micro shaeet # 14 - Haneen thnebat

بسم الله الرحمن الرحيم
Micro lec#14
18/10/2010
*** I apologize for this too long sheet but it's easy , many information are repeated so"2st3n bellah wla t3jz"!
This lecture cover slide#10-26 from streptococci hand-out.
Slide 10:
**Streptococci diseases divide into 2 major category:
1-suppurative(pyogenic/pus forming)streptococcal disease.
2-non-suppurative(non-pyogenic/inflammatory without pus forming)disease.
►Suppurative disease:
-The most imp.disease caused by Streptococci is pharyngitis (sore throat/tonsillitis/streptococcal sore throat) common in childhood.
-relatively short period of incubation, develop (2-4) days after exposure to the organism from an individuals who are shedding the organism.

-Bacteria is usually present in the throat of healthy carrier (carrier: don't show disease but they have the organism (bacteria) in their throat structures like tonsils .they shed it with their respiratory droplets so susceptible individual around them become infected and develop a sudden abrupt onset of: sore throat,fever, malaiseand headache after(2-4)days of exposure.
(وكعة,دعث,شعور بالتعب)
-Sore throat is a manifestation, it's not a disease, but it has been agreeable to called streptococcal disease of the throat as (sore throat).

-sore throat is pale of the throat but pale of the throat are not restricted to Streptococci because it's common to cause by virus. The mostcommon cause of upper respiratory tract infectionlike(common cold, adenovirus…etc) is virus.so theminority of sore throat is due to the bacteria and this common in childhood.While in adult, viruses more common than bacteria as a cause of sore throat.Manifestations of sore throat: fever(may reach 39-40c°),malaise, headache, Posterior pharynx appears erythematous(redness)with an exudate and cervical lymphadenpathy(lymph node in neck become enlarge),enlargement of the tonsils which become follicular in nature and can be covered with a white membrane formed from puss.(inflammatory exudates membrane cover tonsil due to sever inflammation associated with tissue necrosis ,fibrin collection,organism,pus..etc all these collection lead to formation of pus over tonsil and this is characteristic of sore throat.However,this membrane disappearance can be used by other infection like diphtheria(DPT)(bacteria) that cause tonsil enlargement and membrane usually ruptured upon attempt to remove it. Viral infection also can cause soar throat, lymphadenpathy, headache,fever. We conclude that viral and other bacterial infections can cause sore throat with the same manifestations seen in streptococcal sore throat."same clinical picture to streptococcal sore throat".
I will abbreviate streptococci as str. *
-Str.sore throat can't be diagnosed by gram-stained smears,we must isolate the organism to confirm the etiology because sore throat as we mention before can be caused by many organisms(virus,bacteria).

- Str.infection treated by Ampicillin or penicillin(β-lactam antibiotics)but usually they give Ampicillin as oral antibiotic in treatment.

-if it's viral →no improvement take place, individuals will develop skin rash,skin rash seen in 80%of those with EBV(Epstein-Barr virus)infection that cause sore throat"fromWikipedia",treated without penicillin or Ampicillin.Sopenicillin here can use in diagnosis only, that this sore throat is due to viral infection not str.infection and skin rash also is an evidence that this sore throat is due to viral insection.
-The most important bacteria that cause sore throat is streptococci.

-other bacteria also can cause sore throat such(diphtheria,Acinetobacter,and even Neisseria can cause sore throat).

-in childhood usually it's the streptococci that cause sore throat.
-sometimes it's complicated by puss collection ,Peritonsillar and retropharyngeal abscesses are developed but this is rarely to occur.

-retropharyngeal abscesses can opened,raptured,into the airway .block airway passage ,cause asphyxiation(25tena8).so retropharyngeal abscesses serious condition.

-if str. sore throat infection not treat,it will lead toPeritonsillar (more common)and retropharyngeal abscesses(less common),antibiotic treatment here is not useful and the puss must be removed(drainage)by syringe to decrease the pressure in upprer respiratory tract.

-as we mentioned before that str.infection treated by penicillin or Ampicillin .but in case of penicillin-allergic patient we use erythromycin or other antibiotic."the Dr. said that penicillin is the treatment of choice".

