool sample for culture >7 days diarrhoea
Dehydration check
Bloods for ongoing symptoms - U+Es for electrolyte disturbances
Management:
Oral rehydration
Paracetamol for pain and fevers
Consider antibiotics for positive stool sample (only reduce symptoms by 1-2 days) often not given/needed as self-limited
Do NOT give antimotility agents due to complications such as toxic megacolon
Avoid public space (school, work) until 48 hours after V+D has ceased to prevent infection
Inform local public health team as notifiable disease
Prevention:
Good hygiene
E. coli bacteria
Normal intestinal bacteria
Spread via contact with infected faeces, unwashed salads or contaminated water
E.coli 0.157 produces shiga toxin causing cramps, bloody diarrhoea and vomiting and can lead to haemolytic uraemic syndrome therefore should AVOID antibiotics if suspected infection
Campylobacter bacteria
Most common bacterial cause of gastroenteritis (travellers diarrhoea)
Gram negative curved or spiral shaped bacteria
Spread from improperly cooked poultry, untreated water or unpasteurized milk
Usually resolves around 3-6 days, causes abdo cramps, diarrhoea (bloody), vomiting, fever
Consider antibiotics after isolating bacteria if there are severe symptoms or other comorbidities - treat with azithromycin or ciprofloxacin
Staph aureus toxin
Can produce enterotoxins on foods such as eggs, diary, meat
Causes diarrhoea, profuse vomiting, abdo cramps and fever
Resolve within 12-24 hours
Cholera
Background: Acute diarrhoeal infection in the GIT Linked to epidemics and pandemics Not usually seen in the UK Most common in southeast asia, africa and south america 3-5 million people affected annually
Pathology:
Water-borne infection caught by ingestion of faecally contaminated water or shellfish then leads to infection of the GIT
Incubation is usually 2-5 days but can sometimes be a few hours and are infectious for 7-14 days.
Produces an AB type enterotoxin (binds to host cells and viral component) enabling it to enter the cell and increase loss of chloride ions during viral replication process, causing an increase loss in salt and water in the GIT leading to extreme watery diarrhoea which can be fatal if dehydration is not corrected with clean water.
Aetiology:
Caused by the enterotoxin subunit-A of Vibrio cholerae bacterium (gram negative comma shaped bacteria)
There are over 100 serotypes of V. cholerae but only two cause disease - O1 (has two variants called classical and EI Tor) and O139.
cholera risk factors and presentation
Risk factors:
Poor sanitation in endemic areas
Poor water supply/sanitation in endemic areas
Poorly cooked seafoods in endemic areas
Presentation:
75% asymptomatic
High volume of watery diarrhoea (rice water stools)
Severe dehydration and circulatory collapse (hypovolaemia)
N+V
Fluid loss can be up to 20L per day
Cholera investigation and management and prevention
Investigation/diagnosis:
Stool culture and sensitivities
Dehydration status (1kg of weight loss = 1L fluid loss roughly)
Bloods - U+Es, FBC, WCC
Management:
Oral rehydration therapies
IV fluids for severe dehydration
Antibiotic treatment to decrease volume and duration of diarrhoea by 50% is recommended for patients with mod-severe dehydration (tetracycline, doxycycline or ciprofloxacin often used) but avoid if possible for resistance purposes
Prevention:
Improved sanitation
Boil water before drinking, add chlorine tablets or drink bottled water
The UK has licensed oral vaccines for those travelling to remote areas where access to medical treatment is limited or aid workers in disaster relief/refugee camps. It is effective against serotype O1 only for up to 2 years preventing 50-60% of cholera episodes.
Primary immunisation for ages 6+ is two doses of oral vaccine (sachets) given 1-6 weeks apart with an advised booster to be taken within 6 months (ages 2-6) or 2 years (6+) since primary vaccination
Botulism
Background:
Widespread environmental (soil) bacteria that can cause rare infection
There are three naturally occurring forms as a result of biological warfare.
It is regarded as the most lethal substance known, an estimated 1g could kill 1 million people.
