Core Microbiology Pathology Flashcards
Why do Certain Bacteria Cause Particular Infections?
3 Factors:
Host factors (Immune system and devices)
Opportunity (Exposure and Normal flora)
Bacterial Factors ( Virulence, Resistance, Environmental survival)
Where are E.coli & UTIS found what happens?
Part most peoples NORMAL bowel flora.
•Colonise urethral meatus & surrounding area e.g. perineum.
•Females- short urethra.
•Use pili to adhere to uroepithelial cells/ urinary catheter materials triggers host inflamm response (infec).
•Can develop resistance to antibiotics that treat UTIs.
Where are S.aureus &; Skin Infecs found, what happens?
- In NASAL CARRIAGE in 50% people.
- Can adhere to damaged skin e.g. eczma, surgical wound, burn etc.
- Makes exoenzymes &; toxins damage tissues &a provoke host inflamm response (pus formation by WBCs).
What is Staphylococcus aureus? What does it cause?
- Gram +ve coccus.
- Primary pathogen.
- 30-50% carry in nose.
- Causes skin/ soft tissue infecs- commonest; of surgical site infecs.
- Can get into blood stream.
- Bacteraemia/ septicaemia.
- Osteomyelitis/ septic arthritis.
- Endocarditis
- Pneumonia
- UTI
- Meningitis
What is Staphylococcus epidermidis? What does it cause?
- Opportunistic pathogen.
- SKIN commensal.
- Most people carry it on skin as part of normal flora.
- Is a ‘coagulase –ve staphylococci’ (coagulase lab test).
- Causes infec in association with ‘foreign bodies’ which it sticks to e.g. intravascular catheters, Prosthetic joints, prosthetic cardiac valves.
- Adheres to plastics/ metals using glycocalyx (slime), forming biofilms.
- Causes inflamm response.
- Over time joint loosens rocks pain.
What is Streptococcus pyogenes? What does it cause?
•‘Group A Strep’.
•Strawberry tongue
•In chains (not clump- see pic )
•Commonest cause of bacterial sore throat (pustular appearance of tonsils).
•Also causes;
o Scarlet Fever
o Necrotising fasciitis (‘flesh eating bug’)
o Other SSTIs (skin & soft tissue infecs)
o Invasive infecs, such as pneumonia
o Puerperal sepsis (lower genital tracts of females that’ve just delivered)
• Also associated with 2ndry immunological presentations e.g. glomerulonephritis.
What is Streptococcus pneumoniae? What does it cause?
- Commonest cause of bacterial pneumonia & bacterial meningitis (except in neonates).
- Also causes resp tract infeccs & other childhood infecs e.g. otitis media.
What is Streptococcus agalacitae? What does it cause?
- ‘Group B strep’.
* Commonest cause of meningitis & sepsis in neonates (babies under 3 mnths).
What is the Streptococcus milleri complex ?
- 3 closely related species of pus-forming streptococci.
- Normal flora in bowel & upper resp tract.
- Trigger pus formation
- Associated with abscesses; dental, lung, liver, brain & others.
What is Viridans streptococci?
- Collective name for a number of species of α-haemolytic streptococci that inhabit the upper respiratory tract e.g. S. oralis, S. mitis
- Can invade mucosal surfaces into the bloodstream = infec damaged heart valves.
- Classic cause of sub-acute bacterial endocarditis (sub acute as present over couple of weeks e.g. with tiredness etc)
What is Streptococcus gallolyticus?
- Formerly known as Streptococcus bovis
- A type of α- haemolytic streptococcus that forms part of bowel flora
- Bacteraemia with this organism can be associated with colonic malignancies (lower GI malignancies)
What is Listeria monocytogenes?
- Gram +ve bacillus.
- Rare but signinf cause of sepsis & meningitis in pregnancy, neonates & immunosuppressed patients.
- Zoonosis (can be transmitted to humans from animals), able to grow at low temps.
- Associated with consuming cheese from unpasteurised milk &; other foodstuffs
What is Corynebacterium species ?
- Gram positive bacilli
- A number of species are commensals of skin &upper respiratory tract
- Occasional opportunistic infecs associated with devices & trauma
- Corynebacterium diphtheria- classic cause of diphtheria
- Rarely seen now in UK because of immunisation
What is Propionibacterium acnes?
- Gram positive bacillus
- Associated with acne
- Can also cause device-associated & post-procedural infections
What is Enterobacteriaceae (‘coliforms’) ?
- A collective terms for diff gram –ve bacilli species found in bowel flora.
- Gram –ve stain pink & bacilli more sausage shaped.
- Common species; Escherichia coli, Klebsiella pneumoniae and Enterobacter cloacae
What is E.Coli?
- Commonest cause of UTI & bacteraemia (sources include urinary (e.g. catheters), biliary (e.g. gallstones) & intra-abdominal)
- Cause of nosocomial (originate in hospital) infecs e.g. line infections, pneumonia, wound infections
- Certain toxigenic strains (e.g. O157) associated with severe diarrhoea & haemolytic uraemic syndrome (HUS)
- Growing resistance to antibiotics
What is Pseudomonas aeruginosa?
- Multi-resistant gram negative bacillus
- Opportunistic pathogen (can’t cause infec in healthy, needs immunosuppression)
- Can cause resp infecs, UTIs, soft-tissue and other infecs in vulnerable patients
- Often produces characteristic green pigment
What is Neisseria meniingitidis?
- Gram –ve diplococcus
- Causes meningococcal sepsis and/or meningitis
- Classic presentation- purpuric non-blanching rash (sepsis)- can do glass test to help i.d. rash
- Reduction in cases after vaccine intro
What is Neisseria gonorrhoeae?
- Gram –ve diplococcus
- Causes gonorrhoea
- Ophthalmia neonatum (in babies whose mother has gonorrhoea).
- Rarely causes invasive infecs (e.g. septic arthritis) 2ndry to primary sexually transmitted infec
What is Haemophilius influenzae?
