Group B beta hemolytic streptococci:- Gram +ve cocci - Lancefield group B - Form large colonies - Hemolytic but result

t in less hemolysis compared to group A - Catalase ve - Encapsulated; & its capsule made up of sialic acid; used in vaccinations - According to capsule divided into 9 serotypes - Capsule is a virulent factor; an anti-phagocytic by binding with complement factors - Newborns widely affected; result in septicemia, meningitis, sepsis & chorioamnoitiis with high mortality; they considers as immune compromised patients - They are part of normal flora of GIT, vagina (10-30%) - We have to be aware when lady become a pregnant if she is a carrier or not (so checked in 3rd trimester) & if present gives them chemoprophylaxis - Occurs due to premature rupture of the membrane that surround the fetus in uterus; so organism pass to baby & develop septicemia - Premature baby are more susceptible Pathogenesis:- There is balance between organism & host factors (immune response) - Sialic acid capsule as virulent factors; bind to factor H & interfere with the function of the complements - Our bodies have to develop antibodies & this requires 10 days - Because of the capsule (sialic acid); phagocytosis affected because of presence of capsule - Produce enzyme that inactivates C5 factor called C5 peptidase - Specific abs are protective because of the phagocytosis Clinical: - Non specific others; we have to culture & look for organism in the lab - Patient develop: o Septicemia, respiratory distress, fever & lethargy o Meningitis in 5-10% of the cases o Peripartum choriomengitis (related to choriom & amniotic fluid) o Pneumonia & skin infection o Mortality rate approaches 20% Diagnosis - Blood & CSF culture - Group B because of faint weak complete type of hemolysis - Gram +ve - Catalase ve - Direct detection from vagina is not effective; because group B are normal flora in vagina (10-30%) Treatment: - Penicillin drug of choice - Less susceptible to beta-lactams - Combinations with aminoglycosides - When septicemia caused we use combination therapy because we need synergism Prevention - Reduce contact & eradicate carries by 1. By checking 3rd trimester pregnant women & must taking vaginal swap 1

2. If mother had premature rupture in the membrane; go to hospital because delay result in higher chance of infection 3. We use intapartum chemopropohylaxis with beta lactam 4. Using purified GBS polysaccharide as vaccine We do not need to premature babies unless there is a reason Positive CAMP test (not used)

Listeria monocytogenes:- Associated with infection of newborns - Causes still-birth baby died - Like GBS cause meningitis - Name of disease is listeriosis - Problem with this organism: 1. Affect adult pregnant can be affected 2. Associated with still birth; baby death & has multiple granulomatous lesion granulomatosis infantiseptica (similar to TB patient) 3. Granulomatous lesion caused by macrophages General features: - Gram +ve - Short rods coccobacilli - Catalase +ve - Beta-hemolytic & to differentiate from streptococci we use catalase test which is: o Catalase ve in strep o Listeria is +ve - They resist phagocytosis by listeriolysin - Grow & enriched at cold temperature - Tumbiling type of motility spiral movement at 25 C - Also test called umbrella motility test; by inoculate organism in motility media at cold & organism result in shapes like umberall - 3 serotypes based on thichoic acid most virulent factors - Infection caused in fetus & newborns infections - Sources o Found in humans & animals intestines o From diary products; soft cheese - Cause still birth - Seen in extreme age group - Trasplacental like group B beta-hemolytic streptococci - If there is premature; meningitis will occurs Pathogenesis: - Cell mediated immunity (CMI); with monocytes so macrophages as defens mechanism - If patient if there is immune deficiency then patient is more susceptible to severe infections - Little humoral but more CMI. PMNs - Common in AIDS patient - Attachement to phagocytes; to escape phaogcytosis by mechanism of actin rearrangement (similar to shigella)

o Bacterium attach into surface protein called internalin; then produce LLO (listerial listeriolycin oxygenase) which result in holes in cell membranes so entering cytosol o Involves proteins like: ActA, Gelsolin o Cytoskeleton rearrangement: start by actin polymerization to produce Actin tail Clinical aspect: - Food borne breaks - In majority of cases no GIT manifestations - CNS predilections; associated with bacterial meningitis - Neonatal & puerperal sepsis - Elderly & immunecompromised - Women in late pregnancy - Diagnosis: by blood & CSF culture Treatment: - Penicillin, ampicillin, TMP-SMX & combination of ampicillin & gentamicin - Gentamicin not affected in meningitis unless injected intrathecally Prevention: - By screening of food products - No vaccination Mycobacterium Lepare: - Affect peripheral nervous systems ( nerve endings in particular) - Cause leprosy - Clinical presentation is granuloma in face, disfigurement; loss of sensation, parethesia & so on - Acid fast bacilli - Cannot be grown on artificial media differentiation from M.TB) - Grown in pad of mice or armadillo - Slow grower with regeneration time of 12-14 days - Have mycolic acid similar to M.TB; only difference is in one of mycolic acids which is called phenol glycoplid1 (PGL-1) - So PGL-1 only found in M.leprae - Causes chronic granulomatous disease to terminal nerve endings - Unknown mode of transmission; could by respiratory pathway - Reservoir is human - Incubation period is very long as 2-7 years - We can get them from skin granuloma - Called also Hanesn organism; discover them Pathogenosis: - Must multiply in host cells macrophages - PGL-1 & LAM mycolic acid facilitates survival within cells - In peripheral sensory nerve they cause Patchy anesthesia (due to destruction) Clinically: - 2 types: 1) Tuberculoid leposry localized - Localized type with localized immune reaction & result in granuloma - Here the patient will have Lepromin +ve; will respond by cell mediated immunity 3

2) Leromatous type systemic type Organism spread all over the body Patient is severely immuncompromisied Lepromin test will be ve

Notes: - Negative indicates fulminant infection rather than not infection - Tubercoloid type: will have granulomatous & epithelioid; lymphocytosis - Lepromatous type: suppression of cell mediated immunity - Delayed type of hypersensitivity to lepromin is the pathology Diagnosis: - Acid fast stain from infected tissue - To differentiate from M.TB we look form phenolic glycolipd Treatment & prevention: - Drug of choice is sulphones combined with rifampin in tuberculoid leprosy - Added Clofazimine in lepromatous leprosy - Chemorophylaixs with dapsone; BCG (bacillus, Calmette-Guerin) vaccine which activates the macrophages