Medical micro


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Medical micro

  1. 1. Incubation period.Incidence andgeographical distribution.Aetiology and associations.Clinical symptomsand presentation.Pathology.Diagnosis and differential.Treatment - preventative - curativeCourse and prognosis.Complications.
  2. 2. Incubation period.A few weeks to yearsIncidence andgeographical distribution.Worldwide. High in HIV Treatment - preventativeand deprived areas - curative BCG useful for prevention.Aetiology and associations. Triple+ Rx for activeMycobacterium tuberculosis Infections.Rifampicin,Primary and secondary isoniazid, ethambutolinfections + or - pyrazinamideDiagnosis and differential.Microscopy and culture Course and prognosis.Clinical symptoms Slow course usually.and presentation. Prognosis variableFever, cough, organdysfunctions Complications. Healing with fibrosis,Pathology. calcification and/orGranuloma formation. cavitationHeals with fibrosis and Tuberculosiscalcification. Cavitationin lungs
  3. 3. Incubation period. Diagnosis and differential.2-10days, commonly Microscopy of organism on3-4 days sin scarification. Culture from blood and/or CSFIncidence and Treatment - preventativegeographical distribution. - curativeEpidemic and endemic. Give contacts rifampicinMore common in or ciprofloxacin. Givecrowded conditions patients ceftriaxone orAetiology and associations. Penicillin + treatmentInfection with Neisseria of hypotension etc.meningitidis Course and prognosis.Clinical symptoms Fatal if untreated. Theand presentation. earlier the treatmentMeningitic – fever, headache, The betterneck stiffness, haemorrhagic rash.Septicaemic – hypotension and shock Complications.(meningeal signs may be later) Neurological damage, organ system damage,Pathology. deathOrgan and bloodvessel damage Meningococcal infection
  4. 4. Meningococcal purpuric spots
  5. 5. Conjunctival haemorrhages in meningococcal sepsis
  6. 6. Opisthotonus in meningitis
  7. 7. Other common causes of meningitis include: Streptococcus pneumoniae Haemophilus influenzae
  8. 8. Incubation period. Pathology.Variable, probably a day or Sepsisso from introduction oforganism Diagnosis and differential. Necrotising fasciitis. If onAetiology and associations. lower limb DVTInfection usually with Strep.pyogenes to give erysipelas Treatment - preventative(a superficial infection with - curativesharply defined borders) or Penicillin + flucloxacillinStaph. aureus to give cellulitis An erythromycin or(a deeper infection with less clindamycinwell defined borders).Organism introduction via skinbreeches or other infections (eg. Course and prognosis.Athlete’s foot) Variable.Clinical symptoms Complications.and presentation. Lymphangitis, lymphadenitis,Symptoms and signs of septicaemiainflammation Cellulitis/erysipelas
  9. 9. Incubation period. Diagnosis and differential.2-5 days usually Clinical plus microscopy and cultureIncidence andgeographical distribution. Treatment - preventativeAreas with low immunization - curativerates, often children, Vaccination for prevention Antitoxin + antibiotic +Aetiology and associations. isolationCorynebacterium diphtheriaeInfection, usually of the throat Course and prognosis. VariableClinical symptomsand presentation. Complications.Throat and/or laryngeal Heart and nervousinfection with membrane system damage, respiratory obstruction, deathPathology.Respiratory obstruction +Toxin production to harm heart, Diphtheriaor nervous system
  10. 10. Gastroenteritis
  11. 11. Urinary tract infections(affect 10-15% of healthy women each year)
  12. 12. KidneyPelvisCalyxMedullaPyramidsUreterBladderProstateUrethra
  13. 13. Clinical symptoms and presentation.LOWER URINARY TRACT SYMPTOMS “CYSTITIS”•Possibility of no symptoms Fifty percent chance of UTI•Pain/burning on micturition if one or more symptoms.•Frequency and nocturia Exclude vaginal discharge/•Urgency irritation then chance of UTI•Cloudy urine about 90 percent•Malodorous urine•Suprapubic pain•Haematuria if “full house” of other symptomsPatients are usually afebrile do not have lateralised back pain do not have chills or rigors
  14. 14. Aetiology and associations. Diagnosis and differential.CAUSES OF “CYSTITIS”•Bacterial urinary tract infection•Chlamydia•Trichomonas•Candida•Viruses•Trauma – sexual intercourse•Allergies•Senile vaginitisE.coli in 89 percentStaphylococcus saprophyticus in 5-15 percent
  15. 15. Clinical symptomsand presentation.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.
