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Year 3 SOFIA CONDITIONS > Infection > Flashcards

Infection Flashcards

1
Q

What is an abscess?

A

A collection of pus walled off by an area of inflammation

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2
Q

What is the aetiology of an abscess?

A
  • Pyogenic abscesses are caused by infection that the body’s defences have failed to completely overcome
  • Common bacteria include S. aureus, streptococci, enteric organisms, other coliforms and anaerobes.
  • TB classically causes ‘cold’ abscesses
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3
Q

What are the risk factors for abscesses?

A
  • Local: tissue necrosis, a closed underperfused space of foreign body that provides a focus for infection e.g. tooth or root fragment, splinters, mesh of hernia repairs, embedded hair, malignancy
  • Systemic: Diabetes, immunosuppression
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4
Q

What is the epidemiology of abscesses?

A

Common in all ages

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5
Q

What are the presenting symptoms of abscesses?

A
  • Pt may complain of local effects of pain, swelling, heat, redness and impaired function of the area where abscess is present
  • And/or systemic effects such as fever and feeling unwell
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6
Q

What are the signs of abscesses on examination?

A
  • Local effects as presenting symptoms

- If present within organ, localising signs may be absent, only sign being swinging pyrexia

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7
Q

What are the investigations for abscesses?

A
  • Bloods: FBC, increased neutrophils
  • Imaging: Ultrasound, CT, MRI scanning may be used to search for site
  • Aspiration: Pus is low in glucose and acidic. Culture of pus for organisms and sensitivity to organisms
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8
Q

How are abscesses prevented?

A

Prophylactic antibiotics (e.g. during operations) or if given early during an infection. Often not effective once abscess has formed

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9
Q

How are abscesses managed by surgery?

A

Drainage of pus is carried out by incision and drainage, with debridement of cavity and subsequent free drainage by packing of cavity (if superficial) or by drains (if deep)

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10
Q

How are abscesses generally managed?

A

Principles involved include drainage of pus, removal of necrotic and foreign material, antimicrobial cover and correction of the predisposing cause

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11
Q

What are the possible complications of abscesses?

A
  • Spread may result in cellulitis (in skin) or bacteraemia with systemic sepsis
  • If focus of infection is not removed, a chronic abscess or discharging sinus or fistula may form.
  • Occasionally, antibiotics may penetrate and result in the formation of a sterile collection or antibioma
  • If constrained by strong facial planes, slow expansion can cause pressure necrosis of surrounding tissues
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12
Q

What is the prognosis for abscesses?

A
  • Good, if adequately drained and predisposing factor removed
  • If left untreated, abscesses tend to ‘point’ to the nearest epithelial surface and may spontaneously discharge their contents
  • Deep abscesses may become chronic, undergoing dystrophic calcification
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13
Q

What is oral candidiasis?

A
  • Infection of oral tissues

- Can also cause oropharyngeal, oesophagitis, vulvovaginits, endopthalmitis, meningitis, endocarditis

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14
Q

What is candidaemia?

A
  • Infection of blood, pleural, peritoneal fluid with Candida
  • Usually fever, hypotension, leukocytosis
  • Disseminates to retina, kidney, liver, spleen, bones, CNS
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15
Q

What is the epidemiology of candidiasis?

A
  • Oral: Infants, older adults, immune suppression

- Candidaemia: Pts in hospital, intravascular catheters, neutropenia

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16
Q

What are the causes and risk factors of candidiasis?

A

C. Albicans is most common infection

  • Oral candidiasis: HIV infection, Xerostomia, dentures, malnutrition, advanced malignancy, cancer chemo or radiotherapy, pregnancy, diabetes, immunosuppressive therapy
  • Candidaemia: Central venous catheter, use of broad spectrum abx, haemodialysis, surgery, parenteral nutrition, immunosuppressants
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17
Q

What are the presenting symptoms of candidiasis?

A
  • Fever due to sepsis
  • Dysphagia
  • Odynophagia
  • Hoarse voice
  • Genital candidiasis: vulval pruritis, burning, swelling, dyspareunia
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18
Q

What are the signs of oral candidiasis on examination?

A
  • Creamy white or yellowing plaques
  • Adheres to oral mucosa
  • Removal of plaque may show erythamatous base of bleeding surface
  • Cracks, ulcers, crusted fissures from angles of mouth
  • Lesion anywhere on oral mucosa
  • Immunodeficiency: patchy loss of filiform papillar, spotty red areas on buccal mucosa
  • Lesion confined to outline of dental prosthesis
  • Burning oral pain
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19
Q

What are the signs of candidaemia on examination?

