Infection Flashcards

1
Q

What is pyrexia of unknown origin (PUO)?

A

PUO is a documented fever persisting for >2 weeks, with no clear diagnosis.
Occult infection is the commonest cause of PUO in adults

Causes include infection, malignancy, vasculitides and drugs, IBD, sarcoidosis, thyrotoxicosis.

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2
Q

What is bacteraemia?

A

Transient presence of organisms in the blood. Usually causes no symptoms

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3
Q

What is septicaemia?

A

Clinical picture that results from systemic inflammatory response (SIR) to infection

Inflammation is intended to be a local contained response to infection. In some causes, this goes outwith the boundaries of the local environment so the inflammatory process becomes systemic instead of remaining localised.

Clinical features include:

  • fever
  • tachycardia
  • increased respiratory rate
  • hypotension

High mortality rate if untreated

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4
Q

What is the common causative microorganism in biliary tree infection?

A

Enterococcus faecalis, or E.oli (Gram -ve)

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5
Q

What are the two big microorganisms that cause infection in IVDU?

A

Staph. Aureus

Pseudomonas

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6
Q

What is toxic shock syndrome? (TSS)

A

This is caused by staphylococci. These bacteria produce an exotoxin. TSS is characterised by an abrupt onset of fever, rash, diarrhoea and shock.

Associated typically with tampon users, but can occur in anyone including children

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7
Q

What is Waterhouse-Friderichsen syndrome?

A

Usually caused by Neisseria meningitidis. Rapidly datal illness if untreated. Causes purpuric skin rash and shock. Adrenal haemorrhage (and subsequent hypoadrenalism) may occur.

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8
Q

What are the features, complications and management of measles?

A

Measles is caused by an RNA paramyxovirus. Spread by droplet.

Period of infectivity is 4 days before and after rash, after which they can return to work/school.

Two stages:

1) Pre-eruptive and catarrhal stage: fever, cough, rhinorrhoea, conjunctivitis and pathogonomic Koplik’s spots (grey spots on buccal mucosa).
2) Eruptive stage: maculopapular rash starts on face, spreads to whole body. Fades after a week.

Complications:

  • Gastroenteritis
  • Otitis media
  • Encephalitis
  • Myocarditis

Pregnant ladies need not worry about congenital malformations but there is increased risk of miscarriage as with most infections.

Rarely the virus reactivated before puberty and causes panencephalitis with mental problems and death

Management

Symptomatic.

UK - All kids given MMR vaccine (measles mumps rubella)

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9
Q

What are the features of mumps and its management?

A

Mumps is caused by paramyxovirus. Spread by droplets. (Same as measles)

Features: Primarily school aged children and young adults.

  • Fever
  • Headache
  • Malaise
  • PAROTID SWELLING
  • (orchitis, meningitis, pancreatitis, oophoritis, myocarditis, hepatitis)

Management:

Symptomatic treatment.
Children can return to school 5 days after ONSET of swelling.

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10
Q

What are the features and management of Rubella?

A

Also called ‘german measles’, this is caused by an RNA virus. Peak age of 15 years. Incubation period 2-3 weeks.

Prodrome of malaise, fever, lymphadenopathy.
The pinkish rash on face and trunk after about a week, lasting for 3 days.
Clinical diagnosis but antibodies can be measured

Management:

Symptomatic.
Return to school 6 days after onset of rash
Complications - arthralgia, encephalitis, thrombocytopenia

Congenital rubella syndrome:

Maternal infection during pregnancy may affect the fetus if infection during first trimester when the fetus is most vulnerable:

  • heart defects
  • cataracts
  • microcephaly
  • mental handicap
  • deafness

(DUMB HEARTLESS BLIND BABY)

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11
Q

What are the three herpes viruses?

A

Herpes Simplex Virus (HSV)

Varicella zoster virus (chicken pox virus and shingles)

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12
Q

What are the features and management of HSV?

A

HSV1:

  • Herpetic stomatitis with buccal ulceration, fever and local lymphadenopathy
  • Herpetic whitlow: damage to skin over a finger allows access of the virus, allowing irritating vesicles to form (i.e. if you touch sore area of skin allowing virus to enter the cut)
  • Keratoconjuncivitis (inflammation of both conjunctiva and cornea)
  • Acute encephalitis
  • Disseminated infection in the immunocompromised

HSV2:

  • Transmitted sexually
  • Genital ulcers (can also occur in HSV1)
  • Fever
  • Lymphadenopathy
  • Anorectal infection in homosexuals
  • Systemic infection in immunocompromised

Recurrent HSV infections occur when virus lies dormant in ganglion cells and is reactivated by trauma, illness, UVR. This leads to recurrent labialis (cold sores) or recurrent genital herpes.

