Microbiology Flashcards

1
Q

What is a sinus?

A

A sinus is an abnormal communication from deep tissue to the skin, and it indicates active infection underneath (they can’t have a treated or cured infection).

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2
Q

Define osteomyelitis

A

A progressive infectious process resulting in inflammatory destruction, bone necrosis (sequestrum) and new bone formation (involucrum).

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3
Q

What are the 3 types of osteomyelitis I should know about?

A

Haematogenous, Contiguous and Diabetic

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4
Q

Tell me about haematogenous osteomyelitis

A

Following bacteraemia, especially in children (because their bones are very vascular), metaphyseal area of long bones (because this is where most of the metabolic activity is).

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5
Q

Tell me about contiguous osteomyelitis

A

After trauma or surgery, or overlying soft tissue infection. May be associated with prosthesis/pins/plates. Direct spread of infection. Affects all ages, any bone

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6
Q

Tell me about diabetic osteomyelitis

A

A consequence of reduced vascularity, neuropathic skin changes, decreased local immunity and metabolic disturbance. Often associated with foot ulcers. Assume osteomyelitis if bone evident at the base of the ulcer. Very hard to treat. Often results in amputation

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7
Q

What might you see on an x-ray in a patient with osteomyelitis?

A

Periosteal thickening/ elevation

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8
Q

What is the overall most common pathogen to cause osteomyelitis?

A

Staphyloccocus aureus

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9
Q

What is the most common pathogen to cause osteomyelitis in newborn babies? (Note this is not the most common cause of osteomyelitis overall)

A

Group B streptococci (normal vaginal flora)

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10
Q

What is the most common pathogen to cause septic arthritis?

A

Staphylococcus aureus

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11
Q

Is reactive arthritis a joint infection?

A

Not a joint infection, it is a post-infectious phenomenon that involves the joints and makes them painful. It is a sterile type of arthritis and if you aspirate the joint there will be white cells but no organisms present because there was never an infection in the joint itself- it is an immune response to an (usually GI/GU) infection

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12
Q

What is the most common pathogen to cause prosthetic joint infections?

A

Coagulase negative staphylococci

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13
Q

What are the treatment options for prosthetic joint infection?

A

Conservative - DAIR - debridement, antibiotics, implant retention Radical i.e. remove prosthesis- either 1 stage or 2 stage Lifelong suppressive therapy if unfit for surgery Do nothing- if elderly, comorbidities and current symptoms do not impact QOL

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14
Q

What tend to be the antibiotic treatment durations for osteomyelitis (paediatric and adult), septic arthritis and prosthetic joint infections?

A

2-3 weeks for septic arthritis 4 weeks for paediatric osteomyelitis 6-8 + weeks for adult osteomyelitis but PJI may require months if prosthesis still in, or years if persistent and can’t cure

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15
Q

What antibiotics tend to be given to treat a bone/joint infection caused by staph aureus?

A

Flucloxacillin + rifampicin, fusidic acid or gentamicin

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16
Q

What does ‘facultative’ mean with regards to optimum atmospheric conditions for bacteria?

A

Organisms that can grow in the presence or absence of oxygen.

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17
Q

What is meant by the terms ‘psychrophile’, ‘thermophile’ and ‘mesophile’ with respect to optimum temperature of bacteria.

A

Psychrophile = organisms capable of growth in low temperature ranging from -200 to 10 degrees Thermophile= organisms that thrive at unusually high temperatures between 40 and 122 degrees e.g. campylobacter Mesophiles= organisms that grow happily at 37 degrees e.g. E-coli

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18
Q

How do staphylococcus and streptococcus organisms sit next to each other?

