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FRCEM Primary > Pathology 5.3 - Infection > Flashcards

Pathology 5.3 - Infection Flashcards

1
Q

Causes of upper respiratory tract infections

A

Mainly viral, 15% bacterial. Commonly Streptococcus

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2
Q

Pathological process of URTI

A

Person to person spread
Invades mucosal lining
Incubation period 1-5 days

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3
Q

Investigation of URTI

A

Mononucleosis in young people with sore throat, lymphadenopathy and hepatosplenomegaly
Immunocompromised.

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4
Q

Causes of LRTI

A

Bacterial - Haemophilus influenzae, Streptococcus pneumoniae, Moraxella cattarrhalis. Rarely Staphylococcus aureus (Post viral), Legionella, Chlamydia psittaci (exposure to birds)
Viral - Influenza, Parainfluenza, RSV
Fungal - Candida, aspergillus (usually in immunocompromised)

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5
Q

Pathological process of LRTI

A

Inhalation of pathogen causing fever, cough, pleuritic chest pain and extrapulmonary features in atypical pathogens.
Acute inflammation causes migration of neutrophils which phagocytose microbes and trap them in a chromatin meshwork containing antimicrobial proteins - neutrophil extracellular traps (NETs)

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6
Q

Investigation of LRTI

A

CXR, sputum culture, U&E, CRP, FBC, ABG
LFTs rise mildly in psittacosis, Q fever and Legionella
Phosphate drops in Legionnaires
Urinalysis for legionella antigen and microscopic haematuria in Legionnaires Disease

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7
Q

Causes of meningitis

A

Bacterial - New Born - Group B Strep, E Coli
Children - Neisseria meningitides, Strep pneumonia, HIB
Adults - Neisseria meningitides, Strep pneumonia
Viral - Enterovirus, Herpes simplex type 2, varicella zoster, mumps, HIV
Fungal - Cryptococcus neoformans, Candida, Aspergillus
Non infectious - cancer, systemic inflammatory conditions like SLE and vasculitis

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8
Q

Pathological processes of meningitis

A

Infective agent reaches the meninges via the blood stream through the nasal cavity or through CSF via skull fractures or indwelling devices. They enter the subarachnoid space through a weakness in the BBB like the choroid plexus causing inflammation which makes the BBB more permeable, leading to cerebral oedema. Inflammation of the meninges causes interstitial oedema. Cerebral vasculitis decreases blood flow and cells die from hypoperfusion causing more oedema. Oedema increases ICP.

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9
Q

Investigations for meningitis

A

FBC, CRP, blood culture, viral serology, meningococcal PCR, LP
LP findings - bacterial: high WBC, high protein, low glucose
LP findings viral: high WBC, normal or high protein, normal glucose

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10
Q

Causes of encephalitis

A

Viral - herpes simplex, varicella zoster, HIV, rabies

Bacterial - Syphilus, spread from meningitis

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11
Q

Pathological process of encephalitis

A

Inflammation of the brain parenchyma causing fever, headache, photophobia, confusion and sometimes seizures

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12
Q

Investigation of encephalitis

A

FBC, CRP, blood cultures, LP, MRI

LP findings: high WBC, normal protein, normal glucose

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13
Q

Causes of myocarditis

A

Viral - HIV, coxsackie, CMV, enterovirus, rubella, polio
Bacterial - Brucella, gonococcus, Haemophilus influenza
Fungal - Aspergillus, Candida
Drugs - ETOH, chemo, antipsychotics, antibiotics (penicillin, chloramphenicol)
Bites/stings - scorpion, snake, black widow spider
Toxins - arsenic, lead, mercury
Physical - radiation, electrical shock
Systemic inflammatory disorders - SLE, sarcoidosis, RA, systemic vasculitis

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14
Q

Pathological process of myocarditis

A

Symptoms result from inflammation of the myocardium or the weakness that it causes. Damage arises either directly from the causative agent or from the inflammatory response to it. It can be acute or chronic with continuing damage from an autoimmune abnormal expression of HLA human leucocyte antigen.

