medical micro
TRANSCRIPT
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Complications.
Course and prognosis.
Treatment - preventative - curative
Diagnosis and differential.
Pathology.
Clinical symptomsand presentation.
Aetiology and associations.
Incidence and geographical distribution.
Incubation period.
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Tuberculosis
Complications.Healing with fibrosis,calcification and/orcavitation
Course and prognosis.Slow course usually.Prognosis variable
Treatment - preventative - curativeBCG useful for prevention.Triple+ Rx for activeInfections.Rifampicin,isoniazid, ethambutol+ or - pyrazinamide
Diagnosis and differential.Microscopy and culture
Pathology.Granuloma formation.Heals with fibrosis and calcification. Cavitation in lungs
Clinical symptomsand presentation.Fever, cough, organdysfunctions
Aetiology and associations.Mycobacterium tuberculosisPrimary and secondaryinfections
Incidence and geographical distribution.Worldwide. High in HIV and deprived areas
Incubation period. A few weeks to years
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Meningococcal infection
Complications.Neurological damage,organ system damage, death
Course and prognosis.Fatal if untreated. The earlier the treatmentThe better
Treatment - preventative - curativeGive contacts rifampicinor ciprofloxacin. Givepatients ceftriaxone orPenicillin + treatmentof hypotension etc.
Diagnosis and differential.Microscopy of organism onsin scarification. Culture from blood and/or CSF
Pathology.Organ and blood vessel damage
Clinical symptomsand presentation.Meningitic – fever, headache,neck stiffness, haemorrhagic rash.Septicaemic – hypotension and shock(meningeal signs may be later)
Aetiology and associations.Infection with Neisseriameningitidis
Incidence and geographical distribution.Epidemic and endemic.More common in crowded conditions
Incubation period.2-10days, commonly3-4 days
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Meningococcal purpuric spots
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Conjunctival haemorrhages in meningococcal sepsis
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Opisthotonus in meningitis
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Other common causes of meningitis include:
Streptococcus pneumoniaeHaemophilus influenzae
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Cellulitis/erysipelas
Complications.Lymphangitis, lymphadenitis,septicaemia
Course and prognosis.Variable.
Treatment - preventative - curativePenicillin + flucloxacillinAn erythromycin orclindamycin
Diagnosis and differential.Necrotising fasciitis. If onlower limb DVT
Pathology.Sepsis
Clinical symptomsand presentation.Symptoms and signs ofinflammation
Aetiology and associations.Infection usually with Strep.pyogenes to give erysipelas (a superficial infection with sharply defined borders) orStaph. aureus to give cellulitis(a deeper infection with lesswell defined borders).Organism introduction via skinbreeches or other infections (eg.Athlete’s foot)
Incubation period.Variable, probably a day or so from introduction of organism
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Diphtheria
Complications.Heart and nervoussystem damage, respiratoryobstruction, death
Course and prognosis.Variable
Treatment - preventative - curativeVaccination for preventionAntitoxin + antibiotic +isolation
Diagnosis and differential.Clinical plus microscopy and culture
Pathology.Respiratory obstruction +Toxin production to harm heart,or nervous system
Clinical symptomsand presentation.Throat and/or laryngeal infection with membrane
Aetiology and associations.Corynebacterium diphtheriaeInfection, usually of the throat
Incidence and geographical distribution.Areas with low immunization rates, often children,
Incubation period. 2-5 days usually
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Gastroenteritis
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Urinary tract infections(affect 10-15% of healthy women each year)
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Kidney
PelvisCalyxMedullaPyramids
Ureter
Bladder
ProstateUrethra
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LOWER URINARY TRACT SYMPTOMS “CYSTITIS”
•Possibility of no symptoms•Pain/burning on micturition•Frequency and nocturia•Urgency•Cloudy urine•Malodorous urine•Suprapubic pain•Haematuria if “full house” of other symptoms
Patients are usually afebrile do not have lateralised back pain do not have chills or rigors
Fifty percent chance of UTI if one or more symptoms.Exclude vaginal discharge/irritation then chance of UTIabout 90 percent
Clinical symptomsand presentation.
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CAUSES OF “CYSTITIS”
•Bacterial urinary tract infection •Chlamydia•Trichomonas•Candida•Viruses•Trauma – sexual intercourse•Allergies•Senile vaginitis
E.coli in 89 percentStaphylococcus saprophyticus in 5-15 percent
Aetiology and associations. Diagnosis and differential.
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UPPER URINARY TRACT INFECTIONS“PYLEONEPHRITIS”
•Usually, but not always, symptoms of cystitis•Fever•Chills or rigors•Lateralised back pain•Pain on percussion over kidneys•Patients are systemically unwell.
Clinical symptomsand presentation.