A

Staphylococcus organisms = grape like Streptococcus = in a chain

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19
Q

Summarise key points about the gram stain

A

Exploits differences in the bacterial cell wall in the staining process. Purple = gram positive. Pink= gram negative - pink has an ‘n’ in it so it is gram negative

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20
Q

Tell me about cross linking within peptidoglycan

A

The strands (comprised of N-acetylmuramic acid and N-acetylglucosamine) are cross linked by short runs of amino acids. Gram negative bacteria have only a single layer, gram positive bacteria contain up to 40 layers of peptidoglycan.

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21
Q

How does penicillin work as an antibiotic?

A

Note that the last two amino acid molecules in peptidoglycan are always alanines. Penicillin (which is a beta-lactam antibiotic) is an analogue of alanine. The enzymes which add the alanine to the chains have a greater affinity for penicillin, and so the organism is unable to make its cell wall and in an osmotic environment, the cell will lyse.

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22
Q

What is endocarditis?

A

Bacterial (or fugal) infection of a heart valve or area of endocardium. Clinical presentation traditionally classified as either acute or subacute. If you have a short history and present acutely it is more likely to be staph aureus, whereas if you have been unwell for weeks/months it might be more likely to be one of the viridans streptococci.

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23
Q

What do people with endocarditis generally die of?

A

They don’t tend to die of the bloodstream infection, they die of the cardiac complications such as heart failure (because of the damaged heart valves). In treatment, we aim to reduce the amount of damage that is accred (whether that be medical or surgical Tx).

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24
Q

What are the four categories of infective endocarditis?

A

Native valve infective endocarditis Prosthetic valve infective endocarditis IVDU-associated endocarditis Nosocomial infective endocarditis

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25
Q

Tell me about native valve endocarditis

A

Congenital heart disease (high to lower pressure gradients greatest risk) Rheumatic heart disease Mitral valve prolapse Degenerative valve lesions

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26
Q

What organisms are typically involved in native valve endocarditis?

A

Viridans streptococci

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27
Q

Tell me about prosthetic valve endocarditis and the commonest organism which causes it

A

Only 1-5% of cases. Coagulase negative staphylococci predominate (e.g. staph epidermis, staph saprophyticus).

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28
Q

Tell me about IVDU associated endocarditis and the organism most likely to cause it

A

Right sided infection more common. Tricuspid 50%, aortic 25%, mitral 20%. Staphylococcus aureus predominates, but other organisms including fungi (e.g. candida tropicalis) sometimes responsible.

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29
Q

What are the HÁČEK organisms in infective endocarditis?

A

Although, staph aureus, streptococcus species and enterococci together are responsible for >80% of cases of IE, there is a group of gram negative organisms (bacilli) which can cause IE they are often found in the upper airway and usually younger people with underlying cardiac problems tend to present with these organisms.

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30
Q

What infecting organisms may be ‘culture negtive’ in IE?

A

Q fever (coxiella burnetti) -zoonotic infection from goats Bartonella app Trypheryma whipplei

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31
Q

What are the clinical features of infective endocarditis?

A

Malaise (95%), pyrexia (90%), arthralgia (25%) Cardiac murmurs (90%), cardiac failure (5%) Oslers nodes (15%) Janeway lesions (5%), splinter haemorrhages (10%), Roth spots (5%). Oslers nodes are painful whereas janeway lesions are painless. Roth spots are flame-shaped haemorrhages on the retina. Splenomegaly (40%), cerebral emboli (20%), haematuria (70%) haematuria because they have a degree of glomerulonephritis

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32
Q

How does the clinical criteria work for IE? (Duke’s criteria, Durack et al.)

A

(2 major) or (1 major and 3 minor) or (5 minor)

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33
Q

What are the major criteria for IE?

A

Positive blood culture- typical organisms for IE from 2 separate blood cultures. Persistently positive blood cultures. Evidence of endocardial involvement- positive echocardiogram- vegetation’s, abscess, new partial dehiscence of prosthetic valve, new valvular regurgitation

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34
Q

What are the minor criteria for IE?