-at age of(4-16)the chance of which sore throat develop to rheumatic fever is high and that's why it's very imp. to treat all faces of str.soar throat to avoid the development of rheumatic fever at this age.
-children with recurrent str.sore throat infection must treated by the 2 form of penicillin (long-acting time penicillin→Benzathine& short acting time penicillin→procain) "back to page 9 in hand-out Antibacterial agent (classes of penicillin) to remember "they are given together to cover long&short term effect of str.infection so disease will not develop to rheumatic fever.

-after treatment ,especially in partial treated individuals,pharyngeal carriage is common and up to 20%of school children has streptococci in their throat which is high!they can infect country not school!spread of infection is easily among classmates,teachers .That's why treatment should last for minimal 10 days until organism eradicate.
-symptoms usually disappear in the third day ,that's why many parents stop giving antibiotic to their children in the second or third day as their children impove,feelbetter,start to play.This is an abuse of antibiotic that will enhance the pharyngeal carriage state.

Laboratory diagnoses:
"the dr. explanation wasn't clear so it's recommended to back to textbook p.103-104"
Diagnosis made by isolation of the organism in broth culture .it's imp.to take the swab from the infected area because oral cavity is heavily inhibited by normal flora ,normal flora will over growth the streptococci so swab must taken from the infected area(such as tonsil).The configurations of diagnoses are made by 2 methodes:serotyping with anti-A-antibody and if agglutination pattern occurs .this is an evidence that the organism is str. of group A.

Alternative method can use Bacitracin(antibiotic) ,it's active against gram + bacteria &can't use in treatment because of high toxicity but can used in lab to confirm the identify of streptococci .we add Bacitracin to our plate(swab from infected region culture in blood agar plate and show small ,translucent β-hemolytic colonies )if clear zone appear then we conclude that inhibition of growth of β-hemolytic colonies occur. So according to conformation (type of str.),treatment will start.
Slide 10
Scarlet fever:
-common complication that follow sore throat.
-develop Within 1 to 2 days of the development of pharyngitis.
- A diffuse erythematous(27merar) rash initially appears on the upper chest and then spreads to the extremities.
- The area around the mouth is generally spared→meanperi-oral area lackerythematous rash.
احمرار الجلد لن يظهر في المنطقة حول الفم.
-The rash disappears in 5 to 7 days and is followed by desquamation of the skin that involve palms& soles(desquamation of the whole area that affected by rash).
Desquamation :تقشر الجلد
-Scarlet fever is due to (pyrogenic)erythrogenic toxin that release by the organism in the course of pharyngitisso it's not due to the organism it self but due to the toxin release by it).
-3 types of erythrogenic toxin (A,B,C). (A) is th common one, but A don't protect against B&C.That's why children who develop scarlet fever due to erythrogenic toxin type A, will develop another attack by type B&C,but here(in case of B&C) the attack is secondary so the scarlet fever associated with type B&C less severthan those with type A.
Slide 12
You can see the color of rash appear in the patient'schest .InSlide 13you can see strawberry tongue "tongue appear redden like strawberry"this is characteristic for children with scarlet fever.Slide 14:desquamation of palms.
Slide 15
Pyoderma(impetigo)
-infection by group A str. and usually affects the sun exposed area (face,arm,leg).
-common to affect children especially those with poor hygiene.
-can cause by staphylococci.we can't differentiate between staphylococcal impetigo and streptococcal impetigo exept by isolate and cultureof the causative agent.
*Order of development of impetigo is:
1-formation of vesicle at localized area of skin.
2-vesicle develop to bullae(7owy9leh),that usually filled with clear fluid .
بثر 3-bullae undergo depressionto form pustule.
4-pustulewill rapture and crust over,and the crust (8shor)will shed from the adhesion.
بكوّن قشور
-child usually scratch the area because this area of lesions are itching,which cause infection(auto-infect)to other area, that's why infection spread ."so it's not single lesions &should be treated with penicillin".
-the target group is young children (2-5 years) with poor personal hygiene and occurs during the warm, moist summer months." Sweating provide the environment suitable for development of str. so increase the risk of such infection."
-strain that cause skin infection differ from that cause pharyngitis (sore throat infection).this imp. because throat infection is associated with rheumatic fever as post-streptococcal disease, whereas skin infection is associated with the ….."I will check it from Dr. 2nshallah".so we have 2 different groups of streptococci.
Slide 16
Erysipelas (erythros = red, pella = skin )
-infection was common in past but less nowadays.
-Local pain and inflammation, lymph node enlargement and systemic signs (chills, fever, leukocytosis).
-Involved area is typically raised and distinctly differentiated from the uninvolved skin.→this is imp.here there is clear differentiation between infected skin(raised above other area) and non- infected skin, ,unlike Cellulitis(explained later) where it is difficult to differentiate between involved&un- involved areas.
-in past it was called (the disease of the face) usually bilateral involvement of the cheeks.Butnow ,occur mostly common in children &older adult and commonly develop in the leg.
-Usually preceded by respiratory tract or skin infection with group A streptococci.→so it's a complication of respiratory or skin infection that caused by group A streptococci. Slide17&18: clear distinguish between involved/un-involved skin.
Slide 19
Cellulitis :
-infection of the subcutaneous tissue, spreading of str. infection from the skin to subcutaneous tissue result in condition known as Cellulitis.
-simply it's infection in the connective tissue subsequent to the break in skin(introduction of organism through the broken skin ,continuity of the skin lost).
-cellulitis can't be diagnosed in clinical…..,we have to isolate the organism,because cellulitis can caused by any organism. Any organism that can penetrate through the skin ,can cause Cellulitis,so not only gram+but also gram- bacteria can cause Cellulitis because the subcutaneous area is the spreading area.
- cellulitis don't involve muscle and fat,involve only subcutaneous tissue "muscle is spared".
Necrotizing Fasciitis:
-more serious,fatalillnessinfectionthatinvolve destruction of muscle,fat unlike cellulitis.
-most imp.and common cause of Necrotizing Fasciitis is str.(β-hemolytic str.,group A str.)
-can cause by staphylococci but rarely.
-str. that causesNecrotizing Fasciitis was called (flesh – eating bacteria)"term by press".
الصحافة أطلقت هذا المصطلح.
-The dr. read the slides .about third point in slide19→in bothcellulitis&Necrotizing Fasciitis, the organism introduce into the tissue through braked skin, that's why Necrotizing Fasciitis usually start as cellulitis "cellulitis if not treated it will lead to Necrotizing Fasciitis".