- Gram negative bacillus
- Part of normal respiratory tract flora
- Can cause resp tract infecs (e.g. pneumonia, infective exacerbations of COPD)
- Capsulated types (e.g. type b) associated with meningitis & epiglottitis (can obstruct airway).
- Only type b infecs prevented by HIb vaccine
What are anaerobes?
• Grow in absence of oxygen.
• CLOSTRIDIUM species- many are spore-forming;
o C. difficile – antibiotic-associated diarrhoea/colitis
o C. perfringens – classical cause of gas gangrene
o C. tetani – cause of tetanus
o C. botulinum – cause of botulism
• Bacteroides species, Fusobacterium species, Prevotella species and many others
• Often part of polybacterial infecs (with other organisms) e.g. dental infecs, lung abscesses, colonic abscesses, post-trauma skin/soft tissue infecs
What is Mycobacterium species?
- Often referred to as ‘Acid Fast Bacilli’ (AFBs)
- Do NOT stain using conventional gram staining (has slightly diff cell wall)
- Mycobacterium tuberculosis – cause of TB
- Other Mycobacterium species sometimes called ‘Atypical Mycobacteria’ &; cause resp infecs in those with chronic lung disease or opportunistic infecs in immuno-compromised patients e.g. AIDS, transplant patients, etc
What are Bacteria without a conventional cell wall
- Not going to stain with gram stain.
- Chlamydia species
- C. trachomatis – commonest cause of STI
- Mycoplasma species
- M. pneumoniae – common cause of resp tract infecs
What is Spirochaetes? What does it cause?
• Treponema pallidum- causes syphilis
• Other species of spirochaetes that can cause important infecs:
oLeptospirosis (in contaminated water/ rats).
oLyme Disease (tic bites you reactive skin lesions).
Which are gram –ve? • A] Streptococcus pneumoniae • B] Mycobacterium tuberculosis • C] Escherichia coli • D] Listeria monocytogenes • E] Neisseria gonorrhoeae • F] Mycoplasma pneumoniae
C & E,
A] Streptococcus pneumoniae (streptococcus is actually +ve)
• B] Mycobacterium tuberculosis (this can’t stain)
Which bacteria is a common cause of skin infection? • A] Klebsiella pneumoniae • B] Streptococcus pneumoniae • C] Haemophilus pneumoniae • D] Neisseria meningitidis • E] Staphylococcus aureus • F] Clostridium difficile
Staphylococcus aureus
Which of the following is the most common sexually transmitted infec? • A] Chlamydia trachomatis • B] Treponema pallidum • C] Corynebacterium diphtheriae • D] Staphylococcus aureus • E] Neisseria gonorrhoeae • F] Viridans streptococci
Chlamydia trachomatis
Which of the following can cause meningitis? • A] Neisseria meningitidis • B] Streptococcus pneumoniae • C] Listeria monocytogenes • D] Streptococcus agalactiae • E] Haemophilus influenzae • F] Staphylococcus aureus
All of them A] Neisseria meningitidis B] Streptococcus pneumoniae C] Listeria monocytogenes D] Streptococcus agalactiae E] Haemophilus influenzae F] Staphylococcus aureus
How do you define the ‘reference range’?
- Way to set up reference range.
- Take normal patients, then can set a normal distribution- reference range roughly -2 standard deviations to +2SDs.
- So certain patients results outside reference range; would be false +ves (so potentially abnormal).
- But reference range not fixed boundaries, are a guide- interpret them in light of patient.
Which factors affect Factors which Affect Reference Ranges?
• Age
• Gender
• Diet
• Pregnancy
•Time of month (menstruation hormones change), day (e.g. cortisol changes), yr (e.g. vit D)
•Weight (e.g. can dilute yourself with water)
•Stimulus (e.g. if given glucose can change reference range)
Need to bear these in mind when interpreting results!!!
What is Diurnal Rhythm of Cortisol?
- Usually only allowed to measure cortisol at 9am or 12pm- are stable.
- During day reference range widens.
- E.g. if stressed cortisol gone up, or gone for a run.
What is the Glucose Tolerance Test?
- E.g. give 75grams of glucose; if fasting increases in a specific range, if diabetic glucose will shoot up.
- Depends on stimulus & what you expect to happen after given stim.
16 yr old boy to hospital in deep coma. Exam; severely dehydrated & has deep sighing respiration.
- What are the two most likely diagnoses?
- What extra information would you like to obtain?
- What tests are needed and why?
- What test(s) would you wish to use to follow-up the patient?
16 yr old boy to hospital in deep coma. Exam; severely dehydrated &; has deep sighing respiration.
- What are the two most likely diagnoses? Diabetes, Salicylate over dose (e.g. in aspirin)
- What extra information would you like to obtain? Previous history - wt loss, polyuria etc.
- What tests are needed and why? Glucose, Gases, U&E, Salicylate, pH (if acidotic)
- What test(s) would you wish to use to follow-up the patient? HbA1c
What is Protein Glycosylation ?
Protein + Glucose —-> Advanced Glycosylated Endproducts (AGE)
• Non-enzymatic process
• Rate of formation proportional to;
– a) glucose concentration
– b) time
• May explain long-term complications of diabetes
• Scientific basis of commonly used monitoring tests
What is HbA1c?
- HbA1c is a stable glycosylated haemoglobin
* Its % concentration indicates cumulative glucose exposure.
What is fungi?
•Separate kingdom of organisms- are eukaryotic microorganisms.
•Single celled to macroscopic (yeasts & hyphae).
•Various growth forms- mainly hyphal or yeast.
•Glucan- chitin cell wall.
•Reproduce sexually and/or asexually, spore formation.
•Lifestyle;
o Saprophytes (decaying organic matter)
o Plant pathogens
o Animal pathogens (small n.o. compared to bacteria, viruses, protozoa)
What are the different types of fungal disease?
Superficial infection- Affects skin, hair, nails &mucocutaneous tissue.
• Dermatophytes
• Candidia
Subcutaneous infection- Affects subcutaneous tissue, usually following traumatic implant).