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15
Q

Investigations for myocarditis

A

ECG (diffuse T wave inversion, saddle ST elevation), FBC, CRP, blood cultures, Trop, Echo, viral titres, myocardial biopsy

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16
Q

Causes of endocarditis

A

Usually infective - Streptococcus, Staphylococcus

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17
Q

Pathological process of endocarditis

A

Turbulence around the endothelial surface from under lying structural problems, damaged or prosthetic valves allows bacteria to adhere. Causes low grade fever, new murmur, petechiae, splinter haemorrhages, Osler’s nodes (tender subcut nodules on the pads of the digits), Janeway lesions (nontender maculae on palms and soles) and Roth spots (retinal haemorrhage). Left sided disease will give systemic infectious emboli

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18
Q

Investigations for endocarditis

A

Duke criteria - 2 major/1 major + 3 minor/ 5 minor
Major - +ve blood culture (2 from 2 draw sites 12 hours apart with typical organisms),
Endocardial involvement on ECHO (vegetation, abscess, new regurg)

Minor - Fever >38,
evidence of embolism,
Predisposing factor (known lesion, IVDU),
Immunological condition,
Positive Echo not meeting major criteria,
Positive blood cultures not meeting major criteria

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19
Q

Viral causes of Hepatitis A

A 
Picornovirus
Single stranded RNA
Faeco-oral spread
Acute, self limiting
Vaccine available
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20
Q

Viral cause of Hepatitis B

A

Hepadnavirus
DNA virus
Blood/body fluid spread
Acute and self limiting (unless in children)
May develop into chronic hepatitis with cirrhosis and hepatocellular carcinoma
Vaccine available

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21
Q

Viral cause of Hepatitis C

A 
Hepacivirus
Single stranded RNA
Blood/body fluid spread
Acute phase is asymptomatic
May progress to cirrhosis
No vaccine
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22
Q

Viral cause of Hepatitis D

A

Deltavirus
Small circular, single standed RNA virus
Occurs in conjunction with Hep B
Associated with IVDU

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23
Q

Other causes of Hepatitis

A

Mumps, rubella, CMV, EBV
Alcohol
Toxins/ drugs - amiodarone, amitriptyline, halothene, ketoconazole, methotrexate, paracetamol, amatoxin containing mushrooms (deathcap)
Autoimmune
Metabolic - haemachromatosis, Wilson’s disease

24
Q

Pathological process of hepatitis

A

Initially non-specific aches, fever, nausea, vomiting, diarrhoea. Later specifically anorexia, dark urine, jaundice, abdo pain, hepatomegaly. Extensive damage causes cirrhosis presenting with hepatomegaly, jaundice, palmar erythema, gynaecomastia, ascites, spider naevi.

25
Q

Investigations for hepatitis

A

FBC, U&E, LFT, clotting, hepatitis serology

26
Q

Causes of gastroenteritis

A

Usually viral - 70% norovirus, 20% rotavirus, adenovirus, astrovirus
Bacterial - salmonella, shigella, staphylococcus, campylobacter, e coli, clostridium

27
Q

Pathological process of gastroenteritis

A

Infectious agents adhere to mucous membranes and produce enterotoxin or cytotoxin which increases fluid secretion and decreases absorption, resulting in dehydration and loss of electrolytes.
Enterotoxins (E coli, Cholera) act on secretory mechanisms to increase watery diarrhoea
Cytotoxins (Shigella, C diff) destroy mucosal cells, decreasing resorption ability.

28
Q

Investigations for gastroenteritis

A

FBC, U&E, Stool culture

29
Q

Causes of urinary tract infections

A

80% are E coli.

Others are : Staphylococcus saprophyticus, Klebsiella, proteus

30
Q

Pathological process of UTI

A

Bacteria ascend into bladder via urethra, may be promoted by SI. Usually a thin film of urine remains after emptying bladder and bacteria are removed by mucosal cell production of organic acids.
Look for underlying anatomical abnormality in males age 3 months to 50 years

31
Q

Investigation of UTI

A

MSU

32
Q

Causes of STI

A

Bacteria - Gonorrhoea, Syphilus, Chlamydia, Non-gonococcal urethritis
Viral - HIV, Hepatitis B, Herpes simplex, Genital warts, Cervical cancer - from human papilloma virus
Fungal - tinea cruris
Parasite - Phthirus pubis

33
Q

Pathological process of STI

A

Infections are transmitted through mucus membranes and some pathogens are more abundant in genital fluids than saliva.

34
Q

Investigation of STI

A

Urethral swabs, vaginal swabs, MSU, bloods for HIV, syphilis serology

35
Q

Causes of pelvic inflammatory disease

A

Gonorrhoea, Chlamydia

36
Q

Pathological process of PID

A

Organisms ascend to the upper genital tract from the vagina and cervix. There is inflammation of the uterus, fallopian tubes +/- ovaries. Can progress to scar formation causing adhesions, infertility and increased risk of ectopics.