Diagnosis: clinical but HSV DNA PCR can be done

Management: Oral aciclovir for 5 days - only beneficial if used while ulcers still forming, useless later…

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13
Q

What are the features and management of varicella zoster virus (VZV)

A

This is the chickenpox virus. It is primary infection with VZV that causes chicken pox, which may produce a mild childhood illness. Note that chicken pox can be very severe in adults and immunocompromised.

Features:

  • 2 to 3 weeks incubation
  • Prodrome of fever headache malaise
  • Rash on face, salp, trunk begins as macules and develops into papules and vesicles, which heal with crusting.
  • VERY ITCHY
  • Complications include pneumonia and CNS involvement. CNS involvement presents as acute truncal cerebellar ataxia

Diagnosis: clinical but viral DNA PCR can be done

Management: No treatment in healthy children. Over 16 y/o given antiviral therapy with aciclovir is they present within 3 days because risk of severe disease is increased.

If pregnant and exposes to VZV, give zoster immunoglobulin (ZIG) and aciclovir if they do go on to develop chickenpox.

Papule is flat circumscribed alterations in skin color. Papule is a solid, elevated lesion with no visible fluid which may be up to ½
cm. in diameter. Vesicles are circumscribed epidermal elevations in the skin containing clear
fluid and less than ½ cm

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14
Q

What are the features of herpes zoster (shingles)

A

After VZV primary infection, the virus remains dormant in the dorsal root ganglia/CN ganglia, and if it reactivates, it causes shingles.

A person with shingles (particularly if rash is weeping) can actually cause chickenpox in a non-immune individual after close contact and touch.

Features:
-pain and tingling in a dermatomal distribution precedes the rash by a few days. The rash consists of papules and vesicles in the same dermatome. The commonest sites are the lower thoracic dermatomes and the opthalmic division of the trigeminal nerve (V1)

Management:
Oral aciclovir ASAP. Main complication is post-herpetic neuralgia (PHN) which can be severe and last for years - ridiculous isn’t it! What a pain! - Treat this with carbamazepine or phenytoin (yes it is an anti-epileptic). PHN can be reduced by prompt aciclovir treatment.

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15
Q

What are the features of infectious mononucleosis and Epstein-Barr virus (EBV)?

A

Infectious mononucleosis (glandular fever) is caused by the EBV and predominantly affects young adults (kissing disease). Transmitted in saliva and aerosol.

Major cause for hairy leukoplakia in patients with AIDS, Burkitt’s lymphoma, nasopharyngeal carcinoma, post-transplant lymphoma and the immunoblastic lymphoma of AIDS patients.

Features:

  • Fever
  • Headache
  • Sore throat
  • transient macular rash (usually if given amoxicillin inappropriately thinking it is just a sore throat)
  • Cervical lymphadenopathy
  • Splenomegaly
  • Mild hepatitis

Rare Cx - splenic rupture, myocarditis, meningitis.

REMEMBER THAT CMV, TOXOPLASMOSIS AND ACUTE HIV PRODUCT SIMILAR ILLNESS.

Investigations:

  • Atypical lymphocytes on peripheral blood film strongly suggest EBV
  • Detection of heterophile antibodies is diagnostic test of choice. ( Heterophile antibodies are antibodies produced against poorly defined antigens)
  • Paul bunnell reaction: the antibodies agglutinate sheep red cells (Monospot test for horse red cells)

Management: No treatment. Corticosteroids if neuro involvement, or when there is tonsillar enlargement causing obstruction and if there is severe thrombocytopenia or haemolysis

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16
Q

What is lyme disease? List its features and treatment

A

This is a multisystem disorder caused by a spherocyte called Borrelia burgdorferi. It is spread FROM dears VIA ticks.
Most likely to occur in summer months in woodland areas.

Features:
-Stage 1: occurs 7-10 days after infection. Erythema migrans (expanding rash) at site of bite + fever, headache, malaise, myalgia. EM IS PATHOGONOMIC OF LYME DISEASE - It looks like a bulls eye

-Stage 2: weeks to months later with neurological problems, cardiac problems and arthritis

Patients may continue to have fatigue and MSK pain for months to years (Chronic Lyme Disease) after acute infection is treated. The term chronic lyme disease is misleading as there is no evidence that this is due to persistent infection with Borrelia.

Diagnosis is mainly clinical. Serology will show IgM antibodies in first months, and IgG later.

Management: Amoxicillin or doxycycline for early disease. IV benpenm or ceftriaxone for later stages.

P.S. tick usually needs to be attached for 48 hours or more to transmit the infection so prompt removal of the tic is encouraged.