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100 90 80 70 60 50 40 30 20 10 0
Fluoroquinolones
Nitrofurantoin
Ampicillin/amoxycillin
Cephalosporins
Co-amoxiclav
Trimethoprim
Percentage susceptibility of E.coli
%
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Protein synthesis impairmentChloramphenicolClindamycinErythromycinFusidic acidLinezolidTetracyclines
Nucleic acid synthesisMetronidazoleNitrofurantoinQuinolonesRifampicin
Formation of poisonsHexamine
MultifactorialAminoglycosides(mostly on bacterialLipopolysaccharides)
MetabolicPyrimethamineSulphonamidesTrimethoprim
Bacterial cell wall damageCephalosporinsPenicillins (ampicillin/Amoxicillin)TeichoplaninVancomycin
Ribosomes (site ofprotein synthesis)
Nuclear apparatus(bacteria do not have a true nucleus)
Treatment - preventative - curative
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Chickenpox
Complications.Secondary bacterialskin sepsis, encephalitis
Course and prognosis.Mostly heals withoutscarring. Pneumoniaespecially in the pregnant
Treatment - preventative - curativeVZV Immunglobulin givenEarly does not preventDisease but reduces itsSeverityAciclovir and similardrugs stop progressinginfection
Diagnosis and differential.Herpes simplex infection.Other rare “poxes”
Clinical symptomsand presentation.1-5 crops of itchy vesiclesover about one week in acentripetal distribution
Aetiology and associations.Infection with Varicella-zoster virus from someonewith chickenpox or shingles
Incidence and geographical distribution.Worldwide, except whereVaccination practiced
Incubation period. About 18 days
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Chickenpox rash
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Chickenpox pneumonia
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Ophthalmic shingles
Course and prognosis.Heals with scarring.Zoster associated pain,Particularly in the elderly
Treatment - preventative - curativeAciclovir and similardrugs, if given early,Will miminse further damage and (slightly)reduce incidence ofzoster associated pain
Diagnosis and differential.Culture or electronmicroscopy of virus
Clinical symptomsand presentation.After a dermatomal prodromeof itching or pain there is adense simultaneous confluentchickenpox eruption.
Aetiology and associations.Reactivation of VZV whichhad been acquired during anAttack of chickenpox.Shingles can thus transmitchickenpox but not shingles
Incidence and geographical distribution.Worldwide
Incubation period. Usually years after chickenpox
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Smallpox Complications.Scarring, death
Course and prognosis.Fatality rate between20-40%
Treatment - preventative - curativeVaccination pre andpost exposure.Certain anti-retroviraldrugs are probably effective
Diagnosis and differential.Chickenpox or monkeypox
Clinical symptomsand presentation.Dense simultaneous eruptionof a centrifugal seep-seated rash
Aetiology and associations.Infection with Variola virus
Incidence and geographical distribution.Who knows what whoMight have in a deep freeze?
Incubation period. 7-17 days, usually10-12 days
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MeaslesComplications.Bacterial pneumonia,encephalitis
Course and prognosis.Rash lasts for about four day and thenbegins to stain
Treatment - preventative - curativeVaccination is highly effective
Diagnosis and differential.Other viral rashes. DrugRashes seldom spread from above downwards andrarely stain.
Clinical symptomsand presentation.Patients have high feverand may be very unwell in the prodrome.Patients have respiratorytract symptoms includingcough and coryza.Rash spreads from abovedownwards and stainswithin a few days
Aetiology and associations.Measles virus
Incidence and geographical distribution.Was worldwide and “everychild had it” before vaccination.
Incubation period.About 10 days to fever inthe prodrome, about 14 days to the rash
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Measles rash
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Measles almost always blanches
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HIV infection
Complications.Of immune deficiency ANDfrom the multiple drugs used
Course and prognosis.Depends on access to hightechnology and highlyexpensive medical care
Treatment - preventative - curativePrevention – avoid or minimise risks!Cure not possible: long term HIVSuppression is the aim. Neither cure notuseful vaccination will occur soon.
Diagnosis and differential.Uncomplicated but unusualinfections or neoplasms
Clinical symptomsand presentation.Mostly opportunistic infections and neoplasms associated with immune deficiency.
Aetiology and associations.Infection with Human Immune Deficiency virus
Incidence and geographical distribution.Worldwide. Main reservoir (2003)is in sub-Saharan Africa.
Incubation period. 6 weeks to 6 months toseroconversion illness (if any), average of 10 years from infection until AIDS (in the untreated), average of 14 months from AIDS to death (in the untreated)
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Organism or cells bearing itsAntigens are attacked directly
T (THYMUS DERIVED) LYMPHOCYTESAre responsible for cell mediated immunitywhich deals with intracellular pathogens andneoplasms. They also produce lymphokinesand inflammatory mediators
B LYMPHOCYTESReacting B lymphocytes react with theirown target antigens and change into plasmacells which produce immunoglobulins (mostof which are antibodies
Localisation and combination withantigens and, ideally, destruction ofassociated organisms
INFECTING ORGANISM ATTACKED BY:OpsonificationPrecipitationAgglutinationNeutralisationComplement activation
PHAGOCYTIC SYSTEMA rapid relatively non-specific defencesystem which eats up invading pathogensand destroys them and/or presents relevant antigens to the immune system
IgE is responsible for some allergicreactions. It does not play a significantpart in most infections
IgM “reacts against surfaces ofinvading pathogens” and is the the first immunoglobulin to risein an acute infection.
IgG “protects bodily fluids” andRises later than IgM and a rise inIgG indicates an infection at someTime. A greater than fourfold change in concentration to a specific organism on paired seraexamination suggest an acuteinfection.
IgA “protects body surfaces.”
HIV AND HOST DEFENCES AGAINST INFECTION
IgD. Function in largely unknown.
Polyclonal stimulation ->hypergammaglobulinamia butfunctionally hypogammoglobulinaemic
Progressivelyreduced in numberand function ->intracellularinfections
Phagocyticfunctions staynormal untillate-stage disease
Pathology.
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HIV pneumonias, notably PCP
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Drug tracks
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HIV seroconversion illness
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Cytomegalovirus retinitis