Streptococcus spp and

Corynebacterium diphtheriae
SGL 11
Ass. Prof. Shler Ghafour Raheem
Department of Basic Science, College of Medicine
shler.raheem@hmu.edu.krd
Genus: Streptococcus

Gram-positive cocci arranged in chains or pairs

Catalase negative
Streptococcus spp

Medically important species

Streptococcus pyogenes (Group A streptococci; GAS)

Streptococcus agalactiae (group B streptococci; GBS)
Streptococcus pneumoniae
Streptococcus pneumoniae
Streptococci can be classified according to

1- Hemolytic patterns on blood agar:

(A)- -Hemolytic streptococci (incomplete lysis of red blood cells)
(B)- -Hemolytic streptococci (complete lysis of the red cells).
(C) - -hemolysis: Some streptococci are nonhemolytic.

2- Serologically on presence of C substance

C substance is located in the cell wall, and its specificity is determined by an
-Hemolytic Streptococci are arranged into groups A U (known as
Lancefield groups) on the basis of antigenic differences in C carbohydrate.
A, B and D are more frequent.
Group A Streptococcus (S. pyogenes)

Distinguishing features
-hemolytic. It shows beta-hemolysis after 24 hours. In
contrast, harmless streptococci of the upper respiratory system are
either nonhemolytic or alpha-hemolytic.
Bacitracin sensitive
Pyrrolidonyl arylamidase (PYR) positive.

Reservoir: Human throat

Transmission: Respiratory droplets

Streptococcal Respiratory Diseases

Strep throat or streptococcal pharyngitis, is an inflammation

of the pharynx caused by streptococci.
Lancefield group A Streptococcus is the major cause of
bacterial pharyngitis, scarlet and rheumatic fevers.
One strain of group C Streptococcus (also called S.
equisimilis) is also a pathogenic beta-hemolytic bacterium that causes
some cases of streptococcal pharyngitis. However, unlike group A strep
throat, this kind of group C pharyngitis does not lead to scarlet or
rheumatic fevers.
Signs and Symptoms

The back of the pharynx appears red, with

swollen lymph nodes, abscesses covering the
tonsils. Pain during swallowing, bad breath, fever,
malaise, and headache,

Bacteria spread into the lower respiratory tract,

they may cause inflammation of the larynx
(laryngitis) or bronchi (bronchitis).

Laryngitis manifests as hoarseness; bronchitis

reduces airflow, encourages mucus accumulation in
the lungs, and triggers coughing.
The disease scarlet fever, can accompany
pharyngitis caused by a strain of Streptococcus
carrying a lysogenic bacteriophage that codes for
pyrogenic toxins, which are also erythrogenic
(reddening).
Typically, after one to two days of pharyngitis, such
streptococci release their toxins, triggering fever and a
rash that begins on the chest and spreads across the
body.
The tongue usually becomes strawberry red. The rash
disappears after about a week, and the skin sloughs
off in a manner reminiscent of staphylococcal scalded
skin syndrome.
Untreated streptococcal pharyngitis sometimes leads to
complications such as acute glomerulonephritis, a
disease of the kidneys, and rheumatic fever, in which
inflammation leads to damage of heart valves and muscle.

Though the exact cause of such damage is unknown, it

appears that this disease is an autoimmune response in
which antibodies directed against streptococcal antigens
cross-react with heart antigens.
Strains of group A streptococci have a number of structures, enzymes, and
toxins that enable them to survive as pathogens in the body. These include
the following:

M protein causes inhibition of complement component C3b, thereby

interfering with opsonization and lysis
The hyaluronic acid capsule
C5a peptidase. With this enzyme, S. pyogenes decreases the movement of
leukocytes into the site of infection.

Streptokinases: break down blood clots, enabling to spread rapidly through

damaged tissues.
Pyrogenic toxins (erythrogenic toxins) stimulate leukocytes to release
cytokines that in turn stimulate fever, rash, and shock.
Streptolysins lyse erythrocytes, leukocytes, and platelets
Pathogenesis

S. pyogenes frequently infects the pharynx, but the resulting

disease is usually temporary, lasting only until adaptive immune
responses against bacterial antigens clear the pathogen, usually within a
week.

Typically, strep throat and streptococcal bronchitis occur only when

normal, competing microbiota are missing, when a large inoculum enables
the bacterium to gain a rapid foothold before antibodies are formed against it,
or when adaptive immunity is impaired.

S. pyogenes can invade deeper tissues and organs through a

break in a mucous membrane to cause necrotizing fasciitis
 Diagnosis, Treatment, and Prevention
50% of patients diagnosed with strep throat actually
have it; the rest have viral pharyngitis. bacterial and viral
pharyngitis are nearly identical, a sure diagnosis requires
serological testing.

The most common bacterial infection is Group A beta-

hemolytic streptococci, which causes around 36% of
cases of acute pharyngitis. Other bacterial
etiologies include Group B streptococci, Chlamydia
pneumoniae, Mycoplasma pneumoniae, Haemophilus
influenzae, Candida, and Neisseria meningitidis

https://www.google.com/search?q=Pharyngitis&source=lnms&tbm=isch
&sa=X&ved=2ahUKEwjWvcGAtbbtAhWGDuwKHdg1DxcQ_AUoAXoE
CBEQAw&biw=1366&bih=657#imgrc=Mh30a3Bdv7AImM
Penicillins, or amoxicillin, are very effective against both S.
pyogenes and group C streptococci (S. equisimilis).