A
  • Tachycardia
  • Tachypnoea
  • Hypotension
  • Poor capillary refill
  • Acute mental confusion
  • Decresed urine output
  • Low 02 sats
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20
Q

What are the investigations for candidiasis?

A
  • Oral: Superficial smear of lesion for microscopy, biopsy of lesion, culture of mouth rinse sample
  • Candidaemia: Blood cultures, ABG (hypoxaemia, hypercapnia), high lactate, creatinine, high LFTs
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21
Q

What is cellulitis?

A

Acute non-purulent spreading infection of the subcutaneous tissue, causing overlying skin inflammation

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22
Q

What is the aetiology of cellulitis?

A
  • Often results from penetrating injury (e.g. intravenous cannulation), local lesions (e.g. insect bites, sebaceous cysts, surgery) or fissuring (e.g. in anal fissures, toe web spaces), which allows pathogenic bacteria to enter the skin.
  • Most common organisms: S. pyogenes and S.aureus.
  • If occurring in the orbit: H. influenzae is most common cause
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23
Q

What is the epidemiology of cellulitis?

A
  • Very common

- Main risk factors are skin break, poor hygiene and poor vascularisation of tissue (e.g. diabetes mellitus)

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24
Q

What are the presenting symptoms of cellulitis?

A

There may be a history of a cute, scratch or injury

  • Periorbital: Painful swollen red skin around eye
  • Orbital cellulitis: Painful or limited eye movements, visual impairment
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25
Q

What are the signs of cellulitis on examination?

A
  • Lesion: Erythema, oedema, warm tender indistinct margins. Pyrexia may signify systemic spread
  • Exclude abscess: Test for fluid thrill or fluctuation. Aspirate if pus suspected.
  • Periorbital: Swollen eyelids. Conjuctival injection
  • Orbital cellulitis: Proptosis, impaired acuity and eye movement. Test for relative afferent pupillary defect, visual acuity and colour vision (to monitor optic nerve function)
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26
Q

What are the investigations for cellulitis?

A
  • Blood: WCC, blood culture
  • Discharge: Culture and sensitivity
  • Aspiration: As it is often non-purulent, it is not usually necessary
  • CT/MRI scan: When orbital cellulitis is suspected (to assess posterior spread of infection)
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27
Q

How is cellulitis managed?

A
  • Medical: oral penicillins (e.g. flucloxacillin, benzylpenicillin, coamoxiclav) or tetracyclines are effective in most community acquired cases. In hosp, treat as per microbiological guidelines
  • Surgical: Orbital decompression may be necessary in orbital cellulitis. It is an emergency
  • Abscess: can be aspirated, incised and drained or excised completely
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28
Q

What are the possible complications of cellulitis?

A
  • Sloughing of overlying skin
  • Localised tissue damage
  • In orbital cellulitis, may be permanent vision loss and spread to brain, abscess formation, meningitis, cavernous sinus thrombosis
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29
Q

What is the prognosis for cellulitis?

A

Good with treatment

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30
Q

What is herpes simplex virus?

A

Disease resulting from HSV1 or HSV2 infection

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31
Q

What is the aetiology of herpes simplex?

A
  • HSV is an alpha-herpes virus with double stranded deoxyribonucleic acid (dsDNA)
  • Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse)
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32
Q

What is the epidemiology of herpes simplex?

A
  • 90% adults seropositive for HSV1 by 30 yrs

- 1/3 of world populations has recurrent HSV infections

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33
Q

What are the presenting symptoms of herpes simplex (HSV1)?

A

Primary infection often asymptomatic; usual symptoms:
- Pharyngitis
- Gingivostomatis, may make eating very painful; and
- Herpetic whitlow, inoculation of virus into a finger
Recurrent infection/reactivation; prodrome (6h) peri-oral tingling and burning. Vesicles appear (48h duration), ulcerate and crust over. Complete healing 8-10 days

34
Q

What are the presenting symptoms of herpes simplex (HSV2)?

A
  • Very painful blisters and rash in genital, perigenital and anal area
  • Dysuria
  • Fever and malaise
35
Q

What are the presenting symptoms of herpes simplex (HSV keratoconjunctivitis?

A
  • Epiphoria (watering eyes)

- Photophobia

36
Q

What are the signs of HSV1 primary infection on examination?

