Staphylococcus Streptococcus: Propertie S Morpholo Gy Culture & Biochemi Cal Reactions

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Gram positive bacteria of medical importance

cocci
pg1

Propertie
s
Morpholo
gy
Culture &
biochemi
cal
reactions

Pathogen
icity

Infection
s

bacilli
pg2

Staphylococcus

Streptococcus

-Spherical, resistant to drying , heat and


9% NaCl but inhibited by 3%
hexachlorophene
-Grow(aerobic/microaerophilic)
-Culture on nutrient,blood & mannitol
salt agar.
-Biochem. Reac.
1)Catalase test(diff.staph from
streptococci)
2)Coagulase test(diff.S.aureus from
S.epidermidis & S.sapropyhticus)

-In chains of varying length,large,heterogenous group.

1)Catalase(converts H202H20+O2)
2)Coagulase& Clumping factor
-to clots oxalated plasma & altering
ingestion by phagocytes
-Clump.factor adhere organisms to
fibrinogen & fibrin. Form clumps.
3)Staphylokinase(fibrinolysis)
4)Hyaluronidase(spreading factor)
5)Exotoxins(lysing WBC, necrosis &
severe inflammation)
6)Panton-Valentine leucocidin(lysis
WBC)
7)Exfoliative toxins(Superantigens &
dissolving mucopolysaccharide matrix of
epidermis)
8)Toxic shock syndrome
toxin(fever,shock,desquamative skin
rash,multisystem involvement)
9)Enterotoxins(S.aureus cause food
poisoning,vomiting & diarrhea)
#S.coccal=normal flora on skin & mucous membrane but
S.aureus(major pathogen for human)

1)S.aureus infections:
-focal suppuration(abscess)
-pneumonia
-empyema
-meningitis
-endocarditis
-osteomyelitis
-sepsis
-acne,pyoderma,impetigo
-scalded skin syndrome
-bullous exfoliation
-toxic shock syndrome
-food poisoning
2)S.epidermidis infections:
-normal flora to skin,respiratory & git
-may infect orthopedic/CVS prostheses
and cause disease in immunosuppressed
persons
3)S.saprophyticus infections:
-urinary tract infections in young women

1)S.pyogenes:blood agar complete hemolysis(B),Lancefield A,


antigenic structures of M protein,T & P substance.
2)S.agalactiae:Group Bpart of normal flora in women
3)S.viridans:a haemolytic,normal flora of upper respiratory tract &
important in healthy state of mucous membrane
4)S.pneumoniae:diplococcic,permits typing with antisera
5)Enterococci:nonhemolytc,normal enteric flora
6)Peptostreptococcus:normal flora of mouth,respiratory
tract,bowel & female genital tract.
1)S.pyogenes:
-Streptokinase(fibrinolysin)
-Streptodornase(depolymerizes DNA)
-Hyaluronidase(spreading factor)
-Pyrogenic exotoxins(erythrogenic toxin)
-Diphosphopyridine nucleotidase(kill leukocytes)
-Haemolysins(for haemolytic zones)
2)S.pneumoniae:
-its infections causes outpouring of fibrinous edema into
alveoli,followed by RBC & leukocytes, results in consolidation of
portion of lung.
-found in exudate
-sudden fever,chills & sharp pleural pain.

1)S.pyogenes:
*by invasion
Erysipelas(brawny edema)
-Cellulitis(acute rapidly spreading infection on skin & subcutaneous)
-Necrotizing Fasciitis(flesh-eating)
-Puerperal fever
-Sepsis(can be fatal)
*by local infection
-Pharyngitis(sore throat)
-pyoderma
*by Group A invasion
-S.coccal toxic shock syndrome(shock,bacteremia,respiratory failure
& multiorgan failure)
-Scarlet fever
*Poststreptocaccal diseases
-Acute glomerulonephritis
-Rheumatic fever(damage heart muscle and valves)
2)S.agalactiae
*in first month of life:neonatal sepsis,meningitis,respiratory
distress syndrome.
*in elderly/immunosuppressed host:bacteremia,skin,soft
tissue,respiratory and genitourinary infections
3)S.viridans
-Endocarditis on abnormal heart valves
-Genesis of dental caries
4)S.pneumoniae
-Bacteremia has a triad of severe
complications:meningitis,endocarditis & septic arthritis
5)Enterococci
-nsocomial infections
-most common sites of infection are urinary & biliary tract,wounds &
blood
-Meningitis & bacteremia in neonates
-Endocarditis in adults
6)Peptostrepococcus
-occur in wounds,in breast,in postpartum endometritis,following

rupture of abdominal viscus,the brain/in chronic suppuration of lung

Treatmen
t

*S.cocci variably sensitive to many


antimicrobial drugs
*Meaningful S.coccal isolates tests help
in choice of systemic drugs.