A

Predisposition (heart condition, IVDA) Fever Vascular phenomena (major arterial emboli, septic pulmonary infarcts, intracranial haemorrhage, Janeway lesions) Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor Microbiological evidence: positive blood culture but not meeting major criteria Echocardiogram: consistent with IE, but not meeting major criteria

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35
Q

When is surgery indicated in IE?

A

Extensive damage to valve, infection of prosthetic valve, worsening renal failure, persistent infection but failure to culture organism, embolism, large vegetation’s

36
Q

What treatment do we give for IE that is caused by a Viridan’s streptococci?

A

Benzylpenicillin (+ low dose gentamicin for synergy). In most cases at least 4 weeks of parenteral therapy will be required.

37
Q

What about treatment for IE in Q fever and chlamydiae IE?

A

Q fever - tetracyclines plus hydroxychloroquine, >year therapy Chalmydiae- tetracyclines

38
Q

What is meant by the term ‘intercurrent bacteraemia’ ?

A

Occurring during the progress of another disease such as cardiac

39
Q

What conditions did NICE say are and are not associated with a risk of developing IE?

A

Associated with risk: acquired valvular heart disease with stenosis or regurgitation, valve replacement, structural congenital heart disease, hypertrophic cardiomyopathy, previous IE. The following are not associated with a risk of IE: isolated atrial septal defect, repaired ventricular septal defect, repaired patent ductus arteriosus, closure devices that are judged to be endothelialised.

40
Q

What is a summary statement for the guidelines of antibiotic prophylaxis for IE?

A

In summary, this guideline recommends that antibiotic prophylaxis solely to prevent IE should not be ‘routinely’ given to people at risk of IE undergoing dental and non-dental procedures. If a person at risk of IE is receiving antimicrobial therapy because they are undergoing a GI or GU procedure at a site where there is a suspected infection, the person should receive an antibiotic that covers organisms that cause IE.

41
Q

What virological tests do you do for both acute and chronic presentations?

A

Acute presentation- virus antigen or genome (serology/ PCR). Antibody - IgM early (the first immunoglobulin you make against a pathogen in an infection) Chronic disease- antibody- IgG - appears later, persists (so if you wanted to know whether someone has EVER had a certain infection you would look for IgG).

42
Q

What are some viral ‘exotic’ emergencies?

A

Viral haemorrhagic fevers (including Ebola- the bat is the natural host), mortality rate of up to 90% (25%-90%, average 50%), region: particularly Africa. Rabies (mostly an infection of dogs or other animal bites that is transmitted to human through bite or scratch; 100% fatal once you present clinically. Particularly in developing countries). MERS CoV (middle east respiratory syndrome coronavirus)- an infection of camels, causes quite a high mortality rate (40%). Is hasn’t evolved to become a human -> human pathogen yet. Avian influenza A- he influenza we get is not the same as bird flu. Influenza A is a natural infection of water birds, region: Asia (China), mortality around 50%.

43
Q

Tell me about measles (Rubeola)

A

High temperature (39/40 degrees), florid maculopapular rash (flat, red area on the skin that is covered with small confluent bumps), conjunctivitis, Koplik’s spots (clustered white lesions on the buccal mucosa - pathognomonic for measles), almost always symptomatic.

44
Q

Tell me about rubella (German measles)

A

Less florid red-pink skin rash made up of small spots (so the rash isn’t as marked as in measles). Post-auricular lymphadenopathy. Arthralgia- more common in adults. May be subclinical

45
Q

Tell me about parvovirus b19 (erythema infectiosum)

A

Rash maculopapular (typically), more florid on the face (children)- slapped check. Moves to trunk, limbs. Central clearing leads to reticular, lace-like appearance. Re-appears with heat (e.g. after a warm bath). Aching/ painful joints. May be subclinical

46
Q

Tell me about varicella zoster rash

A

Itchy, vesicular rash all over the body. Fever, tiredness and headaches can last up to a week

47
Q

How do most anti-viral drugs act?

