Gram positive rods-2

Gram positive rods-2

Corynebacterium diphtheriaeCaused by toxin producing strains of C.diphtheriaeCause life threatening respiratory obstructionRare in resource rich countries due to effective immunisation with toxoid vaccineNon toxigenic strains colonise the nasopharynx; bacteria lysogenised with phage produce toxin and diseaseTransmission (person to person)Colonise the pharynx, larynx, nose and skin (tropics)Spread from person to person in respiratory droplets

Non immunised individuals susceptibleToxigenic strains carried and transmitted by asymptomatic convalescents and healthy individualsTransmission within the bodyInfection of nasopharynxBacteria multiply locally do not invade deeper tissue and release exo toxinToxin destroys epithelial cells, polymorphs

2NOT ALL ARE INFECTIVE ONLY THOSE THAT HAVE BEEN INFECTED BY THE PHAGE THAT CARRIES ITMAY NOT BE THE TOXIN PRODUCING STRAINS..WHAT DS DOES CORYNEBACTERIUM DIPHTHERIAE PRODUCE? TOXIN PRODUCING STRAINS CAUSE LIFE THREATENING RESPIRATORY OBSTRUCTIONSO WHERE DO YOU FIND DIPHTHERIAE ON THE BODY? COLONIZE THE PHARYNX, LARYNX AND NOSE AND SKINHAVE NON TOXIGENIC STRAINS COLONISE THE NASOPHARYNX, THEN BACTERIA LYSOGENNISED WITH PHAGE PRODUCE TOXIN AND DSHOW IS DIPTHERIAE TRANSMITTED? PERSON TO PERSON IN RESPIRATORY DROPLETSWHERE DO THEY MULTIPLY? INFECTION OF NASOPHARYNX, MULTIPLY LOCALLY NOT INVADE DEEP TISSUE BUT RELEASE EXO TOXIN WHICH DESTROYS EPITHELIA CELLS, POLYMORPHS..

Clinical manifestation:Diphtheria; lymphadenopathy (bull neck) and pseudomebranous pharyngitisDirty Gray, exudative, adherent pseudomembrane made of necrotic dead cells and fibrin and bacteria, which bleeds when attempt to remove. Diphtheria (Greek) leatherExtensive inflammation, swelling, enlargment of cervical lymph nodes (bull neck)Involvement of larynx; respiratory obstructionDeath by mechanical obstruction and action of toxinToxin absorbed into blood has several effectsFever, pallor, exhaustionMyocarditisPolyneurtis (demyelination)

Grey pseudomembraneBull neck3INHIBITS PROTEIN SYNTHESEIS TWO WAYS 1. ELONGATION FACCTOR AND BINDING TO 60 S RIBOSOMES.ITS CYTOTYOXICPSUDOMEMBRA THAT BLEEDS IS INDICATIVE OF DSIT STARTS BLEEDING WHEN TRY TO TAKE IT OUTWhat are the clinical manifestation? LPDPELDTPPELT.DDoLLWHEN THE TOXIN IS ABSORBED INTO BLOOD WHAT ARE THE EFFECTS? FPEMPFat..PEMP.FAT PIMPToxinA-B toxin; coded by lysogenised phage; beta prophageInhibit protein synthesis ADP ribosylation of EF-2Shuts down protein synthesis and kills the cellCardiotoxic- myocarditisCytotoxicNeurotoxic- demyelination

4HOW DOES THE DIPTHERIAE TOXIN CAUSE PROBLEMS? HAVE A-B TOXIN PROTEIN SYNTHESIS OF ADP RIBOSYLATION OF EF-2 WHICH SHUTS DOWN PROTEIN SYNTHESIS AND KILLS THE CELL.TELL ME ABOUT THE A-B TOXIN? CODED BY LYSOGENISED PHAGE; BETA PROPHAGE WHICH CARDIOTOXIC (MYOCARDITIS), CYTOTOXIC AND NEUROTOXIC (DEMYELINATION)Life threatening disease, clinical diagnosis urgentLaboratory diagnosisStain: demonstration of metachromatic granules by Alberts stain