Systemic infection- Affects deep-seated organs.
• Aspergillus
• Candida
What are Dermatophytes ?
- Keratinophilic fungi- cause of disease in skin, hair & nail.
- 3 genera: Trichophyton, Microsporum, Epidermophyton.
- Slow growing moulds.
- Originate in soil (geophilic), other animals (zoophilic) or confined to humans (anthropophilic).
What is Tinea pedis? What else is it known as?
Dermatophyte Infections of Foot skin
Athletes foot
•Athletes foot- more common than onychomycosis, common in males, younger adults &sportsmen
- Uni- or bilateral
- Itching, flaking, fissuring of skin.
- Little inflamm- fungi adapted to not cause host response, so can survive.
- Interdigital: toeweb skin wet & macerated.
- Plantar: soles of feet dry & scaly, if skin of whole foot affected ‘Moccasin foot’.
- Hyperhidrosis, 2ndry to infection may increase severity.
- 2ndry to bacterial infec.
- May spread to infect toe nails.
- Trypical causes: Trichophyton rubrum
What is Tinea unguium? What else is it known as?
Dermatophyte Infections of Nail (toe or finger) (onychomycosis)
Fungal nail disease
Fungal nail infec- common in general adult pop (5-25% rate), increasing incidence in elderly.
• Thickening, discolouring, dystrophy of nail 4 main types;
1. Lateral/ distal subungual (getiing in on top & sides of nail)
2. Superficial white (on top of nail)- usually in immunocompromised
3. Proximal
4. Total nail dystrophy (usually affects whole nail)
• Typical causes: Trichophyton rubrum & ; T. interdigitale.
What is Tinea cruris? What else is it known as?
Dermatophyte Infections of Groin area skin
Jock itch
- More prevalent in men.
- Itching, scaling, erythematous plaques with distinct edges.
- Satellite lesions sometimes present.
- May extend to buttocks, back & lower abdomen.
- Typical cause: T.rubrum
What is Tinea corporis? What else is it known as?
Dermatophyte Infections of Limbs and torso skin generally
Tinea corporis
- Circular, single or multiple erythematous plaques.
- May extend from e.g. scalp or groin.
- Invasion of follicle ‘Majocci’s granuloma’ (more intense disease).
- Typical cause: wide range of dermatophytes, anthropophilic or zoophilic
What is Tinea capitis? What else is it known as?
Dermatophyte Infections of Scalp skin and hair
Scalp ringworm
•Scalp ringworm- most common among prepubertal children (US survey- tinea capitis in 6.6% children). Tinea capitis more common in deprived areas & black children (rates up to 41%), global prevalence 200 million cases
• Ranges in presentation depending on organs involved; from slight inflamm, scaly patches, with alopecia, balck dots, grey patches to severe inflamm.
• Kerion celsi: boggy, inflamed lesions,hair loss, usually from zoophilic dermatophytes (from animals).
• Favus: presence of cup shaped crusts or scutula.
•These diseases associated with hair invasion:
o Endothrix, spores inside hair shaft (lead to black dots)
o Exothrix, spores outside hair shaft
o Favic, hyphae only in hair shaft (favus)
How do you treat tinea capitis ?
Treat ALL tinea capitis cases with SYSTEMIC antifungals; Griseofulvin, terbinafine. Topical therapy will NOT be curative (role in reducing spread).
What is Candidia ?
•Large genus of yeast.
•Colonises GI tract mucosal surfaces in healthy people.
•Cause of superficial mucosal (oral &; vaginal) disease ‘thrush’, also occasionally skin disease & keratitis.
•Cause of systemic disease when in circ, system, can infect almost any organ in body.
• Caused by range of Candidia species;
o Candida albicans
o Candida glabrata
o Candida parapsilosis
o Candida krusei
What are Superficial Candida Infections- Oral Mucosa- the different types?
• Acute pseudo-membranous; o White plaques in mouth o Low CD4 count (<200 cells/ul) o Younger patients o Asthma with steroid inhalers (dampens down mouths mucosal immunity) • Chronic atrophic o Older patients o Erythema • Angular cheilitis • Chronic hypoplastic o Oral leukoplakia o Lesions may undergo malignant transformation
What is the epidemiology of Oral candidosis ?
- See it in HIV/AIDS- sometimes even if on Anti-retroviral therapy, T-cell immunity important to prevent mucosal candidosis.
- Antibiotic use- supress normal bacteria flora, less competition for yeasts.
- Patients with head & neck cancer- radiotherapy & chemo affect immune responses & salivary secretions.
- General debilitation in hospitalised patients- increases colonisation &; risk of oral disease.
What is Candida vulvovaginitis ?
- Affects 70-80% women at least once during child-bearing years.
- Pruritis, burning sensation, +/- discharge.
- Vaginal epithelium inflamm, may extend to labia majora.
- Often more florid infecs during pregnancy (becomes worse)
- 10% women- recurrent vulvovaginal candidosis (probably relates to subtle immune defect).
- Diagnosis: +ve culture in symptomatic patients (from swab).
What is the Diagnosis & Treatment of Superficial Candidosis?
- Diagnosis: culture with i.d. & antifungal sensitivity testing where appropriate.
- Treatment; usually oral azoles, fluconazole highly effective resistance in normally sensitive species (e.g. Candida albicans) or naturally resistant species (Candida krusei) can be a prob.
Which antibiotics should NOT be given to PREGANANT women?
REMEMBER- do NOT use oral fluconazole or other azoles in PREGANANT women- this increases risk of teratologies (e.g. heart defects), treat with topical azoles e.g. clotrimazole.
What is Systemic Candidosis ?
- Candida sp can infect almost any organ in body, defined by site of infec
- Usually acquired from colonised skin, mucosal sites, or GI tract
- Usually seen in the compromised host
- Candida albicans most common, other species also occur
- Disseminated disease may be identified from blood culture
What is Candida oesophagitis ?