37
Q

Investigations of PID

A

FBC, CRP, urinalysis, high vaginal swab

38
Q

Causes of cellulitis

A

Group A strep, staphylococcus aureus.

Facial cellulitis is usually HIB and Strep pneumonia

39
Q

Pathological process of cellulitis

A

Microorganisms invade disrupted skin, either overtly or through microscopic breaks from dry and irritated skin.

40
Q

Investigations of cellulitis

A

Not usually required, but if severe do FBC, U&E, blood cultures, wound swabs.

41
Q

Causes of osteomyelitis

A

Staphylococcus aureus is most common

Occasionally Enterobacter or Streptococcus species

42
Q

Pathological process of osteomyelitis

A

Infection may be localised or spread through periosteum, cortex, marrow and cancellous bone. It can be direct from contact of tissue and bacteria from trauma or surgery, or haematogenous from bacteria seeded from blood. Once infected leucocytes enter to engulf the bacteria but release enzymes that lyse the bone. An involucrum is an area or new bone forming around the site of necrosis.

43
Q

Investigations for osteomyelitis

A

FBC, CRP, blood cultures, XR - periosteal elevation becoming cortical or medullary lucencies seen after 14-21 days.

44
Q

Causes of septic arthritis

A

Staphylococcus aureus, Streptococcus species.
HIB in children
Neisseria gonorrhoea in young adults
TB - especially in the spine

45
Q

Pathological process of septic arthritis

A

Bacteria comes via the blood from a focus elsewhere, extends from an adjacent tissue or directly from a joint penetrating wound.
Knee is 40-50% of cases
Hip 20-25%
Hip more common in infants and young children.

46
Q

Investigations for septic arthritis

A

FBC, CRP, blood cultures, Xray, joint aspiration

47
Q

Cause of AIDS

A

HIV

48
Q

Pathological process of AIDS

A

Spread by sexual contact, blood, blood products and mother to child. HIV enters macrophages and CD4 T cells. Reverse transcriptase copies the single stranded RNA from the viral proteins and copies it into a DNA molecule to be transported into the cell nucleus and integrated into the host genome by the enzyme Integrase.

49
Q

Investigations for HIV

A

Serological tests for HIV

50
Q

Causes of pyrexia of unknown origin

A

Infections - Extrapulmnary TB, endocarditis
Neoplasms - lymphoma
Collagen vascular disorders - temporal arteritis
Other - drug reactions

51
Q

Investigations for PUO

A

Repeated thorough history and examination.
FBC, U&E, cultures (blood, sputum, urine, CSF, stool), Viral serology, autoantibodies, CRP, ESR, CXR, Consider abdo US or CT.

52
Q

Causes of malaria

A

Plasmodium vivax
Plasmodium ovale
Plasmodium malariea
Plasmodium falciparum - most morbidity and mortality

53
Q

Pathological process of malaria

A

An infected female Anopheles mosquito bites a human, injecting sporozoits through the saliva intot he blood stream. These infect hepatocytes and multiply asexually for 6-15 days. They differentiate into merozoites and rupture the hepatocyte, escaping into the blood stream where they infect red blood cells. They multiply asexually in the RBC and occasionally break out to infect more RBC, causing the classic swinging fever. Some merozoites differentiate to gametocytes and are picked up by another feeding mosquito, reproducing in its gut to sporozoites that migrate tot he salivary glands. P vivax and P ovale can lie dormant in the liver as hypnozoites for up to 3 years.

54
Q

Investigations for malaria

A

Thich and thin blood films to identify the protozoa. FBC, U&E, blood cultures

55
Q

Causes of fungal infections

A 
Superficial - Tinea versicolour (Malassezia globosa: yeast infection causing lighter and darker patches of skin)
Ringworm - caused by dermatophytes
Tinea capitis - scalp
Tinea corporis - trunk and extremities
Tinea cruris - groin
Systemic - Candida, Aspergillus
56
Q

Pathological process of fungal infections

A

Systemic fungal infections are caused by opportunistic pathogens. Superficial fungi thrive in warm, moist conditions. They are spread by person to person contact and may be present on the skin without active infections

57
Q

Investigations for fungal infections

A

Skin or nail scrapings. Direct examination with a UV (Woods) light will fluoresce 50% of ringworm fungi.

FRCEM Primary (32 decks)

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