Infection Flashcards

1
Q

Cellulitis

A

severe inflammation of dermal and subcutaneous layers of the skin

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2
Q

Candidiasis

A

Candida albicans and other Candida species

infections have various manifestations, depending on the site and the degree of immune-incompetence of the patient.

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3
Q

Oral candidiasis (thrush)

A

yeast Candida albicans and other Candida species

raised, white plaques on the oral mucosa, tongue, or gums. The plaques can become confluent and ulcerated and spread to the throat

treated topically with nystatin or clotrimazole

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4
Q

Vaginal candidiasis

A

yeast Candida albicans and other Candida species

itching and burning pain of the vulva and vagina, accompanied by a white discharge.

treated topically with nystatin or clotrimazole

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5
Q

Pneumonia

  • Definition
  • Pathenogenesis
  • Clinical features
A

Pneumonia is infection of the terminal air sacs (“alveoli”) and tissue of the lung.

Pneumococci, characteristically in pairs (diplococci), multiply rapidly in alveolar spaces and induce extensive oedema =incite an acute inflammatory
response in which neutrophils and congestion are prominent. As the inflammatory process progresses, macrophages replace the neutrophils and ingest debris. The
process usually resolves.

fever, malaise, tachypnea (increased respiratory rate),
and tachycardia, cough

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6
Q

Pneumonia

  • Definition
  • Pathenogenesis
  • Clinical features
A

Pneumonia is infection of the terminal air sacs (“alveoli”) and tissue of the lung.

Pneumococci, characteristically in pairs (diplococci), multiply rapidly in alveolar spaces and induce extensive oedema =incite an acute inflammatory
response in which neutrophils and congestion are prominent. As the inflammatory process progresses, macrophages replace the neutrophils and ingest debris. The process usually resolves.

fever, malaise, tachypnea (increased respiratory rate),
and tachycardia, cough

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7
Q

Community-Acquired Pneumonia

A

pneumonia (infection of the lung parenchyma seen on chest X-ray) which develops outside the hospital

2 years old+: S.pneumoniae
Under 2 years old: Respiratory syncytial virus (RSV)
No causative agent is found in up to 40% of patients with CAP.

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8
Q

X ray patterns of acute pneumonia

A

Lobar pneumonia is pulmonary consolidation demarcated by border of lung segment or lobe.
 Bronchopneumonia is seen as patchy consolidation around the larger airways
 Interstitial pneumonia is demonstrated by fine areas of shadowing in the lung fields and there is usually no sputum production at presentation. It is usually seen in mycoplasma, legionella, and viral pneumonia

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9
Q

Meningitis

A

Meningitis is inflammation of the meningeal lining of the brain and spine.

A patient will have:
 General features of an infection such as fever, increased pulse rate
 Symptoms and signs due to inflammation of the meninges:
a. headache
b. photophobia (difficulty looking at bright lights)
c. vomiting
d. neck stiffness on flexion of the neck
e. irritable (progressing to reduced level of consciousness)
f. Other findings dependent on severity (e.g. sepsis) or complications.

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10
Q

Sepsis

A

a syndrome of life-threatening organ dysfunction caused by a dysregulated host response to infection. It is usually caused by a bacterial infection.

Septic shock: subset of sepsis where particularly profound circulatory, cellular and metabolic abnormalities substantially increase mortality.

Causative agents depend on the syndrome, host and clinical context. Gram-negative infections account for an increasingly large proportion of cases,
particularly of healthcare-associated infections

Common presenting syndromes include pneumonia, intra-abdominal and urinary sepsis, and skin and soft tissue infections.

Management and treatment: prompt recognition, early appropriate
antimicrobial therapy and supportive treatment- Sepsis 6 bundle

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11
Q

Neisseria meningitidis infection

A

Neisseria meningitidis is a Gram negative diplococcus that may be found within polymorphonuclear leukocytes (neutrophils)

Rates of meningococcal disease are highest for young children and increase again
for adolescents and young adults.

Neisseria meningitidis causes both meningitis and septicaemia. They can occur
together or separately.