A

Most interfere with the replication of the genome (block nucleic acid synthesis)

48
Q

Tell me about antiviral nucleosides (which are very typical antivirals)

A

Mimic natural nucleosides (base+sugar), but are deoxy derivatives of A,C,T,G. They require to be phosphorylated to act as substrates for DNA polymerase enzymes. They act as competitive inhibitors and DNA chain terminators. Classic examples are anti-herpes anti-virals e.g. aciclovir.

49
Q

What is aciclovir usually used to treat?

A

Effective against HSV types 1 and 2 and VZV infections. Main indications are: severe primary labial and genital herpes, ophthalmic HSV and VZV, eczema herpeticum, herpes zoster, chickenpox, herpes encephalitis, prevention and Tx of disseminated herpetic disease in the immunocompromised patient.

50
Q

What is the main limitation with aciclovir?

A

Limited oral bioavailability so requires to be given 5 times a day for 5-7 days. So patients rarely take them as they should. Topical therapy of limited value with the exception of eye drops used in ophthalmic herpes and ophthalmic zoster

51
Q

Tell me about the influenza virus

A

Single stranded helically shaped RNA virus of the orthomyxovirus family. Three basic antigen types: A,B,C.

52
Q

What is the main reservoir for the flu virus?

A

Water birds

53
Q

What does ‘drift’ and ‘shift’ mean in relation to viruses?

A

Drift= when there are minor changes to the virus that occur during replication. These changes can be sufficient to create a new strain that can infect people again. These small drift changes are the reason the flu vaccine is different every year. Shift= when there are major antigenic changes that occur when two different viruses co-infect a ‘mixing host’. The two viruses in the mixing host can form a whole new completely different virus. Pigs are common mixing hosts.

54
Q

What antivirals do we have against the influenza virus?

A

Neuraminidase inhibitors- neuraminidase is an enzyme that helps the virus slip out of one cell and infect another cell in the respiratory tract. Oseltamivir (Tamiflu) and Zanamivir (Relenza)- prevents enzyme function in the virus.

55
Q

What are the features used to define SIRS (systemic inflammatory response syndrome)?

A

Defined as two or more of: Temp >38 or <36 Heart rate >90 Resp rate >20 White cell count >12 or <4 x 10^9 cells/L Altered mental status Hyperglycaemia >7.7 mmol/L Hypotension <90mmHg SBP

56
Q

Tell me about the sepsis-3 definition which came about in 2016

A

The original sepsis definition was focussing on how much of the body was responding to an infection in terms of inflammation compared to how much damage the inflammation is causing to the body. The sepsis-3 definition focuses not on the degree of inflammation or the degree of shock or sepsis, but it focuses on the degree of organ dysfunction caused by the infection (and the response to that infection)

57
Q

What scoring system does the sepsis-3 definition use?

A

SOFA score- stands for sequential (sepsis related) organ failure assessment (SOFA) score

58
Q

What does the SOFA score take into account?

A

Respiratory damage (by looking at resp rate) Liver damage (looking at bilirubin, LFTs, clotting, albumin) Cardiovascular damage (by looking at MAP and serum dopamine levels) CNS damage (using GCS) Renal damage (looking at creatinine and urine output) So it looks t how much impairment the infection is causing in the wider system. Generates a score from 0-4.

59
Q

So what are the updated (2016) definitions of sepsis?

A

Sepsis= a life-threatening organ dysfunction caused by a dysregulated host response to an infection. The clinical criteria for sepsis is: a suspected or documented infection AND an acute increase of 2 or more SOFA points (a proxy for organ dysfunction).

60
Q

How do we define septic shock?

A

Sepsis AND vasopressor therapy needed to elevate MAP >65mmHg and a raised lactate of >2mmol/L despite adequate fluid resuscitation. Remember that lactate is a surrogate marker of anaerobiosis.

61
Q

What is a qSOFA?