Three types: infant botulism (honey), food-borne (home canning) and wound botulism (contaminated wounds)
Seven types of exotoxin exist, only A, B, E and F affect humans
Exotoxins affect the neurological system
Pathology:
Found commonly in the soil, it is neutralised by water so cannot be dispersed in this.
Only survives in anaerobic conditions, produces spores
Food-borne - when spores germinate and bacteria reproduce in an environment outside of the body producing toxins, causes illness when food is ingested
Wound botulism - organism enters an open wound and produces spores, it is the most common in IV drug use
Infant botulism - rare aside from the USA where it is the most common type. Babies ingest spores which germinate in the gut and release toxins, only occurring in children due to not having natural defences against spores to prevent germination.
Aetiology:
Botulinum toxin of Clostridium botulinum (anaerobic gram positive bacillus)
Botulism risk factor and presentations
Risk factors:
IV drug use
Presentation: Occurs within 2-8 days after toxin exposure Symmetric descending flaccid paralysis Ptosis, accommodation failure, pupil fixation (facial and oculomotor nerve paralysis) Dry mouth and throat Dysphagia N+V Abdominal distension Problems urinating Constipation Blurred vision Diplopia Slurred speech Tachycardia Respiratory paralysis Muscle weakness
botulism investigation, management and prevention
Investigation/diagnosis: Bloods - serum toxin Urinalysis Stool microscopy Vomit or gastric fluid samples Spirometry Pulse oximetry ABGs
Management:
Monitor for respiratory failure
Polyvalent antitoxin (A, B, E types) must be given promptly
With supportive care of patient to monitor paralysis
Mechanical ventilation if respiratory paralysis
Prevention:
Good food preparation and sanitation helps minimise cases
There is no current vaccine licensed in the UK or effective against all serotypes
Tetanus
Background:
Rare in the UK, largely a disease where there is inadequate vaccination
Pathology:
Found in soil, particularly soil rich manure as well as dust and faeces.
Produces spores that enter a wound and cause muscle rigidity and spasms 3-21 days post infection
One exotoxin is produced by spores.
Infection spreads via lymph and blood, transported up nerves and binds irreversibly to neurons
Prevents inhibition of motor reflex responses to sensory stimuli, resulting in muscle spasms which can be severe enough to tear muscles, cause long-bone fractures or spinal compression fractures and rigidity
Aetiology: Clostridium tetani (anaerobic gram positive bacillus).
tetanus risk factors and presentation
Risk factors: >60 YO Lack of immunisation Drug addiction Contaminated wounds (soil, rusty metals, manure) IM injections in surgery Poor obstetric techniques Neonatal tetanus - rural areas where deliveries are at home without sterile procedures
Presentation: Exaggerated muscle reflexes and uncontrolled muscle spasms Lockjaw (trismus) Dysphagia Risus sardonicus (sneering appearance) Neck stiffness Opisthotonos (in neonates) Complications - aspiration pneumonia, laryngospasms and asphyxia, fractures, apnoea, HTN, cardiac arrest, PE
tetanus investigation and prevention
Investigation/diagnosis:
Clinical diagnosis
Spatula test - touch back of the pharynx with spatula to elicit bite reflex instead of gag reflex in tetanus infected individuals
Prevention:
Vaccine given as a standard tetanus, diphtheria and polio dose for adults and school leavers
Primary course for those under age 10 also contains acellular pertussis and pre-school booster given.
Doses given at 2, 3 and 4 months old then after age 10 given 3 more doses with an interval of at least 1 month in between doses.
Give booster three years after completion of primary course (under 10) or five years after primary dose if over age 10.
Second booster given to everyone after 10 years after first booster
CI in allergies, neurological conditions, unwell with fever
tetanus management
Management:
Human anti tetanus Ig given via IV in ICU
Penicillin or metronidazole given to prevent bacterial growth (which produces more exotoxin)
Clean the wound
Consider prophylactic sedation and intubation, benzodiazepines to prevent/control spasms
Botulinum toxin may reduce symptoms
Tetanus toxoid booster vaccine injection
Recovery can take months and significant weight loss if always seen
Management of tetanus prone injuries:
Wounds sustained >6 hours before surgical treatment or any wound with exposure to soil/manure, foreign bodies, compound fracture or clinical evidence of sepsis.