Erythromycin or another macrolide to treat penicillin-sensitive

patients.

Antibodies against M protein provide long-term

protection against S. pyogenes; however, antibodies directed
against the M protein of one strain provide no protection against other
strains. For this reason, a person can have strep throat more than once.
 Alpha hemolytic streptococcus
S. pneumoniae

General characteristics
Gram positive
Lancet-shaped diplococci
Non motile Sputum gram-stain showing the typical lancet-
shaped gram positive diplococci of S.
Encapsulated If an etiology is
pneumoniae

hemolytic identified, therapy

should be de-escalated
Optochin sensitive
and directed at that
Lysed by bile pathogen
https://microbiologyinfo.com/biochemical-test-and-identification-of-streptococcus-pneumoniae
 Reservoir: Human upper respiratory tract
Transmission: Respiratory droplets
- Not considered highly communicable
- Often colonizes the nasopharynx without causing
disease

Predisposing Factors
Influenza or measles infection
Chronic obstructive pulmonary disease (COPD)
Congestive heart failure ( CHF)
Alcoholism (dominant cause of pneumonia)
 Pathogenesis
Polysaccharide capsule is the major virulence factor

- Antiphagocytic

- Antigenic and opsonized by host antibodies

IgA protease enhances the ability to colonize the mucosa of the URT
Pilli
Teichoic acid
Pneumolysin: hemolysin/cytolysin
-Damages respiratory epithelium
- Inhibits leukocyte respiratory burst and inhibits classical complement fixation
Diseases

Typical pneumonia
- Most common cause (especially in sixth decade of life)
- Shaking chills, high fever, lobar consolidation, blood-tinged, "rusty"
sputum
Adult meningitis
- Most common cause
- CSF reveals high WBCs (neutrophils) and low glucose, high protein
Otitis media and sinusitis in children
Bacteremia/sepsis
Laboratory Diagnosis

Direct Gram staining

Optochin sensitive (P disk)
Hemolysis ( )
Catalase (-ve)
Bile solubility test (+ve)
Streptococcus pneumoniae
Lancefield (none)
 Quellung reaction
- Using specific anti-capsular antisera
- Capsule fixed and swells
- Capsular swelling is visible microscopically

Latex particle agglutination

- Detection of capsular antigen Quellung reaction
 Treatment
Bacterial pneumonia: Macrolides
Adult meningitis: Ceftriaxone or cefotaxime. Vancomycin is
added if penicillin resistant S. pneumoniae has been reported in the
community
Otitis media and sinusitis in children: amoxicillin, erythromycin
for allergic individuals

Prevention: Antibody to the capsule (over 80 different capsular

serotypes) provides type-specific immunity
Corynebacterium diphtheriae
General characteristics

Gram positive bacilli

Pleomorphic ( v or k or L shape ).
Chinese letter pattern, angular
arrangement
Nonmotile, noncapsulated, Gram stain
nonsporing
Facultative anaerobes
Have metachromatic granules

Albert stain
 Reservoir
throat and nasopharynx

Transmission
Humans are the only natural host of C. diphtheriae. Both
toxigenic and nontoxigenic organisms reside in the upper
respiratory tract and are transmitted by airborne droplets.
Pathogenesis
Organism not invasive; colonizes epithelium of
oropharynx or skin in cutaneous diphtheria
Diphtheria toxin consists of fragment A and
fragment B.
Diphtheria toxin binds to diphtheria toxin
receptor via fragment B
Fragment A then passes through the endosomal
membrane into the cytosol and inactivates
elongation factor2, (EF2), resulting in the
inhibition of protein synthesis in the host cell.
 Diseases
Respiratory diphtheria
- presents as pharyngitis or tonsillitis
with fever, sore throat, and malaise.
- Can be accompanied by plaque-like
pseudomembrane in the throat and
severe lymphadenopathy (bull neck).
 Effect on oropharynx: Dirty gray pseudomembrane (made up of dead cells
and fibrin exudate, bacterial pigment)
obstruction
heart and nerve damage
Host cell death
Laboratory diagnosis

Involves both isolating the organism and demonstrating toxin

production.
Decision to treat with antitoxin is a clinical one and cannot wait
for the laboratory results
Sample collection: Throat swab or swab from membrane
Microscopy: Gram stain and Alberts stain
Culture: Tellurite blood agar (selective medium)
 sterile filter paper with C. diphtheriae antitoxin

Biochemical tests Ab-Ag precipitation line

PCR assay for the presence of the

bacteria
toxin gene in the organism isolated
from the patient
Testing for toxigenicity. Gel
Precipitation Test

Gel Precipitation Test

Treatment

Diphtheria antitoxin
Penicillin or erythromycin

prevention
Immunization with diphtheria toxoid
Reference

Robert W. Bauman, Todd P. Primm. 2018. Microbiology with

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Warren E. Levinson, Peter Chin-Hong, Elizabeth Joyce, Jesse

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Patrick R. Murray, Ken S. Rosenthal and Michael A. Pfaller. 2021.

Medical Microbiology. 9th edition. Elsevier

Kaplan. 2018. USMLE Step 1 Lecture Note. Immunology and

Microbiology.
Stefan Riedel, Thomas G. Mitchell, Jeffery A. Hobden, et al. 2019. Jawetz,
Melnick, & Medical Microbiology. 28th edition. McGraw-Hill
Education.
Cowan, M. Kelly. 2012. Microbiology: A systems approach, 3rd edition.
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