Culture: potassium tellurite agar, LoefflersDemonstrate toxin by tissue culture or Eleks gel test

Treatment: antitoxin and antibiotics; erythromycin, penicillin GPrevention: active immunisation with DTa PContacts of patients should be tested for carriage of toxigenic strains

5MATCHED SHAPE OR CHINESE LETTERING..USED TO DO ELEKS NOW DO THE PCR.WHY IMPRT TO PRODUCE TOXIN HAVE TO PROVE IT.TOXINS ARE PROTEINS.WHICH ANTIBIOTICS INHIBIT PROTEIN SYNTMACROMIDLES..HOW DO LAB DIAGNOSE DIPTHERIAE? ACDCApD..HOW DO DEMONSTRATE THE DIPTHERIAE TOXIN? ELECKS GEL TESTNOW CAN DO PCR.WHAT IS THE TREATMENT FOR CORYNEBACTERIUM DIPTHERIAE? Antitoxin and antibiotics, PENERYTHRO PENICILIN GHOW DO U PREVENT CORYNEBACTERIUM DIPTHERIAE? ACTIVE IMMUNISATION WITH DTaPWHAT SHOULD BE DONE WITH CONTACTS OF PATIENTS? SHOULD BE TESTED FOR CARRIAGE OF TOXIGENIC STRAINS.ActinomycesOrganism with no respect for anatomical barriers6WHAT IS ACTINOMYCES KNOWN FOR? ORGANISM WITH NO RESPECT FOR ANATOMICAL BARRIERSActinomyces israeliiMorphologyGram positive rods to branching filamentsNon acid fast (distinguish from nocardia)Anaerobic (distinguish from nocardia)

ReservoirNormal colonizer of oral mucosa, gingival crevices and female genital tract

InfectionsInfections (endogenous)When mucosal barrier compromised As in oral trauma, dental extraction, manipulation of IUD (intrauterine device)Grows rapidly in tissues

7TELL ME ABOUT ACTINOMYCES ISRAELLI? GNARRANG.R= RESERVOIRWHAT IS THE RESERVOIR FOR ACTINOMYCES ISRAELII? ORAL MUCOSA, GINGIVAL CREVICES AND FEMAL GENITAL TRACTHOW DO U GET ACTINOMYCES ISRAELII INFECTIONS? ENDOGENOUS INFECTION WHEN MUCOSAL BARRIER BROKE EG DENTAL EXTRACTIONOR IUD AND GROWS REALLLY FAST IN TISSUESAbdominal/pelvic actinimycosisArise from pelvis (IUD) in women or Ileocecal region following surgery or traumaBrain abscess, (solitary abscess)Spread from other fociMycetomaSubcutaneous implantation through traumasinus tracts opening to the skin

Sulfur granules in pus

Treatment: penicillin, surgical drainage

DiseaseCervicofacial actinomycosis (lumpy jaw)Trauma to oral cavity, dental extraction with poor oral hygieneTissue swelling and fibrosis at the angle of jaw and neck

Thoracic actinomycosisInvolves lungs and ribsAspiration from oral cavity or from other focus through muscle fascia