A
  • Tender cervical lymphadenopathy
  • Erythematous
  • Oedematous pharynx
  • Oral ulcers filled with yellow slough (gingivostomatitis)
  • Digital blisters/pustules (herpetic whitlow)
37
Q

What are the signs of herpes labialis on examination?

A

Perioral vesicles/ulcers/crusting

38
Q

What are the signs of HSV2 infection on examination?

A
  • Maculopapular rash
  • Vesicles and ulcers (external genitalia, anal margin, upper thighs)
  • Inguinal lymphadenopathy
  • Pyrexia
39
Q

What are the signs of HSV keratoconjunctivits on examination?

A
  • Characteristic lesion is a dendritic ulcer

- May be visualised following staining with 1% fluorescein

40
Q

What are the investigations for herpes simplex virus?

A

Usually a clinical diagnosis

- Vesicle fluid: Electron microscopy, PCR, direct immunofluorescence, growth of virus in tissue culture

41
Q

What is human immunodeficiency virus (HIV) infection?

A

Infection with the human immunodeficiency virus (HIV)

42
Q

What is the aetiology of HIV?

A

Transmitted by:

1) Sexual intercourse: risk increased with homosexuals in West
2) Blood (and other body fluids): Mother to child (intrauterine, childbirth or breastfeeding), needles (injecting drug users, health care workers), blood product transfusion, organ transplantation

43
Q

How does HIV cause infection?

A
  • HIV enters the CD4 lymphocytes following binding of its envelope glycoprotein (gp120) to CD4 and a chemokine receptor.
  • Reverse transcriptase (in viral core) reads RNA to manufacture DNA, which is incorporated into the host genome
  • Dissemination of virions leads to cell death and eventually to T-cell depletion
44
Q

What is the epidemiology of HIV?

A

On the rise in Africa and Asia

More than 40,000,000 adults affected worldwide

45
Q

What are the 3 phases of HIV infection?

A

1) Seroconversion: (4-8 weeks post-infection), self-limiting- fever, night sweats, generalised lymphadenopathy, sore throat, oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea
2) Early/asymptomatic: (18 months to 15+ years), apparently well- some pts may have persistent lymphadenopathy. Progressive minor symptoms e.g. rash, oral thrush, weight loss, malaise
3) AIDS: Syndrome of secondary diseases reflecting severe immunodeficiency or direct effect of HIV infection

46
Q

What are the presenting symptoms of HIV infection?

A
  • Neurological: Polyneuropathy, myelopathy, dementia
  • Lung: Lymphocytic, interstitial pneumonitis
  • Heart: Cardiomyopathy, myocarditis
  • Haematological: Anaemia, thrombocytopenia
  • GI: Anorexia, HIV enteropathy (malabsorption and diarrhoea), severe wasting
  • Eyes: Cotton wool spots
47
Q

What secondary infections can arise from immunodeficiency associated with HIV?

A
  • Bacterial: Mycobacteria (lungs, GI, skin
  • Viral: CMV
  • Fungal: Pneumocystitis pneumonia (PCP)
  • Protozoal: Toxoplasmosis
  • Tumours: Kaposi’s sarcoma, squamous cell carcinoma, Hodgkin’s lymphoma
48
Q

What are the investigations for HIV?

A
  • HIV testing (after discussion and consent): HIV antibodies, PCR for viral RNA or incorporated proviral DNA
  • PCP: CXR bilateral perihilar/’ground glass’ shadowing, bronchoalveolar lavage
  • CMV: colonoscopy
  • Toxoplasmosis: Brain CT
49
Q

What is incision and drainage of an abscess?

A

Minor surgical procedure that releases pus or pressure built up under the skin from an abscess.

  • Performed by treating the area with an antiseptic, then making a small incision to puncture skin using or scalpel or lancet
  • This allows pus fluid to escape by draining out through incision
50
Q

What are the indications for an incision and drainage of an abscess?

A
  • Most pts with skin abscesses should undergo incision and drainage
  • Needle aspiration is insufficient
51
Q

What are the possible complications of incision and drainage of an abscess?

A
  • Uncommon
  • Inadequate drainage may result in local extension, resulting in development of larger abscess that may be followed by osteomyelitis, tenosynovitis, septic thrombophlebitis, necrotising fasciitis or fistula formation
  • Overaggressive drainage, especially with sharp dissection, may damage adjacent structures (e.g. nerves and vessels) and may lead to bacteraemia
52
Q

What is infectious mononucleosis?