- Mainly in HIV
- In 10-20% patients with oropharyngeal disease
- Pain/difficulty on eating/swallowing
- Diagnose: endoscopy with biopsy
What is Candida endocarditis ?
- Rare consequence of candidaemia
- IV drug abusers, valve surgery
- Vegetations on heart valves
- Fever, weight loss, fatigue, heart murmur
- Difficult to treat without valve replacement
What is Renal candidosis ?
- Candida from blood lodges in kidney tissue during filtration
- Abscesses form in kidney
- Immunocompromised premature neonates
- Associated with fever, abdominal pain, oliguria, anuria
What is a Urinary Tract Candida Infection?
- Ascending from genital tract infec/colonsation or from catheterisation
- More common in women, diabetics, damaged/abnormal urinary tracts
- May be hard to manage as few antifungals secreted in urine (so hard to get to the source of the fungi in body).
- Candiduria (isolation of Candida from urine) common, may or may not be significant
What is Candida peritonitis ?
- Peritoneal dialysis complication
- Bowel perforation during surgery (mixed bacterial/yeast infec)
- Fever, abdominal pain, nausea, vomiting
- Diagnosis: Candida culture from peritoneal fluid
- Treat: source control/ drainage & antifungals
What is a Hepatosplenic candidosis ?
- Dissemianted form of Candidosis
- In patients with leukaemia, other haematological malignancy
- Candidaemia (Candida in blood) during period of neutropenia (when have low levels of neutrophils in blood) (may or may not be detected)
- During neutrophil recovery yeasts lodge in liver and spleen (rarely also kidney)
- Abscesses form (bulls eye sign), fever, liver function disturbance
- Antifungal therapy may be ineffective as dead fungus still triggers inappropriate inflamm response
What is Candidaemia ?
•Candida in blood culture
•40 cases a year in LTHT (3000 beds), 3.3 cases per 1000 ICU admissions (UK study).
•Response;
o Remove lines (where possible)
o Start antifungal therapy
o Check heart and eyes (fungi can cause probs here)
What is Aspergillus ?
• Genus of moulds (filamentous fungi)
•Make airborne spores
•Aspergillus spores exposure universal by inhalation
•Airways may be colonised by Aspergillus sp.
•Not all people get it- how you react to it.
• Medically important species;
o Aspergillus fumigatus
o Aspergillus niger
o Aspergillus flavus
o Aspergillus terreus
What is Aspergillosis?
- Reaction to inhaling Aspergillus (usually people with affected lungs get it);
- Space occupying/non invasive – if have a lung cavity can get e.g. Aspergilloma (fungal ball)
- Allergic reaction – Asthma, cystic fibrosis (CF) e.g. Allergic bronchopulmonary aspergillosis, allergic sinus disease
- Chronic infection – Chronic lung disease (e.g. COPD) e.g. Chronic pulmonary aspergillosis
- Invasive infection – immunocompromised (leukaemia) e.g. Invasive pulmonary aspergillosis, invasive aspergillus sinusitis
What is Aspergilloma?
- Patients with cavities from previous TB, sarcoid, surgery
- Form solid balls of fungus
REMEMBER- Aspergillomas often indolent, but fungi balls may break up causing haemoptysis & are potentially fatal.
What are ALLERGIC FORMS of Aspergillosis?
Asthma & CF
Asthma
•Severe asthma with fungal sensitisation
•Wheezing, breathlessness
•IgE reac to fungi (including Aspergillus)
•Responds to antifungal therapy &; steroids
CF
•Allergic Broncho- pulmonary aspergillosis
•Wheezing, breathlessness, loss of lung function, bronchiectasis
•Airways inflammation
•IgE and G reaction to Aspergillus
•Responds to antifungal therapy & steroids
What is Chronic pulmonary aspergillosis (CPA)?
- COPD
- Chronic resp symptoms; cough, breathlessness, wheezing, chest pain
- Chest CT: consolidation & cavitation (occupies cavity it forms)
- +ve Aspergillus culture from sputum &; BAL
- +ve for Aspergillus IgG
What is Invasive aspergillosis
- Haematological malignancy, stem cell & solid organ transplant
- Low neutrophil counts
- Angioinvasion of lung tissue (can disseminate to other parts of body e.g. brain, kidney, cause skin lesions)
- Dissemination in c. 25% of cases to extrapulmonary sites
- Halo & air crescent signs on CT
- Moderate to poor prognosis, even with aggressive antifungal therapy
What is Aspergillosis, Diagnosis & Treatment?
Aspergillosis, Diagnosis & Treatment
• Diagnosis:
o Culture
o Serology;
Antibody detection- immunocompetent
Antigen detection- immunocompromised (=neutropenic).
o Imaging
•Treatment (depends on type of disease):
o Aspergilloma- resection
o Allergic aspergillosis- steroids +/- antifungals
o CPA and invasive aspergillosis- antifungals e.g. itraconazole & voriconazole (not fluconazole), amphotercin B
What are common Fungal pathogens?
•DERMATOPHYTES
o Infect skin, hair & nails
o Low morbidity, high incidence
•CANDIDA
o Causes superficial & systemic disease
o Can infect any organ in body
o Infec usually form patients own colonised mucosa
•ASPERGILLUS
o Causing pulmonary or sinus disease
o Inhalation of Aspergillus spores
o Effect depends on host reac or lack of reac, allergy to invasive disease
What are Eukaryotes?
- DNA in memb bound organelle (nucleus)
- Other memb bound organelles: mitochondria (& chloroplasts in plants)
- Ribosomes large 18S + 25-28S
- Genes may have introns
- Larger than prokaryotes
What are Prokaryotes?
- DNA not organised into nucleus
- No organelles
- Ribosomes smaller 16S + 23S
- Genes lack introns
What are Keratinophilic?
Can grow on & utilise substrates rich in keratin protein like skin, hair & nails.
What are Viruses?
•Simple micro-organisms NOT capable of independent existence (rely on host).
•Need energy, metabolic intermediates & (some) enzymes from host cells to replicate.