8WHAT ARE THE DS ASSOCIATED WITH ACTINOMYCES ISRAELII? CTABMBATCuMWHAT IS CERVICOFACIAL ACTINOMYCOSIS? LUMPY JAWDUE TO TRAUMA TO ORAL CAVITY, POOR HYGEINE SO GET TISSUE SWELLING AND FIBROSIS AT THE ANGLE OF THE JAW AND NECK.EG. DENTAL EXTRACTIONWHAT IS THORACIC ACTINOMYCOSIS?....INFECTION OF LUNGS AND RIBS FORM ASPIRATION FROM ORAL CAVITY OR FORM OTHER FOCUS THRU MUSCLE FASCIAWHAT IS ABDOMINAL/PELVIC ACTINOMYCOSIS.INFECTION DUE TO PELVIS IUD IN WOMEN OR ILEOCECAL REGION AFTER SURGERY OR TRAUMAWHAT IS BRAIN ABSCESS? SPREAD FROM OTHER FOCIWHAT IS MYCETOMA? INFECTION IN THE SC THRU TRAUMA EG SINUS TRACTS OPENING TO THE SKINGET SULFUR GRANULES IN PUS..HOW DO U TREAT ACTINOMYCES ISRAELII? PuSPENICILLIN AND SURGICAL DRAINAGENocardia asteroides; N. brasiliensisGram positive filamentous bacteria (break up into rods)Partially acid fast ( distinguish from Actinomycetes which has similar morphology but not acid fast)Found in soilAerobic

Opportunistic infectionsPulmonary nocardiosisin patients with low CD4 counts, AIDS, neutropenia, on chemotherapy, malignancyResembles tuberculosis, disseminate to other organs and brain Brain abscess

TreatmentSulfonamides

Gram stainModified acid fast stain9TELL ME ABOUT NOCARDIA? GPFAO.FAGPopeWHAT ARE THE TWO SPECIES OF NOCARDIA? ASTEROIDES AND BRASILIENSISWHAT DS DOES IT CAUSE? PULMONARY NOCARDIOSIS AND BRAIN ABSCESSWHAT HAPPENS IN PULMONARY NOCARDIOSIS? SEE IN PATIENTS WITH LOW CD4 COUNTS, AIDS, NEUTROPENIA, CHEMO, CANCER, RESEMBLES TUBERCULOSIS AND GOES TO OTHER ORGANS AND BRAINHOW DO U TREAT ASTEROIDES AND BRASILIENSIS? SULFONAMIDES.

Listeria monocytogenes

Physiology and structure (useful identification features)Gram-positive coccobacilli often arranged in pairs. Facultative anaerobe Weakly -hemolyticMotile at 250C with end over end tumbling motilityCapable of growth at 4C (psychrophile) and in high-salt concentrationsVirulence Facultative intracellular pathogen that can avoid antibody-mediated clearance Virulent strains produce cell attachment factors (internalins inla, B,C), hemolysins (listeriolysin O, two phospholipase cs), and a protein that mediates actin-directed motility (acta)

MEAT, CHEESE, TELL ME ABOUT LISTERIA MONOCYTOGENES? G FWMC.......CoW...MGF..MGF MY GIRLFRIENS IS A COWWHAT ARE THE VIRULENCE FACTORS? FACULTATIVE INTRACELLULAR PATHOGENT AND CAN AVOID AB MEDIATED CLEARANCE, CELL ATTACHMENT FACTORS. LIKE INTERNALINS, INLA, B,C,....HEMOLYSINS (LISTERIOLYSIN O, TWO PHOSPHOLIPASE CS AND PROTEIN THAT MEDIATES ACTIN-DIRECTED MOTILITY (ACTA)10PathogenesisHost cells enterocytes or M cells of Peyers patchesAttaches to host cells- internalin proteins Inl A,B,CInternalised in phagocytic vacuole escapes phagocytosis by exotoxin listeriolysin O (membrane damaging)Grows in cytosol and passes from cell to cell using Actin filabinding protein ActA- comet tail ments and actin to propel the bacteriaEnters adjacent cell through (filopod) to secondary vacuole ( avoid intercellular region)Escape (phospholipase C and LLO)

DESCRIBE THE PATHOGENESIS OF TEH LISTERIA MONOCYTOGENES? HAIGEE.....11

EpidemiologyIsolated in soil, water, and vegetation and from a variety of animals, including humans (low-level gastrointestinal carriage) Disease associated with consumption of contaminated food products (e.g., soft cheese, milk, turkey, raw vegetables [esp. cabbage]) or Growth in contaminated foods in the refrigerator can lead to high concentrations of bacteriatransplancental spread from mother to neonate; The young, elderly, and pregnant women, as well as patients with defects in cellular immunity, are at increased risk for disease sporadic cases and epidemics occur throughout the year but peak in warmer months

