medical micro

Complications.

Course and prognosis.

Treatment - preventative - curative

Diagnosis and differential.

Pathology.

Clinical symptomsand presentation.

Aetiology and associations.

Incidence and geographical distribution.

Incubation period.

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

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

Meningococcal purpuric spots

Conjunctival haemorrhages in meningococcal sepsis

Opisthotonus in meningitis

Other common causes of meningitis include:

Streptococcus pneumoniaeHaemophilus influenzae

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

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

Gastroenteritis

Urinary tract infections(affect 10-15% of healthy women each year)

Kidney

PelvisCalyxMedullaPyramids

Ureter

Bladder

ProstateUrethra

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.

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.

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.

100 90 80 70 60 50 40 30 20 10 0

Fluoroquinolones

Nitrofurantoin

Ampicillin/amoxycillin

Cephalosporins

Co-amoxiclav

Trimethoprim

Percentage susceptibility of E.coli

%

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

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

Chickenpox rash

Chickenpox pneumonia

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

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

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

Measles rash

Measles almost always blanches

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)

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.

HIV pneumonias, notably PCP

Drug tracks

HIV seroconversion illness

Cytomegalovirus retinitis