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12
Q

Septicaemia

A

the bacteria in the blood

Neisseria meningitidis in the blood triggers an intense host immune response.
- Fever:
- Sepsis: reduced level of consciousness, tachycardia, low blood pressure, poor peripheral circulation,
reduced urine output.
- Disseminated Intravascular Coagulation (DIC)
- Non-blanching Rash (30-75% pts)

Management:
Early recognition
 Early administration of antibiotics. 
 Urgent investigation
 Supportive care, often in an intensive care unit to manage organ
dysfunction and DIC.
 Notify Public Health
 Prevention

Treatment: ceftriaxone

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13
Q

Disseminated Intravascular Coagulation (DIC)

A

syndrome of widespread intravascular activation of coagulation.

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14
Q

Clostridioides difficile infection

A

gram-positive, anaerobic, spore-forming bacillus that is
responsible for the development of antibiotic-associated diarrhoea and colitis
(bowel inflammation).

Spore (faecal-oral) transmission

The diagnosis of C. difficile colitis should be suspected in any patient with
diarrhoea who has received antibiotics within the previous 3 months, has been
recently hospitalised, and/or has an occurrence of diarrhoea within 48 hours or more after hospitalisation

CDI clinical picture can vary from the asymptomatic carrier state to life-threatening colitis

Treatment:
-Asymptomatic carriers: No necessary treatment
-Mild, antibiotic-associated diarrhoea without fever, abdominal pain, or
leucocytosis: Cessation of antibiotic(s) may be the only treatment
necessary
-Mild to moderate diarrhoea or colitis: Metronidazole (P.O or IV)
or vancomycin (oral) for 10 days
-Severe or complicated disease: Vancomycin is considered to produce faster symptom resolution and fewer treatment failures than metronidazole; in
fulminant cases, combined therapy with IV metronidazole and
oral vancomycin may be considered

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15
Q

MRSA

A

a type of Staphylococcus aureus that is resistant to most beta-lactam antibiotics, antistaphylococcal penicillins (e.g., methicillin, oxacillin), and
cephalosporins.

Skin to skin transmission

Treatment:

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16
Q

Norovirus

A

a small, non-enveloped single stranded RNA virus that is a major cause of acute gastroenteritis outbreaks.

There is no specific treatment available so
treatment consists of supportive measures.

Transmission is mainly faecal-oral and also thought to be respiratory. Can be spread following ingestion of contaminated food, direct person-to-person contact or through contact with contaminated surfaces.

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17
Q

HIV

A

Retrovirus that infects cells with CD4 surface receptor. It destroys the cell, causes inflammation and spreads to/infects to more cells

Clinical features: oral candidiasis, Kaposi’s sacroma, PCP

Transmission: contact of infected bodily fluids with mucosal tissue/blood/broken skin

Treatments: anti-retroviral drugs

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18
Q

Malaria

A

One of the most common and deadly infections

Vector transmission: female Anopheles mosquito

Presentation: headache, fever, fatigue, pain, chill, pallor, sweating, dry cough, splenomegaly, nausea, vomiting] bite marks, low BP, high HR (110bpm)

Treatment dependant of species:
P. faciparum= artesunate, quinine + doxycycline
P. vivax, ovale, malariae = chloroquine,

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19
Q

Endocarditis

A

Formation of vegetation that binds to valves or mural endocardium. Aberrant flow predisposes to a collection of fibrin, platelets and scant inflammatory cells

Clinical features of Endocarditis
 Fever
 Heart murmur
 Other cardiac complications
 Embolic features: These are small bits of the vegetation (or biofilm) that become loose and travel to small capillaries where they can block the
capillary or cause local infection at that site.
e.g Janeway lesions, splinter haemorrhages, roth spots in the eye, oslers nodes

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20
Q

Chicken pox/shingles

A

Chicken pox: varicella
Shingles: Herpes zoster

Presentation: fever, malaise, headache, and abdominal pain. The exanthem begins on the scalp, face, or trunk as erythematous macules, which evolve into virus-containing vesicles that begin to crust over after about 48 hours

Treatment: acyclovir

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21
Q

Examples of disease caused by healthcare infection viruses

A

blood borne viruses (hepatitis B, C, HIV)
norovirus
influenza
chickenpox

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22
Q

Examples of disease caused by healthcare infection bacteria

A
Staph aures including MRSA
Clostridium difficle
Escherichia coli, Klebsiella pneumoniae
Pseudomonas aeruginosa
Mycobacterium tuberculosis
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23
Q