SPONTANEOUS ABORTION, NEONATAL SEPSIS, MENINGITISMENINIGITIS IN AIDS PATIESNTS..PREGNANT WOMEN, NEONATAL , AIDS, PTS, WHERE DO U FIND LISTERIA MONOCYTOGENES? SWVAH.....SHAW...V.....HUMANS..LOVE LEVEL GI CARRIAGELISTERIA USUALLY GET FROM? CONSUMPTION OF CONATIMINATED FOOD PRODUCTS....CMTRG...CuRT GuM CHEESE, RAW VEG ES CABBAGE, TURKEY, GROWTH IN CONTA IN THE FRIDGE, MILKHOW IS SPREAD TO THE NEONATE? TRANSPLACENTALWHO ARE THE GREATEST RISK FOR LISTERIA MONOCYTOGENES? YOUNG AND ELDERLY PREGENT, IMMUNE DECREASED13Disease (listeriosis)Neonatal disease Early-onset disease ("granulomatosis infantiseptica"): acquired transplacentally in utero and is characterized by disseminated abscesses and granulomas in multiple organs Late-onset disease: acquired at or shortly after birth and presents as meningitis or meningoencephalitis with septicemia

Disease in healthy adults: typically an influenza-like illness with or without gastroenteritis Disease in pregnant women or patients with cell-mediated immune defects (AIDS): can present as a primary bacteremia or as disseminated disease with hypotension and meningitis may lead to abortion of foetus

SO WHAT KIND OF DS LISTERIOSIS DO U SEE? NHP...PHiN NEONATAL DS, HEALTHY ADULTS AND PREGNANT WOMEN OR IMMUN DEFECDESCRIBE NEONATAL DS IN LISTERIOSIS? HAVE EARLY AND LATE ONSET DS...IN EARLY SEE GRANULOMATOSIS INFANTISEPTICA....ACQUIRED IN UTERA AND SEE ABSCESS AND GRANULOMAS IN LOTS OF ORGANS.......IN LATE WHICH IS ACQUIRED SHORTLY AFTER BIRTH AND U SEE MENINGITIS OR MENINGOENCEPHALITIS WITH SEPTICEMIA...DESCRIBE LISTERIOSIS IN HEALTHY ADULTS? INLUENZA LIKE WITH OR WITHOUT GASTOENTERITIS...HOW DOES IT PRESENT TO PREG WOM AND REDUCED IMMUNE? AS PRIMARY BACTEREMIA OR DISSEMINATED DS WIHT HYPOTENSION ADN MENINGITIS WHICH LEAD TO ABORTION OF FETUS14Diagnosis

Organism isolated from blood, CSF, amniotic fluid, genital tract of mother and contaminated food source

Culture on blood agar may require incubation for 2 to 3 days or cold enrichment at 4c

Beta hemolytic colonies, catalase positive and tumbling motility in broth medium at 250c

Treatment:

Severe disease is penicillin or ampicillin, alone or in combination with gentamicin, trimethoprim-sulfamethoxazole People at high risk (pregnant and immunocompromised) should avoid eating raw or partially cooked foods of animal origin, soft cheese, and unwashed raw vegetables

WHERE CAN U ISOLATE THE ORGSM? BCAGC.....BAG..CoCWHAT TESTS DO U ORDER? CULTURE ON BLOOD AGAR WHICH REQUIRES 2 TO 3 DAYS OR COLD ENRICHMENT AT 4 DEGREES WITH BETA HEMOLYTIC COLONIES, CATALASE POSITIVE AND TUMBLING MOTILITY IN BROTH MEDIUM AT 25 DEGREESHOW DO YOU TREAT LISTERIA MONOCYTOGENES? PAC....PENICILLIN , AMPICILLIN OR COMBO OF GENTAMICIN AND TRIMETHOPRIM SULFAMETHOXAZOLE.

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