• Viruses contain up to 4 components;
1. Genome (RNA or DNA)
2. Capsid (protein coat)
3. Envelope (lipid bilayer)
4. Some viruses- own enzymes (inside capsid)
•Whole particle called a virion.
What are the steps in the lifestyle of a virus?
- Attachment
- Entry
- Uncoating
4-6. Synthesis - Assembly (replicate)
- Release
How are viruses classified?
• Viruses classified according to; 1. GENETIC MATERIAL; o DNA vs. RNA o Single vs double stranded o If single, +ve vs. –ve sense 2. PRESENCE/ ABSENCE OF AN ENVELOPE (all have protein caspule)
What is the Herpes virus?
• Double-stranded enveloped DNA virus.
• 9 types known to infect humans.
Characterised by their ability to establish latency (existing but not manifesting) after primary infec & reactivate;
What is HSV-1 ?
‘cold sores’
What is HSV-2 ?
HSV-2 ‘genital herpes’
What is the Herpes Simplex virus?
• Epidemiology:
oWorld wide (humans only known reservoir)
o 80% UK pop experience HSV-1 in their lives
o10-20% pop had HSV-2
•Mode of transmission: direct skin, genital or eye contact with vesicle fluid (from blisters) form HSV lesions.
•Important clinical syndromes that link to herpes simplex virus:
o Ulcers to skin/ mucous membs (typically mouth/ genitals)
o Encephalitis- (inflamm of brain) e.g. get headaches often severe/ fatal (>95% cases are HSV-1)
o Meningitis (inflamm of meninges)- associated with HSV-2, often follows genital lesions
o Neonatal herpes- severe disseminated viraemia (viruses in blood) usually consequence of vertical transmission from mothers genital tract at delivery (make sure check if mother has herpes- so are aware at time of delivery).
What is the Varicella Zoster Virus ? How is it transmitted? What does it result in?
Herpes Viruses: Varicella Zoster Virus
• Disease names:
o Primary infec= ‘chicken pox’
o Reactivation= ‘herpes zoster’ or ‘shingles’
•Epidemiology:
o In UK 95% ppl had chicken pox by the time their age 20
o In the tropics- decreases to 50% (decreases as get closer to equator)
•Mode of transmission:
o Resp droplet from person with primary infec
o Vesicle fluid (from blisters) from person with primary infec or reactivation
o After primary infec- latency established in dorsal root ganglion
•Important clinical syndromes:
o Chicken pox- febrile illness with widespread vascular rash (blisters filled with fluid) usually start at torso and go distally, usually uncomplicated but complications; pneumonitis (esp. adults), encephalitis, acute cerebellar ataxia
o Shingles/ herpes zoster- reactivation causing unilateral vesicles in a dermatomal distribution
What is the Epstein Barr Virus ? How is it transmitted? What does it result in?
•Disease names: ‘Glandular fever’ or ‘infectious mononucleosis’ or ‘EBV’
• Epidemiology:
o 90-95% in UK in infected by age 25
o Of these 50% infected before 5 yrs
•Mode of transmission: virus shed in saliva & genital secretions (‘kissing disease’)
•Important clinical syndromes that it can cause;
o Infectious mononucleosis (primary infec);
sore throat, lymphadenopathy, hepatosplenomegaly,
atypical lymphocytes on blood film (looked like monocytes- ‘mononucleosis’)
80-90% of clinical infectious mononucleosis is caused by EBV, rest is caused by cytomegalovirus
o Reactivation- especially if unwell/ immunosuppressed (prolonged shed of virus- often asymptomatic)
What is the Cytomegalovirus ? How is it transmitted? What does it result in?
• Disease names: CMV
Epidemiology: In UK % prevalence= age (e.g. 20% of 20 yr olds)
•Mode of transmission:
o Saliva or genital secretions
o Infected donated blood/ organs
• Important clinical syndromes;
o Infectious mononucleosis (primary infec) (see above box)
o Congenital infec- on infants born to mothers with primary infec during pregnancy (e.g. can cause microcephaly), neonate has retinitis, deafness, microcephaly, hepatosplenomegaly in neonate
o Immunosuppressed transplant recipients (solid organ or bone marrow)- either primary infec from transplanted organ/ blood product, or reactivation as a result of immunosuppression.
o Patients with advanced HIV/AIDS- latent CMV reactivation, causing retinitis or colitis
What is Rhinovirus? How is it transmitted? What does it result in?
•Disease names: ‘common cold’ (rhino= ‘nose’)
•Epidemiology: worldwide distribution, occur in epidemics in autumn, winter & spring.
•Mode of transmission: aerosolised resp secretions (secretions that contain virus) & droplets from nose &; eyes
• Important clinical syndromes:
o ‘Common cold’- sneezing, nasal obstruc & discharge, sore throat, cough, headache & fever
What is Influenza ? How is it transmitted? What does it result in?
•Virology & epidemiology:
o Infects humans & animals (can spread between species)
o 3 distinct types: influenza A, influenza B, influenza C (B &; C more stable, A mutates more)
o Influenza A mutates regularly- strains vary yearly
H &; N are 2 important viral surface proteins (have multiple variants- 16 diff Hs and 9 diff Ns)- use in nomenclature e.g. H1N1
•Mode of transmission: aerosolised respiratory secretions
•Important clinical syndromes:
o Primary influenza illness- fever, myalgia (muscle aches), then headache, cough, sore throat, nasal discharge.
o Post-influenza 2ndry bacterial lung infec (with S.pneumoniae, H. influenza, S. aureus)
What is Respiratory Syncytial Virus ? How is it transmitted? What does it result in?
• Disease names: ‘RSV’
• Epidemiology:
o Worldwide distrib, in epidemics in winter (esp. Nov & Dec)
o Commonest in young children: 70% infected &; 30% have had clinical illness in their 1st yr of life
• Mode of transmission: aerosolisation of respiratory secretions
• Important clinical syndromes:
o Bronchiolitis (smallest airways before alveoli)- affects children under 2 yrs;
Inflamm of smallest airways- bronchioles
Causes cough, wheeze, hypoxia & fever
What is HIV?How is it transmitted? What does it result in?