Thoroughly clean the wound
Give human tetanus Ig ASAP if high risk
Where fully vaccinated or up to date with schedule, no further doses are recommended
If unknown status, immunocompromised or not up to date, reinforcing dose of Td/IPV should be given when treated and further doses given to complete recommended five dose schedule
Diphtheria
Background:
Acute URTI that can sometimes infect the ski
Cases are now rare due to herd immunity
Mainly occurs in epidemics
Pathology:
Pathogenic only in humans, spread via respiratory droplets
Incubation usually 2-5 days but can be up to 10 days
Pharyngeal or cutaneous infection is caused by toxigenic strains
Exotoxin produced affects a number of tissues including the heart, peripheral nerves and kidneys
Aetiology:
Corynebacterium diphtheria AB toxin (gram positive aerobic bacillus)
Risk factors:
Poor hygiene and living conditions
Lack of immunisation
Adults at risk of losing immunisation without boosters
Diphtheria presentation, investigation, management and prevention
Presentation: Early symptoms - common cold/URTI Rhinnorhoea which begins very watery then becomes purulent and blood stained Fibrinous pseudomembrane usually on the respiratory mucosa which may cause respiratory obstruction Dysphagia Paralysis Heart failure Asymptomatic
Investigation/diagnosis:
Throat/sputum swab culture is diagnostic
Management:
Antitoxin prevents entry to cells
Antibiotics - erythromycin, azithromycin, clarithromycin or penicillin
Can give antibiotic prophylaxis to those who have had close contact
Prevention:
DTP vaccine - inactivated toxin
erythema infectiosum
Background:
AKA slapped cheek
Very common childhood infection occurring between the ages of 3-15 years
Pathology:
Spread via droplet transmission, blood/bone marrow transplant or vertical transmission (mum-baby)
Typically takes 4-20 days incubation
Lifelong immunity after being exposed to the virus
Aetiology:
Parvovirus B19
Risk factors:
Most common in children
erythema infectiosum presentation and differentials
Presentation:
Asymptomatic in 25% of infections
Non-specific coryza symptoms
Headaches
Rhinitis
Sore throat
Low grade fever
Typically 7 days after being symptoms free develop facial rash - slapped cheek red face rash
Can spread to the rest of the body 2-3 days after appearing on the face
Arthropathy (more common in adults than children)
Differentials:
Rubella: very similar rash over the whole body
Measles: check for Koplik spots
Scarlet fever: look for strawberry tongue
Roseola: similar rash
Drug eruption: new medications?
erythema infectiosum investigation and management and pregnancy
Investigation/diagnosis:
Clinical diagnosis
If uncertain/pregnant - PCR test for parvovirus B19
Bloods - specific to IgM and IgG checking for immunity and current infection
Management:
Self limiting viral infection
Regular OTC analgesia, symptomatic management
Avoid any immunocompromised or pregnant people
Do NOT need to avoid school, but do need to make anyone pregnant at the school aware
Pregnancy:
30% chance of passing infection onto baby
Baby fatality 10% if infected, higher in the first trimester
Can cause congenital abnormality
If been in contact with someone infected, must be investigated (ask if any previous history of parvovirus in childhood, bloods and PCR)
If they have active infection: refer to foetal medicine unit to check for foetal infection
rabies
Background:
Occurs in >150 countries
Viral infection affecting the nervous system, causing encephalitis or meningoencephalitis
Not all individuals exposed to rabies virus develop the disease, however once symptoms occur, rabies is almost always fatal
Pathology:
Carried by warm blooded animals (foxes, bats, dogs, raccoons)
Transmitted by saliva into bite wounds most commonly. The virus is weak and inactivated by drying, UV rays and detergents
4-13 weeks incubation
Virus infects neural tissue and evades the immune response, amplification occurs and the virus spreads along the nervous system, entering spinal ganglions
Once in ganglions the onset of pain or paraesthesia begins and spreads rapidly with marked encephalitis
Finally the virus spreads peripherally including salivary glands
Aetiology:
Rhabdovirus (bullet shaped) single stranded RNA virus
rabies risk factors and presentation
Risk factors:
Children are more at risk as are more likely to approach animals without caution
Travel to areas with high prevalence
Presentation: Insidious onset Pain and paraesthesia around wound Malaise, fever, headaches, pruritus that spreads around the body Muscle spasms Sore throat Hydrophobia due to difficulty swallowing Hallucinations Behavioural disturbances Ascending flaccid paralysis with sensory disturbances and coma Respiratory paralysis resulting in death