A

Clinical syndrome caused by primary EBV infection

Also knows as glandular fever

53
Q

What is the aetiology of infectious mononucleosis?

A
  • EBV is gamma-herpes virus (dsDNA), present in pharyngeal secretions of infected individuals and is transmitted by close contact e.g. kissing or sharing eating utensils
  • EBV infection of the oropharyngeal epithelial cells lead to B cell infection with incorporation of the viral DNA into host DNA
  • Infected B cells disseminate and proliferate in lymphoid tissue throughout the body
  • There is humoral and cellular immune response and production of interleukin and interferon-gamma cytokines
  • Despite, immune responses, which control the initial lytic infection, EBV remains latent in lymphocytes
  • Reactivation may occur following stress or immunosuppression
54
Q

What is the epidemiology of infectious mononucleosis?

A

Common

- 2 age peaks: 1-6 years and 14-20 years

55
Q

What are the presenting symptoms of infectious mononucleosis?

A

Incubation period: 4-8 weeks

- May have abrupt onset: sore throat, fever, fatigue, headache, malaise, anorexia, sweating, abdominal pain

56
Q

What are the signs of infectious mononucleosis on examination?

A
  • Pyrexia
  • Oedema and erythema of pharynx, fauces and soft palate, with white/creamy exudate on the tonsils which becomes confluent within 1-2 days, palatal petechiae.
  • Cervical/generalised lymphadenopathy, splenomegaly (50-60%)
  • Jaundice (5-10%), widespread maculopapular rash in patients who have received ampicillin
57
Q

What are the investigations for infectious mononucleosis?

A
  • Bloods: FBC (leukocytosis), LFT (raised aminotransferases)
  • Blood film: Lymphocytosis (more than 20% atypical lymphocytes)
  • Paul-Bunnell/monospot test: Detects the presence of heterophile antibodies that are produced in response to EBV infections
  • Throat swab to exclude streptococcus tonsilitis
  • IgM or IgG to EBV viral capsid antigen (VCA)
  • IgG against EBNA (Epstein-Barr nuclear antigen)
58
Q

How is infectious mononucleosis managed?

A
  • Bed rest, paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) for fever, throat discomfort and malaise
  • Corticosteroids may be indicated for severe cases (e.g. haemolytic anaemia, severe tonsilar swelling, obstructive pharyngitis)
  • Caution: Most pts develop widespread maculopapular rash when given amoxicillin or ampicillin
  • Advice: Against contact sports for 2 weeks as increased risk of splenic rupture
59
Q

What are the possible complications of infectious mononucleosis?

A

Lethargy for several months following the acute infection

  • Respiratory: airway obstruction by oedematous pharynx, secondary bacterial throat infections, pneumonitis
  • GI/renal: Splenic rupture (caused by persistent splenomegaly, fulminant hepatitis, pancreatitis, mesenteric adenitis, renal failure
  • CNS: Guillain-Barre syndrome, encephalitis, viral meningitis, brachial plexitis
  • EBV-associated malignancy: Burkitt’s lymphoma, nasopharyngeal carcinoma, post-transplant lymphoma, Hodgkin’s lymphoma
60
Q

What is the prognosis for infectious mononucleosis?

A
  • Most make uncomplicated recovery in 3-21 days

- Immunodeficiency and death can occur very lately

61
Q

What is malaria?

A

Infection with protozoan Plasmodium

- Most serious is Plasmodium falciparium which is potentially fatal

62
Q

What is the aetiology of malaria?

A

Plasmodium spp. are transmitted by bite of the female Anopheles mosquito. The protozoa infect red blood cells and grow intracellularly

63
Q

What are the stages that take place for Plasmodium spp. to infect red blood cells?

A

1) Infection of sporozoites into bloodstream by bite of female Anopheles mosquito
2) Invasion and replication in hepatocytes (exoerythrocytic schizogeny).
3) Parasites may reinvade the blood. Inside RBC’s they develop from trophozoites into multinucleated schizonts
4) RBCs rupture and release merozoites which may reinfect new RBCs
5) Gametocytes taken up by Anopheles mosquitos develop into sporozoites in their gut and migrate to the salivary gland of mosquito to be transmitted in their bite

64
Q

What populations have innate immunity to malaria?

A
  • Sickle cell trait
  • G6PD deficiency
  • Pyruvate kinase deficiency
  • Thalassaemias
65
Q

What is the epidemiology of malaria?