HIV- HUMAN IMMUNODEFICIENCY VIRUS
• Epidemiology:
o 36.7 million globally with HIV- 70% in sub-saharan Africa
o 6.5% in Western & central Europe & North America
• Mode of transmission:
o Virus in blood, genital secretions, breast milk
o Transmitted vertically, sexually, needlestick (e.g. contaminated blood products)
• Clinical course:
o HIV targets helper T lymphocytes (CD4)- that are part of cell medicated immune system
o Replicate in CD4 cell (kill CD4 cells, virus levels rise- become immunocompromised)
o 2-6 weeks wks after transmission, patients may develop an acute seroconversion illness (start detecting HIV in their body); fever sore throat, lymphadenopathy, high fever
o Asymptomatic chronic infection follows; steady state between virus & immune system (lasts 5-15 yrs)
o AIDS (severe HIV- when become immunocompromised)= increase in viral load & fall in CD4 count, patient vulnerable to opportunistic infecs.
o AIDS defining illness (if have HIV these illnesses define you as being severe/ having AIDS); TB, pneumocytic pneumonia, cryptococcal meningitis, cerebral toxoplasmosis, Kaposi’s sarcoma
What are the Hepatitis viruses ?
- Many viruses induce hepatitis as part of a wide clinical syndrome.
- Replicate in liver
- A &; E self resolve, B & C have ability to become chronic
- 5 primarily hepatotropic viruses identified;
A&E face-oral spread
B&C- Blood Borne
What is Hep B? How is it transmitted? What does it result in?
Hepatitis B
• Epidemiology: 248 million people chronically infected, >500,000 deaths annually.
• Mode of transmission: vertical, sexual, parenteral (direct inoculation with blood products)
• Clinical course:
o After transmission, acute clinical hepatitis (jaundice, abdominal pain, fever) may occur (but 90% children & 50% young adults asymptomatic of acute infec)
o Hepatitis B after acute phase then cleared by immune system/ persists & becomes chronic.
Risk of chronicity inversely related to age at infection (younger you are- more likely to get chronic);
90% perinatally acquired infec progress to chronic (vertical transmission biggest prob)
Vs. 20-50% aged 1-5 yrs
Vs <5% adult-acquired infections
o Over time chronic hepatitis = cirrhosis = hepatocellular carcinoma
What is Hep C? How is it transmitted? What does it result in?
• Epidemiology:
o 170 million ppl affected worldwide
o Low prevalence in developed countires (0.5-2%)
• In UK, 50% IVDUs have evidence of hep C.
• Mode of transmission: IVDU, needlestick injuries, transfusion of contaminated products, vertical & sexual transmission less common
• Important clinical syndromes:
o After transmission 25% develop acute clinical hepatitis (rest are asymptomatic)
o 15% will then clear the virus, 85% will become chronically infected
o Over time, chronic hepatitis = cirrhosis = hepatocellular carcinoma
What is Norovirus?
- Norovirus- single stranded RNA virus (SSRNA)
* Nororvirus- projectile vomiting (how it’s transmitted; people inhale part of it)
What is Rota virus?
•Rota virus- 1st infec most severe, major cause of infant mortality worldwide (dehydrates infants).
dsRNA
•Rota virus- shed in faeces becomes aerosalised then inhaled
What are Enteroviruses? How is it transmitted? What does it result in?
- Genus is eneterovirus, within this it includes polio, Coxsackie A &; B, enterovirus &; echovirus
- > 70 serotypes exist (most identified in stool during polio research)
- 90% have high fever, rash & feel generally unwell.
- Hand &; mouth syndrome- in palms of hands & mucous membs of mouth (see pics below)
- Hepangina- on back of throat
What is Parvovirus? How is it transmitted? What does it result in?
• Disease names: ‘Slapped cheek syndrome’ or ‘Fifth disease’
• Epidemiology:
o Peak in late winter to early summe
o 50% infected by 15yrs, 90% by 90yrs
Mode of transmission: droplet transmission from resp route (specifically targets & infects erythrocyte proginator cells (immature red blood cells) - causing transient anaemia).
• Important clinical syndromes;
o Erythema infectiosum- fever, coryza, fiery red rash to cheeks
o Transient aplastic crisis;
Affects those with high erythrocyte turnover e.g. sickle cell, thalassemia
Dysponoea, confusion, cardiac failure
o Infec in pregnancy;
7-10% fetal loss if maternal parvovirus in 1st 20wks
2-3% fetus can develop hydrops fetalis (as Hb drops- severe foetal anaemia- heart doesn’t have enough Hb to pump as well = heart failure, oedema, ascites)
What is a prion? How is it transmitted? What does it result in?
Small infectious pathogen containing protein, NO NUCLEIC ACID
•Prion proteins exist naturally in cells, prob when;
o Gene mutation leads to changes in folding pattern
o When struc changes prion becomes resistant to protease enzyme as a result
o Prion accumulates in cell & becomes pathogenic
•Abnormal prions are either;
o Inherites (genetic) defects
o Transmitted via consumption of infected meat/ exposure to infected material
•Human prion diseases share certain properties ;
o Pathological manifestations confined largely to CNS
o Protein accumul produce spongiform change in brain tissue on histology (pic looks like it has spongy holes in it)
o Long incubation time (up to 30 yrs)
o Progressive & fatal
•Transmissible spongiform encephalopathy (disease of brain)
What is New variant CJD (nvCJD)?
• Is diff to sporadic Creutzfeld- Jakob disease
• Sporadic Creutzfeld- Jakob disease= rare; 1 in million, gene mutation, progressive ataxia, depression, dementia then death.
• nvCJD directly linked to BSE (bovine spongiform encephalopathy);
o Same struc prion
nvCJD cases associated with consumption of infected beef
• So sporadic- random gene mutation
• nvCJD- from eating cow
• Is diff to sporadic Creutzfeld- Jakob disease
• Sporadic Creutzfeld- Jakob disease= rare; 1 in million, gene mutation, progressive ataxia, depression, dementia then death.