rabies investigation, managent and prevention
Investigation/diagnosis:
PCR for viral antigens
Nuchal skin biopsy (hairline from base of neck sample)
Post-mortem tissue biopsy
Management:
Clean wound
Immunisation with rabies Ig (RIG)
Prevention:
Vaccine available - attenuated virus
cytomegalovirus
Background:
A member of the human herpes virus family
Infection is worldwide and usually asymptomatic, but can cause severe illness in congenital infection or immunocompromised hosts
Most common presentation is gastroenteritis
Most serious complication is pneumonia
Pathology:
Uses human hosts, transmitted by saliva and sexual contact
UTI moves to kidneys, salivary glands, cervix and testes
May cause a mononucleosis infection in healthy individuals but can cause severe illness in congenital infection or immunocompromised patients
Remains in a persistent state within the host after the initial infection, controlled by the immune system.
Intermittent viral shedding can take place in immunocompetent people
Aetiology:
Human herpes virus
Risk factors:
Congenital infection/pregnancy
Immunocompromised patients
cytomegalovirus presentation and investigations
Presentation:
Often asymptomatic
Glandular fever like symptoms
Foetal malformations in congenital CMV disease
Hepatitis
Pneumonia
In immunocompromised patients - pneumonitis, CNS, colitis, hepatitis
Investigation/diagnosis: Measure CMV load Urinalysis - CMV load Bloods - CMV load, FBC, serum creatinine and LFTs CXR - pneumonia CT - lung infiltrates Biopsy
cytomegalovirus management and prevention
Management:
Antivirals - IV ganciclovir, foscarnet to reduce viral load for a minimum of 14 days
Additional 1-3 months of appropriate prophylaxis should be considered to minimise risk of recurrent infection (determine duration using PCR monitoring of viral load)
Organ transplants
Prevention:
No vaccine
All organ donors and recipients are screening for CMV status before or after transplantation
Antiviral prophylaxis can be given for 3-6 months in some circumstances
Epstein-Barr virus
Background:
EBV AKA human herpesvirus 4 is widespread and one of the most common human viruses worldwide
Member of the herpes virus family
Most people are infected with EBV at some point in their lives
Most common cause of infectious mononucleosis
Pathology:
Spread commonly through bodily fluids (saliva)
Infects B lymphocytes and epithelial cells
Can cause infectious mononucleosis in roughly 50% of primary infections
Also associated with tumours such as Burkitt’s lymphoma, Hodgkin’s disease, B-lymphoproliferative disease
Nasopharyngeal carcinomas and oral hairy leukoplakia can also be associated.
In congenital infection can cause X linked lymphoproliferative syndrome
Can also play a role in autoimmune diseases like SLE, RA and MS but pathology is unknown.
Primary infection is often mild or asymptomatic or causes mumps.
After primary infection the virus becomes latent however in immunocompromised individuals may reactivate
Aetiology:
HHV-4/EBV viral infection
Risk factors:
Immunocompromised - risk of reactivation of latent infection
Epstein-Barr virus presentation, Investigation and management and prevention
Presentation: Fatigue Fever Inflamed throat Lymphadenopathy Hepatosplenomegaly Rash
Investigation/diagnosis:
Clinical diagnosis (difficult due to vague presentation)
PCR and viral antibodies (MONOSPOT test - looks for heterophile antibodies)
Bloods - FBC (WCC and monospot test), LFTs (raised ALT)
Management:
Usually self limiting within 2-4 weeks, fatigue can last for longer
Do not need to isolate from school (with infectious mononucleosis)
Arrange hospitalisation for signs of dehydration, stridor or complication such as ruptured spleen
Avoid exercise for at least one month after recovery due to risk of splenic rupture
Fluid intake
Rest
Regular analgesia as needed
Treat immunocompromised states
Prevention:
Avoiding kissing, sharing personal items, drinks with those showing signs of infection
Herpes simplex virus
Background:
Most individuals are infected with HSV-1 by 1-2 years of age (1 = above waist)
HSV-2 tends to be with onset of sexual activity (2 = below waist)
Usually is asymptomatic
Most contagious when virus filled lesions are present but can also be shed when asymptomatic
In individuals with atopic dermatitis can present with very severe herpes virus blistering in these areas due to weakness of skin barriers (eczema herpeticum) and also can have very similar severe viral blisters in those with burn injuries.