A
  • Endemic in tropics

- Affects 250 million people worldwide yearly

66
Q

What are the preventing symptoms of malaria?

A

High degree of clinical suspicion in any feverish traveller. Clinical symptoms of high fever, flulike symptoms, severe sweating and shivering cold/rigors
Peak temperature may coincide with rupture of the intra-eryhtrocytic shizonts
. every 48 h for P. falciprum (malignant tertian);
. every 72 h for P. malariae (benign quartan); and
. every 48 h for P. vivax and P. ovale (benign tertian).

67
Q

What are the presenting symptoms of cerebral malaria?

A
  • Headache
  • Disorientation
  • Coma
68
Q

What are the signs of malaria on examination?

A
  • Pyrexia/rigors
  • Anaemia
  • Hepatosplenomegaly
69
Q

What are the investigations for malaria?

A
  • Thick/thin blood film (using Field’s or Giemsa’s stain)
  • Blood: FBC (Hb, platelets), U&Es, LFT, ABG
  • Urinalysis: Test for blood or protein
  • Quantitative buffy coat (QBC) test
  • Immunochromatographic (ICT) test
70
Q

What is varicella zoster?

A
  • Primary infection is called varicella (chicken pox)

- Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles)

71
Q

What is the aetiology of varicella zoster?

A
  • VZV is a herpes ds-DNA virus

- Highly contagious, transmission is by aerosol inhalation or direct contact with the vesicular secretions

72
Q

What is the epidemiology of varicella zoster?

A
  • Chicken pox peak incidence occurs at 4-10 yrs
  • Shingles peak incidence occurs at over 50yrs
  • About 90% of adults are VZV IgG positive (previously infected)
73
Q

What are the presenting symptoms of chickenpox?

A
  • Prodromal malaise
  • Mild pyrexia
  • Sudden appearance of intensely itchy spreading rash affecting the face and trunk more than the extremities, the oropharynx, conjunctivae and genitourinary tract
  • As vesicles weep and crust over, new vesicles appear
  • Contagious from 48h before rash and until all vesicles have crusted over (within 7-10 days)
74
Q

What are the presenting symptoms of shingles?

A
  • May occur after period of stress
  • Tingling/hyperparaesthesia in a dermatomal distribution, followed by painful skin lesions
  • Recovery in 10-14 days
75
Q

What are the signs of chickenpox (disseminated varicella) on examination?

A
  • Macular papular rash evolving into crops of vesicles with areas of weeping (exudate) and crusting (vesicles, macules, papules and crusts may be all present at one time)
  • Skin excoriation (from scratching)
  • Mild pyrexia
76
Q

What are the signs of shingles on examination?

A
  • Vesicular macular papular rash, in a dermatomal distribution, skin excoriation
77
Q

What are the investigations for varicella zoster?

A
  • Usually by clinical diagnoses
  • Vesicle fluid: Electron microscopy, direct immunofluorescence, cell culture, viral PCR
  • Chickenpox: Consider HIV testing especially in adults with prior history of varicella infection
78
Q

How is chicken pox managed (primary infections)?

A
  • Children: Treat symptoms (calamine lotion, analgesia, antihistamines)
  • Adults: Consider aciclovir, valaciclovir or famiciclovir if within 25h of rash onset especially if elderly, smoker, immunocompromised or pregnant (especially second or third trimester)
79
Q

How is shingles managed (reactivation)?

A

Aciclovir, valaciclovir or famiciclovir if within 72h of appearance of the rash if elderly, immunocompromised or ophthalmic involvement. Low dose amitriptyline may benefit those with moderate/severe discomfort. Simple analgesia (paracetamol)

80
Q

What are the possible complications of chickenpox?

A
  • Secondary infection
  • Scarring
  • Pneumonia
  • Encephalitis
  • Cerebellar syndrome
  • Congenital varicella syndrome
81
Q

What are the possible complications of shingles?

A
  • Postherpetic neuralgia
  • Zoster opthalmicus (rash involves opthalmic division of trigeminal nerve)
  • Ramsay Hunt’s syndrome
  • Sacral zoster may lead to urinary retention
  • Motor zoster (muscle weakness of myotome at similar level as involved dermatome
82
Q

What is the prognosis of varicella zoster?

A
  • Depends on complications

- Worse in pregnancy, the elderly and immunocompromised

Year 3 SOFIA CONDITIONS (16 decks)

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