  16. 16. Fluoroquinolones Nitrofurantoin Co-amoxiclav Ampicillin/ 100 amoxycillin 90 Cephalosporins 80 Trimethoprim 70 60% 50 40 30 20 10 0 Percentage susceptibility of E.coli
  17. 17. Formation of poisons Bacterial cell wall damageHexamine Treatment - preventative Cephalosporins - curative Penicillins (ampicillin/Multifactorial Amoxicillin)Aminoglycosides Teichoplanin(mostly on bacterial VancomycinLipopolysaccharides) Ribosomes (site ofMetabolic protein synthesis)Pyrimethamine Protein synthesis impairmentSulphonamides ChloramphenicolTrimethoprim Clindamycin ErythromycinNucleic acid synthesis Fusidic acidMetronidazole LinezolidNitrofurantoin Nuclear apparatus TetracyclinesQuinolones (bacteria do not haveRifampicin a true nucleus)
  18. 18. Treatment - preventativeIncubation period. - curativeAbout 18 days VZV Immunglobulin givenIncidence and Early does not preventgeographical distribution. Disease but reduces itsWorldwide, except where SeverityVaccination practiced Aciclovir and similar drugs stop progressingAetiology and associations. infectionInfection with Varicella- Course and prognosis.zoster virus from someone Mostly heals withoutwith chickenpox or shingles scarring. Pneumonia especially in the pregnantClinical symptomsand presentation. Complications.1-5 crops of itchy vesicles Secondary bacterialover about one week in a skin sepsis, encephalitiscentripetal distributionDiagnosis and differential.Herpes simplex infection.Other rare “poxes” Chickenpox
  19. 19. Chickenpox rash
  20. 20. Chickenpox pneumonia
  21. 21. Incubation period. Diagnosis and differential.Usually years after Culture or electronchickenpox microscopy of virusIncidence and Treatment - preventativegeographical distribution. - curativeWorldwide Aciclovir and similar drugs, if given early,Aetiology and associations. Will miminse furtherReactivation of VZV which damage and (slightly)had been acquired during an reduce incidence ofAttack of chickenpox. zoster associated painShingles can thus transmitchickenpox but not shingles Course and prognosis. Heals with scarring. Zoster associated pain, Particularly in the elderlyClinical symptomsand presentation.After a dermatomal prodromeof itching or pain there is a Ophthalmic shinglesdense simultaneous confluentchickenpox eruption.
  22. 22. Incubation period. Diagnosis and differential.7-17 days, usually Chickenpox or monkeypox10-12 days Treatment - preventativeIncidence and - curativegeographical distribution. Vaccination pre andWho knows what who post exposure.Might have in a deep freeze? Certain anti-retroviral drugs are probablyAetiology and associations. effectiveInfection with Variola virus Course and prognosis. Fatality rate betweenClinical symptoms 20-40%and presentation.Dense simultaneous eruption Smallpox Complications.of a centrifugal seep-seated rash Scarring, death
  23. 23. Incubation period. Diagnosis and differential.About 10 days to fever in Other viral rashes. Drugthe prodrome, about 14 days Rashes seldom spread fromto the rash above downwards and rarely stain.Incidence andgeographical distribution. Treatment - preventativeWas worldwide and “every - curativechild had it” before Vaccination isvaccination. highly effectiveAetiology and associations.Measles virus Course and prognosis. Rash lasts for aboutClinical symptoms four day and thenand presentation. begins to stainPatients have high feverand may be very unwellin the prodrome. Complications. Bacterial pneumonia,Patients have respiratorytract symptoms including Measles encephalitiscough and coryza.Rash spreads from abovedownwards and stainswithin a few days
  24. 24. Measles rash
  25. 25. Measles almost always blanches
  26. 26. Incubation period. Diagnosis and differential.6 weeks to 6 months to Uncomplicated but unusualseroconversion illness (if infections or neoplasmsany), average of 10 yearsfrom infection until AIDS Treatment - preventative(in the untreated), average - curativeof 14 months from AIDS to Prevention – avoid or minimise riskdeath (in the untreated) Cure not possible: long term HIVIncidence and HIV infection Suppression is the aim. Neither cure useful vaccination will occur soon.geographical distribution.Worldwide. Main reservoir (2003) Course and in sub-Saharan Africa. Depends on access to high technology and highly expensive medical careAetiology and associations.Infection with Human Immune Deficiency virus Complications.Clinical symptoms Of immune deficiency ANDand presentation. from the multiple drugs usedMostly opportunistic infections andneoplasms associated with immunedeficiency.
  27. 27. Pathology. HIV AND HOST DEFENCES AGAINST INFECTION Localisation and combination withProgressively antigens and, ideally, destruction of Organism or cells bearing its associated organismsreduced in number Antigens are attacked directlyand function -> INFECTING ORGANISMintracellular T (THYMUS DERIVED) LYMPHOCYTES Are responsible for cell mediated immunity ATTACKED BY: Opsonificationinfections which deals with intracellular pathogens and Precipitation neoplasms. They also produce lymphokines Agglutination and inflammatory mediators Neutralisation Complement activation Phagocytic PHAGOCYTIC SYSTEM IgM “reacts against surfaces of functions stay A rapid relatively non-specific defence system which eats up invading pathogens invading pathogens” and is the the first immunoglobulin to rise normal until and destroys them and/or presents in an acute infection. relevant antigens to the immune system late-stage disease IgG “protects bodily fluids” and B LYMPHOCYTES Rises later than IgM and a rise in Reacting B lymphocytes react with their IgG indicates an infection at some own target antigens and change into plasma Time. A greater than fourfold cells which produce immunoglobulins (most change in concentration to a of which are antibodies specific organism on paired sera examination suggest an acute infection. Polyclonal stimulation -> IgA “protects body surfaces.” hypergammaglobulinamia but IgD. Function in largely unknown. functionally hypogammoglobulinaemic IgE is responsible for some allergic reactions. It does not play a significant part in most infections
  28. 28. HIV pneumonias, notably PCP
  29. 29. Drug tracks
  30. 30. HIV seroconversion illness
  31. 31. Cytomegalovirus retinitis