Complications include meningitis or encephalitis if viral infection reaches the brain (typically in the TEMPORAL LOBE)
Pathology:
Primary infection occurs through a break in the mucous membranes of the mouth, throat, eyes, genitals or skin abrasions. Can also be spread via vertical transmission
Virus internalised in cells then begins lytic cycle of proliferation
Cells burst and virus spreads to other cells
Can also infect sensory neurons and lays latent there in the trigeminal ganglia (oral herpes) or sacral ganglia (genital warts) and lies dormant until an immunocompromised state allows for the virus to travel back down the neurons and infect the cells
Triggers include stress, skin damage and viral illness.
Aetiology:
HSV-1 and HSV-2
Enveloped, double stranded DNA viruses
herpes simplex virus risk factors and presentation
Risk factors:
Triggers include stress, skin damage and viral illness.
Presentation: Oral: Often asymptomatic Tingling or burning sensation Blisters appearing on the sides of the mouth, heal within a few weeks and often painful Lesions on palate, lip, gums, tongue LAP Pharyngitis
Genital herpes:
Ulcers and pustules of labia, mons pubis, vaginal mucosa, cervix, shaft of penis
Resolve within a week
Herpetic whitlow:
Finger has been in contact with lesion directly (autoinoculation)
Blisters on fingers
Easy spread to other areas of the body such as the trunk, extremities and head
Eczema herpeticum:
In individuals with atopic dermatitis can present with very severe herpes virus blistering in these areas due to weakness of skin barriers
Eyes: Keratoconjunctivitis Blurry vision Pain Redness Tearing
Neonatal infection:
Skin, eye or mucous membrane infection
CNS infection (lethargy, seizures, irritable, LP changes suggestive of HSV encephalitis)
Disseminated infection (sepsis and organ failure)
Immunocompromised:
More frequent reactivation
More severe blistering
More symptoms such as lesions of the oesophagus or lungs
herpes simplex virus investigation and management
Investigation/diagnosis: Clinical diagnosis PCR viral DNA Viral cultures Viral antibodies LP for meningitis or encephalitis symptoms - shows increased RBCs, WBCs and protein CT, MRI, EEG
Management: Usually self limiting Topical or systemic antivirals within prodromal phase to help speed up recovery Topical analgesic OTC for oral lesions Acyclovir, famciclovir or valacyclovir
influenza
Background:
Types A and B are most common
Type A has different subtypes (H and N) each with different strains e.g. H1N1 is swine flu and H5N1 is avian flu
Outbreaks typically occur in the winter
Pathology:
An RNA virus with three types (A, B and C)
Complications - otitis media, sinusitis, bronchitis, viral pneumonia, secondary bacterial pneumonia, worsening of chronic conditions, febrile convulsions (young children) and encephalitis.
Aetiology:
Influenza RNA virus
Risk factors:
Immunocompromised or long standing comorbidities
influenza presentation, investigation, management and prevention
Presentation: Fever Coryzal symptoms Lethargy and fatigue Muscle and joint aches Headache Dry cough Sore throat Anorexia (loss of appetite)
Investigation/diagnosis:
Usually clinical diagnosis
Viral nasal or throat swabs (PCR) for diagnosis and notification to public health to monitor number of cases
Management:
Public health monitor the number of flu cases and provide guidance on when there is enough cases to justify treatment for suspected flu
Healthy individuals do not require antivirals - self care measures, adequate fluid intake and rest advice, paracetamol PRN for fever and aches
Antivirals (oral oseltamivir 75 mg BD for 5 days OR inhaled zanamivir 10 mg BD for 5 days) should be given within 48 hours of symptom onset to be effective in those at high risk of complications
Post exposure prophylaxis can be given to high risk patients within 48 hours of close contact to someone with influenza (same drugs, same dose but 10 day course instead)
Prevention:
Good hygiene
Vaccination yearly changed to target multiple strains of influenza likely to cause flu that year.