Slide 20
Bullae mean(7oy9leh)-
-Systemic toxicity mean(fever,rash,…)
Third point →heavy antibiotic needed, large dose of penicillin required because of rapid spread of the organism. Whole chest and abdomen can open and destroy. The spreading of str.along facial planes lead to large necrotic tissue that should be removed(debrided) with heavy antibiotic therapy. If patient survive, treatment of the damage skin can achieved by skin grafting.(zra3t jeld).
Slide 21
Streptococcal toxic shock syndrome:
-Similar to that of staphylococci (skin infection with multi- system toxicity).
- Those with underlying disease are at an increased risk(diabetes,cancer,renalfailure,cardiac failure)patient.
-M protein serotypes (1, 3, 12 or 28) are most common cause of Streptococcal toxic shock syndrome.
-It is associated with erythrogenic toxins that cause scarlet fever, So Streptococcal toxic shock syndrome can develop after scarlet fever because it's believed that erythrogenic toxins can mediate this condition.
-erythrogenic toxins are super anti-genes ,mean it can bound directly to T-lymphocyte and activating them without the need to anigenepresentation, they can directly switch on the production of co-inflammatory mediators (substances that promote inflammation)as a consequences of activation of to T-lymphocyte.
-If erythrogenic toxins not present,then activation of
T-lymphocyte require antigene,cross-reacting antibodies with antigene ,and presentation of macrophage.
Slide22
Other infection caused by str. include:
*Puerperalsepsis:
-very common infection of child bed fever or post partumendomyometritis(infection of uterus) and lymphangitis(infection of drainage lymph nodes).
-due to str.group A&B
-Was common in 19thcentury responsiple for up to 20% of those women giving their birth in hospitals because of the spread of organism among nurses,physicion,….etc. who used to examine and caring for women in labor without washing their hand! A scientist obligate them to wash their hand with phenol "I'm not sure" which was available at that time ,the incidence of Puerperalsepsis decrease significantly.
-in past it was due to normal delivery but now it's due to criminal abortion as it is take place in clinic &home not in hospitals so lack of aseptic technique.
*pneumonia:
-bacterial infection can be cause by streptococci.
-No differences between pneumonia that cause by streptococci group A and pneumonia cause byStr.pneumonia.
*Bacteremia:
common in patients with necrotizing fasciitis or toxic shock syndrome (40%).Because in these cases infection spread easily due to destroyed blood vessels "access of organism toward blood stream→Bacteremia.
►non suppurative streptococcal disease:
2 types:1- Rheumatic fever. 2- Acute glomerulonephritis(AGN).
-In both cases ,antibody produce against organism(str.).it has been found that these antibody are structures of the sarcolemma (antigene present in the heart muscle especially in heart sarcolemma)and the antibodies cross reacting with streptococcal M protein.
-So in those 2 type of disease the inflammation caused by antibody produce against streptococcal M protein, butstreptococcal M protein react at the same time with the human hard tissue!So antibodies will react with hard tissue.
-when antibodies produce,they can't differentiate between streptococcal M protein and the hard tissue.
-antigene-antibody complex form→ this activation of complement system→complement products are generated as consequences of inflammation.
-in rheumatic fever,this inflammatory response involve the(mitral and aortic valves)"distruction of the valves".mitral is the most involved result in mitral stenosis(t9'y8 fe al valve).so mitral stenosis is consequence of rheumatic fever which is an immune mediated process/post-streptococcal disease develop 2 weeks after group A str.infection.
-as a conclusion,here the organism don't invade the heart "don't cause infection of the heart ",but the antibodies that produced to resist the organism, will react with tissue of the heart because of similarity between hard tissue component (protein&suguar)and the component of str.M protein.
M protein assotiated with rheumatic fever(M types 18,3,5)in order.