• nvCJD directly linked to BSE (bovine spongiform encephalopathy);
o Same struc prion
nvCJD cases associated with consumption of infected beef
• So sporadic- random gene mutation
• nvCJD- from eating cow
What is a parasite?
- Organism which lives in or on another organism (host) & benefits by deriving nutrients at the other’s expense (habitually relies on/ exploits others &gives nothing in return).
- Doesn’t necessarily cause disease.
- Parasitic disease- parasite derives all benefits from association & host either harmed or suffer consequences of this association.
What is Mutualism?
•Mutualism- association in which both species benefit from interaction.
What is Parasitism?
•Parasitism- association where parasite derives benefit & host gets nothing in return but always suffers some injury.
What is Commensalism?
Commensalism- association where parasite only deriving benefit without injuring host
What are the 3 classes of parasite hosts?
•DEFINITIVE host;
oHarbours adult stage of parasite/ where parasite utilizes sexual method of reproduction
oMajority of human parasitic infections- man definitive host.
•INTERMEDIATE HOST;
oHarbours larval or asexual stages of parasite.
oSome parasites need 2 intermediate hosts to complete lifecycle.
• PARATENIC host;
oHost where parasite remains visible without further development.
What are the types of parasite lifecycle?
DIRECT Lifecycle 1 host (definitive host) e.g. bird, pass eggs in stool, get eaten by another bird etc.
SIMPLE Lifecycle 2 hosts (definitive e.g. bird &intermediate e.g. sow bug), bird infected, egg in faeces, eaten by cell bugs, other birds eat bug
COMPLEX Lifestyle
What is Ascariasis?
Helminths
•Macroparasite- intestinal nematode (round worm), Ascaris lumbricoides.
•Over 1 billion people affected worldwide (approx. 1/7 world pop).
•Peak prevalence 3-8 year olds.
•Areas of poor hygiene e.g. contaminated water.
•1 adult worm can live 1-2 yrs in intestines, can make 200,000 eggs per day.
•Acquired by ingestion of eggs- person infected.
What is Ascariasis Lifecycle?
- Definitive host is us.
- Adult worms in human intestine, released into environment, contaminate food & water, ingested back (travel down intestinal tract, invade mucosa, blood lungs, alveolar space, can find their way back to intestine).
What is Ascariasis’s clinical effects?
Ascariasis- Clinical
•Lung migration: Loefflers syndrome- dry cough, dyspnoea, wheeze, haemoptysis, eosinophilic pneumonitis.
•Intestinal phase: malnutrition, malabsorption, migration (into hepatobiliary tree & pancreas), intestinal obstruct if huge worm burden, perforation.
•(Raised eosinophils).
What is the treatment of Ascariasis?
•Albendazole;
o Prevents glucose absorption by worm.
o Starves worm
o Worm starves-detaches-passed PR.
- WHO ‘Action Against Worms’.
- Improves sanitation.
- Education.
- Community targeted deworming.
What is Schistosomiasis?
Helminths
• Macro-parasite (Helminth- Platyhelminth- Trematode/Fluke)
• Also known as BILHARZIA DISEASE.
• 200 million people affected worldwide (predominantly in Africa- need freshwater snails).
• Caused by fluke (trematodes), Schistosoma:
o S.haematobium
o S.mansoni
o S.intercallatum
o S.japonicum
o S.mekongi
• Causes chronic disease resulting in bladder cancer & liver cirrhosis.
• Snails are intermediate host.
What is Schistosomiasis Lifecycle?
o Only found where intermediate host freshwater snails are.
• Definitive host is us.
• Transmitted via contact with contaminated water (e.g. where infec person urinated).
What is Schistosomiasis’s clinical effects?
- Swimmers itch- immune reac to sceria (rash lasts a week).
- Katayama fever (after a couple weeks)- immune reac to organism; malise, abdominal pain (no treatment just immune reac).
- Chronic Schistosomiasis (can persist for years).
- Effects of eggs in distant sites: spine, lung.
- Adult helminth in blood supply form eggs (eggs cause symptoms ischemic vessels (lodged & can’t get out); if in veous plexus in bladder- haematurea etc, if in small large intestines- abdominal symptoms e.g. portal hypertenssion etc (see next 2 bullet points)).
- Urinary (bladder) (S.haematobium); haematuria, bladder fibrosis & dysfunction, squamous cell CA bladder
- Hepatic/ intestinal (small/ large intes) (S.mansoni, S.intercallatum, S.japonicum, S.mekongi); portal hypertension, liver cirrhosis, abdo pain, hepatosplenomegaly.
What is the treatment of Schistosomiasis?
Schistosomiasis- Treatment
• Praziquantel;
o 40-60mg/kg with food 3 doses 8- hrly.
o Unknown mechanism (↑ ionic permability tetanic contrac, detachment, death)
o Well absorbed, extensive 1st pass metabolism, inactive metabolites excreted in urine.
• Treats long term complications
• Cures them of schistosomiasis but not immunitive (if contact contaminated water will get it again).
HYDATID DISEASE (Helminths):
Schistosomiasis- Control
• Chem treatment of water to kill snail intermediate hosts.
• Chemoprophylaxis
• Avoidance of snail infested waters.
• Community targeted treatment, education & improved sanitation.
What is Hydatid Disease ?
Helminths
•Macro-parasite (Platyhelminth- Cestode-Tapeworm)
•Human accidental intermediate host
•Unusual hosts- sheep & dogs
•Found all over the world wherever sheep are farmed
•Caused by Echinococcus sp
What is Hydatid Disease Lifecycle?
- Dogs definitive host.
- Have adult worm in small intestine= eggs = ingested by sheep/ us = once ingested eggs hatch = penetrates intes wall = circ = liver/lungs/other organs = make cysts.
What are Hydatid Disease clinical effects?