Given free to those aged >65, young children, pregnant women, those with chronic health conditions like asthma, COPD, heart failure and diabetes and healthcare workers and carers
mumps and presentation
Background:
Vaccine offers around 80% protection for mumps so taking vaccination history is very important
Pathology:
Viral infection spread by respiratory droplets
Incubation period of 14-25 days
Usually a self limiting illness lasting around 1 week
Aetiology: Viral infection (mumps)
Presentation: Parotid swelling Fever Muscle aching Lethargy Reduced appetite Headaches Dry mouth Complications - abdominal pain (pancreatitis), orchitis (testicular pain), meningitis or encephalitis (confusion, neck stiffness and headaches)
mumps investigation, management, prevention
Investigation/diagnosis:
Clinical diagnosis
Viral PCR of saliva and antibody testing
Management:
Notify public health (notifiable disease)
Fluids
Rest
Analgesia as needed
Management of complications (pancreatitis, orchitis, meningitis or encephalitis or sensorineural hearing loss)
Prevention:
MMR vaccine programme in children
roseola and presentation
Background:
Sixth disease
Complications include febrile convulsions and rarely encephalitis
Pathology:
Viral human herpes - 6 infection
Self limiting condition
Aetiology:
HHV-6 and possibly HHV-7
Risk factors:
Ages 6 months - 1 year
Presentation:
Abrupt high fever lasting 3-5 days
Followed by an erythematous maculopapular rash that appears as the temperature subsides
Rash initially on the trunk, spreads centrifugally to the face and limbs
Nonspecific viral illness symptoms or asymptomatic
roseola management and investigation
Investigation/diagnosis:
Clinical diagnosis
Viral PCR and antibodies
Management:
Good fluid intake
Calpol for fever and irritability
Bring to hospital if any signs of confusion, excessive drowsiness, not drinking or severely decreased urine output or signs of encephalitis or not improving after 7 days
rubella
Background:
AKA 3rd disease or german measles
Generally mild disease in childhood
Mainly common in spring and summer months
Can cause severe foetal damage in vitro in pregnant women: causes foetal cell cytolysis through vasculitis and immune-mediated inflammation
Is part of MMR vaccine for this purpose
Pathology:
Incubation for 14-21 days
Transmitted via droplet infection
Aetiology:
RNA viral infection
rubella presentation
Prodromal symptoms of malaise, coryza, cough, LAP
Pink macular and papular rash starting on the forehead and spreading on the face, trunk and extremities on the first day of infection (after 1-5 days of illness)
Fades on the second day on the face and rest of the body on the third day
Petechiae on soft palate before the rash
Low fever
Congenital rubella syndrome:
Classic triad of cataract, cardiac deformities and deafness (microcephaly)
Maternal viremia with rubella infections during pregnancy may result in infection of the placenta and foetus causing these developmental defects
Growth cells in foetus are reduced and some reduced after birth
Prevented with effective immunisation
Few cases people develop ear encephalitis: treated with rest, tylenol or non-aspirin pain relief for fever
Congenital rubella has poor prognosis and many children die from heart problems; those who survive need lifelong treatment for deafness, learning disabilities and other congenital problems etc.
