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.