A

Stands for quick-SOFA- it is a short version of the SOFA score which you can do without any blood tests. It only looks at resp rate, BP and mental status.

62
Q

In terms of sepsis pathogenesis, the key pathology lies in the capillaries/ microcirculation. What are the three key things that happen as a result of the cytokines response of the immune system?

A
  1. Platelet activating factor causes increased platelet aggregation and adhesion -> resulting in clogged capillaries. They also attract a fibrin band, resulting in stickiness of the capillaries. 2. Nitric oxide (a secondary mediator in sepsis pathology) causes loss of contractility of vascular smooth muscle (so the vessels have reduced vascular tone and become weak and ‘floppy’) -> dilated capillaries. 3. TNF alpha and C5a cause increased vascular permeability within the capillaries -> leaky capillaries
63
Q

Tell me about cardiac changes and ‘hot’ and ‘cold’ sepsis

A

Initially in sepsis there is a high cardiac output - classic ‘bounding pulse’ of sepsis, the patient will have a fever and be sweaty (like in any other infection) = ‘hot’ sepsis As cardiac muscle becomes affected by organ hypoperfusion and toxic products, cardiac output falls. Patient becomes cold, clammy, (weak pulse with a narrow pulse pressure) resembling a patient with cardiogenic shock = ‘cold’ sepsis

64
Q

Tell me more about the coagulopathy in sepsis

A

Increased platelet activating factor leads to platelet adhesion to vascular endothelium. TNF alpha and IL-1 cause release of tissue factor (thromboplastin) from endothelial cells, leading to activating of the coagulation cascade. Remember you also have consumption of the clotting factors which results in bleeding- DIC. Also, because it causes occlusion of the microcirculation and hypo-perfusion this thereby contributes to the multi-organ failure in sepsis.

65
Q

What is the estimated mortality from severe sepsis and septic shock?

A

Severe sepsis: 30% Septic shock: 60%

66
Q

What are the risk factors for severe sepsis?

A

Immunosuppression Comorbidity (most commonly neoplasia and COPD) Age Invasive devices (vascular, surgical, ventilatory) Use of antimicrobials

67
Q

What is the Mx for sepsis (sepsis 6)?

A

Give: oxygen, fluid challenge, antibiotics Take: lactate, blood cultures, urine output

68
Q

In terms of controlling infectious diseases and food borne illnesses what is good to remember?

A

Can be caused by salmonella, shigella, campylobacter, E.coli 0157 (children at petting zoos can often get this), listeria monocytogenes (often in refrigerated foods e.g. pate and soft cheeses) and clostridium perfringens (anaerobic, particularly canned foods that have spores retained).

69
Q

What can E.coli 0157 cause?

A

HUS (haemolytic uraemic syndrome)

70
Q

Tell me about scarlet fever

A

Scarlet fever is a toxin related reaction you get to group A strep (group A strep is the commonest cause of bacterial tonsillitis).

71
Q

What is the definition of a hospital acquired infection?

A

Infections that are neither present nor incubating when a patient enters hospital but develop during hospital admission or are incubating when a patient leaves hospital.

72
Q

What is the biggest source of hospital acquired bacteraemia?

A

Central venous lines

73
Q

What are the principles of surgical prophylaxis?

A

Clean: non traumatic, no inflammation, no break in technique, no breach of respiratory, alimentary or GU tracts = no prophylaxis, unless metalwork, spine. Clean contaminated: non-traumatic, but break in technique or breach of respiratory, alimentary or GU tract. No significant spillage = one dose Contaminated: major break in technique, gross spillage from a viscus that may include non-purulent material. Dirty traumatic wounds, faecal contamination, foreign body, de-vitalised viscus. Pus encountered from any source during surgery. Treat for 5-7 days.