rubella investigation, management and prevention
Investigation/diagnosis:
Clinical history and exam (difficult as rash is fleeting and mimics any viral rash)
Rubella testing kit confirms diagnosis
Management: self limiting disease
Notify local health teams
Keep children from school for at least 4 days after rash has gone to limit spread to others
Ask about any contact with pregnant women
Complications: Thrombocytopenia Encephalitis Purpura Arthritis
Prevention:
MMR vaccine in childhood
measles (rubeola)
Background:
AKA 1st disease or rubeola
Pathology:
Enters cells and alters RNA transcription
Transmitted through airborne droplets: extremely contagious (if 1 person has it; 90% non-immune people nearby will get it)
Infects respiratory epithelium and spreads to skin and other organs
Incubation roughy 10-14 days
Once infected/immunised have life long immunity
Aetiology:
RNA virus
measles presentation and investigation
4 Cs - cough, coryza, conjunctivitis and very cranky
2 distinct phases: Prodrome (2-4 days) or exanthem (7-10 days)
Prodrome phase: fever, rhinorrhoea, cough, conjunctivitis, Koplik’s spots
Exanthem: maculopapular rash starting behind the ears then spreading to forehead, neck, face, trunk, upper limbs, buttocks and lower limbs. Fever peaks with rash then decreases over 4-5 days
Cough may remain post infection in recovery period
In immunocompromised pts. They may not present with enanthem (Koplik spots) or exanthem (rash) but show higher rates of pneumonia and encephalitis meaning they have higher mortality rates
Investigation/diagnosis:
Clinical exam and history
IgM measles specific swab or serum sample to confirm diagnosis
measles management and prevention and complications
Management:
Supportive treatment; disease is usually self limiting
Human immunoglobulin may be given within 5 days following exposure to unimmunised children (<3years), immunocompromised and pregnant women
Vaccinate other household members PRN
Vitamin A for young children and severely malnourished pts may decrease complication risk and boost antibody response
Notifiable disease: inform local health protection teams of suspected cases
Prevention:
Vaccine given as MMR
Given at 12-15 months then again at 4-6 years
95% efficacy rate
Mothers give transplacental antibodies lasting until 9 months old roughly
Complications
Associated with miscarriage and premature delivery in pregnant women
Post measles encephalomyelitis within 2 weeks onset of rash in immunocompromised children (poor prognosis - autoimmune reaction)
Suppresses immunity for up to 6 wks: Bacterial superinfections: Otitis media or bacterial pneumonia (mostly in young infants)
<2 years: subacute sclerosing panencephalitis (can occur up to 10 years later): caused by persistent measles infection due to abnormal immune response or mutated viral strain leading to inflammation of the entire brain. Symptoms initially subtle like mood changes but lead to seizures, coma, death.
varicella zoster viral infection
Background:
Common illness manifesting as general vesicular rash
Extremely contagious spread by respiratory droplets (in unvaccinated population 90% would become infected)
Predominant age of infection is 5-10 years
Infectious period begins 2 days prior to symptom onset and lasts until all lesions have crusted
Incubation period around 9-21 days
Pathology:
Varicella zoster virus (VZV) infects respiratory cells and liver and spleen in the primary viremia stage; then to the T cells in secondary viremia at around 2 weeks post-infection. T cells release pathogens to skin causing skin lesions as keratinocytes etc are infected.
Aetiology:
VZV infection
Risk factors:
Pregnancy
Immunocompromised
VZV presentation, investigation and complications
Presentation:
Brief prodromal period with fever, chills, headache and malaise
Lesions start to appear over head and trunk, spreading to peripheries
Often very itchy
New lesions generally stop appearing after day 4
Investigation/diagnosis:
Clinical diagnosis
Lesion scraping to confirm PRN
Complications: Secondary bacterial infections leading to necrotising fasciitis or toxic shock syndrome Viral pneumonia Encephalitis Aseptic meningitis Vasculitis Osteomyelitis Otitis media Sepsis
VZV management and prevention
Management:
Self- limiting disease supportive care given
Paracetamol, antihistamines
Avoid contact with pregnant women, neonates, immunocompromised
If pt is immunocompromised then specialist advice needed as may need IV acyclovir (antiviral)
Management in pregnancy:
Check maternal bloods for VZV antibodies
If <20 weeks gestation and not immune, give VZV Igs ASAP preferably within 10 days post exposure
If >20 weeks and not immune, give antivirals (aciclovir or valaciclovir) given on days 7-14 after exposure
prevention:
vaccine for unexposed individuals working in healthcare
