Infectious disease Flashcards

Question

Histoplasmosis presentation, Ix, Mx and prevention

Answer 1

``` 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

Answer 2

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.)

Answer 3

``` 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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

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.

Answer 8

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

Answer 9

``` 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

Answer 10

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

Answer 11

``` 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

Answer 12

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

Answer 13

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

Answer 14

Can produce enterotoxins on foods such as eggs, diary, meat Causes diarrhoea, profuse vomiting, abdo cramps and fever Resolve within 12-24 hours

Answer 15

``` 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.

Answer 16

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

Answer 17

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

Answer 18

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)

Answer 19

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 ```

Answer 20

``` 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

Answer 21

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). ```

Answer 22

``` 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 ```

Answer 23

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

Answer 24

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

Answer 25

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

Answer 26

``` 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

Answer 27

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

Answer 28

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?

Answer 29

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

Answer 30

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

Answer 31

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 ```

Answer 32

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

Answer 33

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

Answer 34

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 ```

Answer 35

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

Answer 36

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

Answer 37

``` 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

Answer 38

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

Answer 39

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

Answer 40

``` 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 ```

Answer 41

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

Answer 42

``` 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

Answer 43

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) ```

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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.

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

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.

Answer 53

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

Answer 54

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 ```

Answer 55

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

Infectious disease Flashcards

(79 cards)