*acute Glomerulonephritis
-occur 2-3 weeeks after skin infection by certain group Astr.types.
-in skin infection the crossrection is between basement membrane of kidney and the organism and that's why,the antibodies released against organism will react with them on glomerular basement membrane"deposition of antibody-antigene complex take place on the glomerular basement membrane"→complement system activationinflammatory response in kidney→proteinurea /hematuriadevelop,loose of the normal function of glomeural that's why it's calledAcute glomerulonephritis AGN.
دم وبروتين في البول
-treatment of rheumatic fever&AGN is by prevention of streptococcal disease and treat it completely as quickly as possible,because it's serious condition" in case of rheumatic fever valve destruction occur "irreversible condition"patient must undergo surgery to get artificial valve. And as you know, artificial valve is target of staphylococci streptococci.
-M protein associated with AGN (12,4,2,49,59,61).


Slide 23,24,25,26
Group B Beta Hemolytic Streptococcus(Streptococcus agalactiae )
-Was initially recognized as a cause of puerperal sepsis.
- Became more notorious as an important cause of septicemia (infection of blood stream), pneumonia and meningitis in newborn children, as well as serious disease in adults.
-Nine serologically distinct serotypes (capsular .antigens of Ps).
-capsule is the base for classification,these serotypes(1,2,….9)composed of polysaccharides and that's why antibodies are produced.
-production of antibodies against str. is more important than exposure to the organism(presence of antibodies is protective).
-Antibodies develop, are protective and their production in mothers is more important than exposure of neonates to the organism. That's mean if female have antibodies ,it's more imp.than exposure because antibodies will cross placenta ,go to newborn protect him against condition of septicemia,pneumonia and meningitis.
-group B str.usuallyColonize the lower gastrointestinal tract and the genitourinary tract.
-Transient vaginal carriage has been observed in 10% to 30% of pregnant women. "amongunpregnant women it less(5-10%)but among pregnant the prevalence of str. group B(str. carriage)is about 10-30%.
-the risk here is that about 60% of those pregnant women who are(+) mean carry the organism ,will transmit the str. to their infant,and those women don't have antibodies so they can't protect their newborns against infection.
-infection of infants are two types:
►early onset disease→infection in infants younger than 7 days "infection can manifested in the first week of life".
-characterized by Bacteremia, pneumonia or meningitis.
-15-30% of survivors have neurological sequelae.so it's serious condition may lead to death.
►late-onset disease→infectionoccurring1 week to 3 months after birth.
-Exogenous source(from member of family, mother…)
-associated with Bacteremia with meningitis.
-Late onset disease is more frequent than early onset disease.
-Adults, especially pregnant women, may be infected (UTI→urinary tract infection, amnionitis→infection of amniotic fluid,endometritis→infection of uterus, wound infection).
*other beta hemolytic streptococci that may cause disease are groups (C,F,G)but these groups rarely cause disease.

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Done by :HaneenThnebat