Borrelia burgdorferi is not classified as either Gram-positive or Gram-negative

17
Q

What is Leptospirosis? List its features and management

A

This zoonosis (infection spread from animals to humans) is caused by a gram-negative organism - Leptospira interrogans, which is excreted in animal urine and enters the host via skin abrasion or intact mucous membranes.

Features:

-10 day incubation period
-Initially fever, headache, malaise, ,yalgia
-Then immune phase - MENINGISM
Most recover uneventfully at this stage.

Some will go on to develop hepatorenal failure, haemolytic anaemia, and circulatory collapse (Weil’s disease)

Investigations:
-Blood or CSF culture will show organisms in first week
-Urine in second week
Serology for IgM

Management:
Doxycycline for mild.
IV penicillin or erythromycin for more severe disease

18
Q

What are causes of fever in the traveller?

A

80% are due to:

  • Malaria
  • Viral hepatitis
  • Febrile illness unrelated to travel
  • Dengue fever
  • Enteric fever (typhoid and paratyphoid)

Others:

  • Gastroenteritis
  • Rickettsia
  • Leptospirosis
  • Schistomoniasis
  • Amoebic liver abscess
  • TB
  • Acute HIV infection

Viral haemorrhagic fever (VHF) is a rare cause of fever in travellers. This presents with high fever and other symptoms before spontaneous haemorrhage kicks in with bleeding into skin gut and lung - isolate!
Lassa fever, Marburg virus and Ebola disease are mainly seen in Sub-Saharan African and Congo-Crimean haemorrhagic fever in Asia and Africa

19
Q

How to assess returned traveller with fever

A

Detailed travel history to work out incubation period, where they visited (rural vs urban, developed vs developing)

Ask about needle and blood exposure, acupuncture, etc.

Vaccination and prophylaxis

20
Q

What are the typical incubation periods for tropical infections?

  • Arboviral infections (including dengue fever), enteric bacterial infections, paratyphoid, plague, typhus, haemorrhagic fevers
  • Malaria, typhoid fever, scrub typhus, Lassa fever, African trypanosomiasis, brucellosis, leptospirosis
  • Viral hepatitis, TB, HIV, schistosomiasis, amoebic liver abscess, visceral leishmaniasis, filariasis
A

Short 21 days:

-Viral hepatitis, TB, HIV, schistosomiasis, amoebic liver abscess, visceral leishmaniasis, filariasis

21
Q

List the pathogenesis, features and management of malaria

A

Malaria is a protozoan parasite. Transmitted by bite of female mosquito. Occasionally transmitted on contaminated blood, equipment, IVDUs.

There are four malaria parasites that infect humans. Most dangerous is Plasmodium falciparum, and the symptoms with this virus can rapidly progress from acute fever with rigors to severe multiorgan failure, coma and death.

Falciparum does not relapse.
The other 3 (ovale, vivax, malariae) are more benign
Ovale and vivax may relapse
Malariae may become chronic.

Pathogenesis:
Passes through skin via bloodstream. Goes to liver to make babies. Few days later infected hepatocytes rupture, releasing the merozoites into the blood where RBCs take them up and here they develop, and then the RBC ruptures, causing anaemia and pyrogen release causing fever.

Falciparum infected RBCs stick to endothelium causing occlusion and therefore severe organ damage, chiefly in gut, kidney, liver, and brain.

Ovale and vivax remain latent in liver and this is the reason these can relapse.

Features:

Incubation is 10-14 days for Vivax, ovale and falciparum.
18 days to 6 weeks for malariae

Onset may be delayed up to 3 months, 1 yea in vivax! woah. This happens in those who have partial immunity or who took chemoprophylaxis.

FALCIPARUM infection is a medical emergency due to rapid deterioration.
The following are more likely to occur if >1% RBCs infected:

  • Cerebral malaria
  • Blackwater fever (dark urine due to RBC breakdown)

Investigations:
-Light microscopy of Giemsa stained thick and thin blood smear.
Thick smears to diagnose malaria; thin smears to quantify % infected cells and species identification

Take 3 smears over 48 hours before you rule out malaria to make sure you don’t miss it.

Do FBC, U and Es, liver biochemistry, and blood glucose in falciparum infection to detect complications.

Management:

Chloroquine for falciparum

22
Q

Dengue fever

A

Transmitted virus by female mosquitoes. 506 day incubation. Causes fever, headache, retro-orbital pain and severe myalgia, often with skin rash.

A severe form is dengue haemorrhagic fever in which there s thrombocytopenia and spontaneous bleeding.

Dengue shock syndrome can occur (hypotension, tachycardia, poor peripheral perfusion)

Detection by PCR.

Treatment is supportive