Genus Bacillus

-large, aerobic, spore forming, in chains


-Bacillus anthracis, cause anthrax,
principal pathogen
-CULTURE
> Blood agar
-MICROSCOPIC EXAMINATION
> Gram stain, Spore stain,
Immunofluorescence stain

1)S.pyogenes:Penicillin G,Erythromycin,rapidly eradicate its from


patient,eliminate antigenic stimulus
2)S.pneumoniae:sensitive to antimicrobial drugs,Penicillin G,early
treatment
3)Enterococci:COMBINATION of Penicillin/Vancomycin +
streptomycin/gentamicin

Pathogenesis of BACILLUS ANTHRACIS (anthrax) :


-CUTANEOUS(by injured skin)
>pruritic papule develops 1-7dys after entry. then, it changes into vesicle that
coalesce & necrotic ulcer develops. 7-10dys eschar fully developed.
-PULMONARY ANTHRAX(inhalation)
>phagocytosed in lung and transported to lymph node & they germinate there &
produce toxin. early manifestation are marked hemorrhagic necrosis & edema of
mediastinum.hemorrhagic pleural effusions follow involvement of pleura. sepsis
occurs. maybe spread to git(bowel ulceration) & meninges
-GASTROINTESTINAL ANTHRAX(ingestion)
>rare in human. abdominal pain, vomiting & bloody diarrhea.

*FOR BACILLUS ANTHRACIS:


-TREATMENT: early treatment
,antibiotics ,recommended=Ciprofloxacin
-PREVENTION: immunization by
attenuated spore based vaccine &
bacteria free filtrate
*FOR BACILLUS CEREUS:
-TREATMENT: vancomycin/clindamycin
with or without aminoglycoside

Pathogenesis of BACILLUS CEREUS (food poisoning) :


-THE EMETIC TYPE : fried rice causes vomiting, nausea, abdominal cramps.
: self-limiting, recovery within 24hrs
-THE DIARRHEAL TYPE : meat dishes and sauces causes profuse diarrhea,
abdominal pain and cramps, fever & vomiting uncommon
:enterotoxin preformed in food or in intestine
ALSO,,B.cereus cause eye infections, severe keratitis, endophthalmitis &
panophthalmitis, endocarditis, meningitis, osteomyelitis & pneumonia.

Corynebacterium
diphtheria

Pathogenesis of diphtheria :
-UPPER RESPIRATORY TRACT INFECTION: by inhalation, oral contact &
ingestion of contaminated food
: production of exotoxin, the toxin absorbed into mucous membranes & destruction
of epithelium with superficial inflammatory response,
: pseudomembrane formed on tonsils, pharynx/larynx. Removal of
pseudomembrane causes bleeding.
: Regional lymph node enlarged and Bull neck formed by edema.
: Continuous toxin production leads to necrosis in heart muscle, liver, kidney &
accompanied by gross haemorrhage. Also nerve damage & paralysis of soft palate,
eye muscle/extremities.
: Diphtheritic inflammation begins causes sore throat & fever.

-club-shaped, arranged in Chinese letter


appearance
-aerobes/facultative anaerobes
-CULTURE
>Loefflers serum slope=quick growth
>Blood agar=small zones of haemolysis
>Blood tellurite medium=brown to black
colonies
-MICROSCOPIC EXAMINATION

>Gram stain
>Alberts stain=metachromatic granules

-TREATMENT: Penicillin/Erythromycin &


early administered specific antitoxin to
site of injury
-PREVENTION : active immunization with
DIPHTHERIA TOXOID in child produces
antitoxin adequate till adulthood.

Listeria
monocytogenes
-Short, non-spore, motile by tumbling endover-end
-causes disease in wide spectrum in human
& animal
-CULTURE
>5% sheep blood agar=small zones of
hemolysis
*catalase positive, produces acid in
carbohydrates & facultative anaerobes
-TREATMENT:Ampicillin, erythromycin/IV
trimethoprim-sulfamethoxazole.

Clinical type of diphtheria :


>Faucial diphtheria (tonsilar region)
>Nasopharyngeal diphtheria
>Nasal diphtheria
>Laryngeal diphtheria

Pathogenesis of listeriosis :
*enters GIT after ingestion of contaminated foods such as cheese. Not destroyed
by phagocytosis.
-EARLY ONSET SYNDROME: granulomatosis infantiseptica from utero infection
characterised by neonatal sepsis, pustular lesions & granulomas containing
L.monocytogenes.
:death may occur before/after death
-THE LATE ONSET SYNDROME: meningitis (from birth to 3 weeks).significant
mortality rate.
ALSO,, adults can develop listeria meningoencephalitis, bacteremia & focal
infections.(immunosuppressed patients)

-LABORATORY DIAGNOSIS: isolation of organism in cultures of blood & spinal


fluid.

GOODLUCK..

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