- Cysts: 70% liver, 20% lungs
- Many remain asymptomatic for years
- Until cyst large enough/ ruptures/ mass effect
- 2ndry bacterial infec
- Cyst rupture = hypersensitivity reacs/ anaphylaxis (can cause death)
Hydatid Disease- Control
• Regularly worm dogs to reduce egg produc
• Hand hygiene
• Safe disposal of animal carcasses/ products of conception.
What is malaria?
Protozoa
• Micro-parasite (protozoa- sporozoan)
• 4 Plasmodium species;
o P. falciparum (most severe)
o P. vivax
o P. ovale
o P. malariae
• Ovale &; vivax has extra stage in lifecycle (dormant) so can recoccur.
• 300-500 million ppl infected/ yr, 1-3 million deaths/ yr (mainly in young children).
• 2000 cases/ yr in UK (70% P. falciparum- travel clinic).
What is malaria Lifecycle?
- Anopheles mosquito as a vector.
- Blood borne, requires a vector.
- 2 hosts
- RBCs to liiver cells replicate here then rupture travel into RBCs then further asexual replication (causes symptoms).
What are malaria clinical effects?
- Parasites rupture RBCs, block capills & cause inflamm reac.
- Fever & rigors (alt. days with falciparum malaria, every 48hrs with benign malaria).
- Cerebral malaria (confusion, headache, coma)
- Renal failure (black water fever)
- Hypoglycaemia
- Pulmonary oedema
- Circulatory collapse
- Anaemia, bleeding &; DIC
RETURNING TRAVELLER + FEVER= MALARIA (until proven otherwise)- make sure take travel history
What is the treatment of malaria?
• Antimalarials;
o Non falciparum malaria: chloroquine + primaquine (prevents relapse)
o Falciparum malaria;
Uncomplicated (oral regime)- quinine + doxycycline, co-artem (artemether/lumefantrine), atovaquone - proguanil
Complicated- IV quinine, artesunate
• Supportive therapy;
o Manage seizures, pul, oedema, acute renal failure & lactic acidosis.
o Exchange transfusion may be helpful in hyperparasitaemia.
• (Diff treatment depending on type of malaria & if complicated/ uncomplicated).
Malaria Control • Spray insecticide in homes. • Larvicidal spraying on breeding pools. • Filling in of breeding pools. • Introduce larvivorus species into mosquito breeding areas. • Insceticide impregnated bed nets. • Still working to make a vaccine.
What is Cryptosporidiosis?
Protozoa
• Caused by Cryptosporidium parvum and hominis (micro-parasite, sporozoan)
• Causes diarrhoeal disease (so in intestine not blood)
• Human to human spread with animal reservoir (cattle, sheep, goats)
• Faecal-oral spread
• World wide distrib (esp. temperate &tropical), sporadic cases can lead to outbreaks
What is Cryptosporidiosis Lifecycle?
- Direct lifecycle
- Human passes in stool
- Infected swimming pools, water
What are Cryptosporidiosis clinical effects?
• Incubation 2-10 days (usually 7 days).
• Watery diarrhoea with mucus (no blood)
• Bloating, cramps, fever, nausea, vomiting
• Usually self-limiting (last up to 2 weeks)- NO TREATMENT in normal patient required
• Can be severe in: very young, very old, immuno-compromised (60% HIV patients infected go on to chronic infection- can loose up to 25 litres fluid/day).
• Those at risk;
o Human- Human Spread (contaminated water);
Regular swimming pool users (can be chlorine resistant)
Child care workers & parents
Nursing home residents/ carers
Healthcare workers
Travellers
o Animal- Human Spread;
Backpackers, campers, hikers
Farm workers
Visitors to farms/petting zoos
Consumers of infected dairy products
What is the treatment of Cryptosporidiosis?
Cryptosporidiosis Treatment • Symptomatic treatment; rehydration, Nitazoxanide • For immunocompromised; o Paromomycin (kill parasite) o Nitazoxanide (unclear effectiveness) o Octreotide (↓ cramps & freq) o HIV patients, quickly initiate HAART.
Cryptosporidiosis Control • Human-Human; o Hand hygiene o Filter/ boil drinking water o Isolate symptomatic patients in healthcare setting o Ensure symptomatic kids kept away from school. • Animal- human; o Pasteurise milk &; dairy products. o Boil/ filter drinking water if camping
What is Trichomoniasis?
Protozoa • Caused by Trichomonas vaginalis • Flagellated protozoan • SEXUALLY TRANSMITTED • Incubation 5-28 days • Symptoms/signs o Men = asymptomatic o Women = smelly vaginal discharge, dyspareunia, dysuria and lower abdominal discomfort, punctuate haemorrhages on cervix (“strawberry cervix”).
What is Trichomoniasis Lifecycle?
- Splits by binary fission
* Sexual transmission
What are Trichomoniasis clinical effects?
ID organism in genital specimens (take swab
• Symptoms/signs
o Men = asymptomatic
o Women = smelly vaginal discharge, dyspareunia, dysuria and lower abdominal discomfort, punctuate haemorrhages on cervix (“strawberry cervix”).
What is the treatment of Trichomoniasis?
Trichomoniasis Treatment
• Metronidazole single dose of 2g or divided doses for 7 days.
• Treat partner simultaneously.
Trichomoniasis Prevention
• General advice about prevention of STIs.
•Use barrier contraceptive methods if sexually active.
What is Giardiasis?
- Flagellated protozoan, is intestinal pathogen
- Faecal oral transmission
- Spectrum of disease: asymptomatic carriage to severe diarrhoea & malabsorption (can cause chronic disease)
- Symptoms: usually last 1-3 weeks (self-limiting, takes couple wks to resolve)
- Diarrhoea
- Abdominal pain
- Bloating
- Nausea and vomiting
What is Giardiasis Lifecycle?
- Direct
- Humans definitive host
- Stools infect env.
- Binary fission
What is the treatment of Giardiasis?
Giardiasis Treatment
• Metronidazole/ tinidazole.
Giardiasis Prevention
• No vaccine available.
• Hygiene measures.
• Boiling water.