74
Q

Tell me about trachoma

A

Chlamydia serovars A-C (not the same chlamydia that causes STIs). Most common cause of preventable blindness worldwide. Transmission: hand to eye contact, flies. Prevention: clean water (because flies lay their eggs in the water, decrease fly populations). Tx: systemic erythromycin or doxycycline (whole towns are given mass Abx Tx).

75
Q

Which individuals cannot have live vaccines?

A

Immunocompromised individuals (they may actually get the disease from it).

76
Q

Tell me about polysaccharide and conjugate vaccines

A

Polysaccharide vaccines are made of extracted and purified forms of the bacterial outer polysaccharide coat. They do not simulate the immune system as broadly as protein antigens such as toxins found in tetanus, diphtheria etc. Protection is not long-lasting and response in infants and young children is poor. Some polysaccharide vaccines have been enhanced by conjugated (eg HiB and MenC vaccines). Conjugation= attachment of a carrier protein to a polysaccharide antigen. Conjugate vaccines generate a better immune response and are effective even in young children. So polysaccharide vaccines aren’t appropriate for children unless they are conjugated.

77
Q

Tell me about pneumococcal vaccination in the UK

A

Pneumococcal conjugate vaccines = all children who are <2 years of age as part of the childhood vaccination programme. Newer version in 2010 protects against 13 capsular types. Pneumococcal polysaccharide vaccine = all adults who are over 65 years of age. All children and adults who are 2-64 and considered to be at higher risk. The PPV provides protection against 23 types of pneumococcal bacteria.

78
Q

Tell me about respiratory syncytial virus (RSV) as an example of passive immunisation

A

RSV can cause a disease called bronchiolitis in the under 1s. Some children are really susceptible to this if they have got underlying heart or lung disease so we can give them antibodies when RSV is most likely to infect them (which is during winter). RSV directed antibodies (Palivizumab). Monthly during RSV season.

79
Q

What are the categories of immune deficiency?

A

Conditions/ co-morbidities e.g. pregnancy, old age, malnutrition, liver/renal failure, splenic dysfunction, diabetes Melli’s is, rheumatoid arthritis, burns Iatrogenic causes: chemotherapy, steroids, radiotherapy, transplantation Disorders of the immune system: HIV, lymphoma, leukaemia, myeloma, congenital causes (SCID), etc

80
Q

How else can we categorise immune deficiency?

A

T cells and cell mediated immunity B cells and humoral immunity Phagocytic cells And within these; number or function Complement, splenic function

81
Q

What is neutropenic sepsis?

A

Neutrophil count <0.5 x 10^9/l plus either Temperature >38 degrees Or other signs/symptoms consistent with sepsis

82
Q

Tell me about invasive aspergillosis

A

Environmental mould with infection occurring through inhalation of spores. Typically patients with prolonged, profound neutropenia. Most frequently causes respiratory infection. Diagnosis: radiology, fungal markers (e.g. beta-glucan), microscopy and culture. Tx: anti-fungal therapy e.g. voriconazole

83
Q

Tell me about mucormycosis

A

Aggressive infection caused my mucoraceous moulds. Immunocompromised or severely hyperglycaemic patients. Clinically manifest as rhinocerebral infection (necrosis of involved areas). Tx: surgical debridement and anti-fungal therapy

84
Q

What are the therapeutic options for neutropenic sepsis?

A

Mono therapy - anti-pseudomonal beta lactam e.g. piperacillin/ tazobactam, imipenem or meropenem, ceftazidime Combination therapy- anti pseudomonas beta lactam plus aminoglycoside e.g. gentamicin

85
Q

diptheria

A

caused by corynebacterium diptheriae diptheric membrane on tonsils (grey coating) sore throat bulky cervical lymphadenopathy (bull neck) neuritis (cranial nerves) heart block

86
Q

bacterial causes of gastroenteritis

A
87
Q

malaria

A

falciparum malaria is the most common and most severe type of malaria

features:

  • schizonts on blood film

temp > 39

hypoglycaemia

severe anaemia

parasitaemia > 2%