Describe the role of E.coli in health and disease

A

Gra m-negative rods, typically lactose-fermenting, facultatively anaerobic

normal part of large bowel microbiota

Possibly protects against invasion by pathogenic species

Can cause:
intestinal infections
toxin-mediated disease
extra-intestinal infections

disease is linked to the presence of virulence factors, frequently restricted to specific E.coli strains

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24
Q

Hepatitis B

A

Inflammation of the liver
Chronic: persistence of HBsAg after 6 months

Double-stranded eveloped DNA virus

Transmission: vertical (75% cases globally), sexual contact, drug injection, needlestick injuries

Presentation: jaundice, fatigue, abdominal pain, anorexia/nausea/vomiting, arthralgia

Treatment: no cure, life-long anti-virals
Vaccine available

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25
Q

Pharyngitis

A

Streptococcus pyogenes

• Peak incidence 5-15
years
• Droplet spread
• Association with overcrowding
• Untreated patients
develop M protein
specific antibody
Clinical features
Abrupt onset sore throat
Malaise, fever, headache
Lymphoid hyperplasia
Tonsillopharyngeal exudates
Throat swab -> Group A strep
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26
Q

Scarlet fever

A
Due to infection with
streptococcal pyrogenic
exotoxin strain of
S.pyogenes
• Local or 
haematogenous spread
• High fever, sepsis, arthritis, jaundice
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27
Q

Typhoid and paratyphoid (enteric fever)

A

Systemic disease

Salmonella typhi, Salmonella paratyphi= rod shaped Gram-negative bacteria

Faecal-oral transmission from contaminated food/water
-poor sanitation, limited access to clean water

Presentation: fever headache, abdominal discomfort, dry cough, relative bradycardia

Treatment: fluoroquinolones (increasing resistance), IV ceftriaxone or azithormycin for 7-14days
Vaccine available (50-75% effective)
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28
Q

Dengue fever

A

commonest arbovirus

Vector transmission: Aedes aegytpo

Presentation: first infection ranges from asymptomatic to non-specific febrile illness

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29
Q

Dengue fever

A

commonest arbovirus

Vector transmission: Aedes aegytpo

Presentation: first infection ranges from asymptomatic to non-specific febrile illness
- lasts 1-5 days: intense headache, fever, muscle/joint pain, widespread red rash

Supportive treatment only: paracetamol, fluids

30
Q

Schistosomaisis/bilharzia

A

Parasitic worms in fresh water snails (cercariae)
- Schistosoma mansoni

Presentation: fever, chills, cough, muscle aches, rash, itchy skin

Treatment: praziquantel

31
Q

Ebola

A

Filovirus

Presentation: flu-like illness with vomiting, diarrhoea, headaches, confusion, rash, internal/external bleeding at 5-7 day

Transition: direct contact with body fluids

32
Q

Zika virus

A

Arbovirus (flavivrius)
Vector transmission: Aedes mosquito and sexual transmission

Presentation: 20% get symptoms which are mild, dengue-like

No treatment, no vaccine

33
Q

Primary immunodeficiency disease

A

due to intrinsic gene defect: missing protein, missing cell, non-functional components

34
Q

Secondary immunodeficiency disease

A

due to an underlying disease/treatment:

35
Q

Primary immunodeficiency disease

A

due to intrinsic gene defect: missing protein, missing cell, non-functional components

65% caused by Ab defects

36
Q

Secondary immunodeficiency disease

A

due to an underlying disease/treatment: decrease production/function of immune components, increased loss of catabolism of immune components

37
Q

X-linked agammaglobulinaemia

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

Patient lacks B cells- defect in B cell development

38
Q

Primary immunodeficiency disease

A

due to intrinsic gene defect: missing protein, missing cell, non-functional components

Presentation: age of symptom onset, type of microbes/sites

Management: supportive treatment (infection prevention, nutritional support), specific treatment ( regular Ig therapy), comorbidities

39
Q

Common Variable Immunodeficiency (CVID)

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

Patient has B cells but do not produce any antibodies

40
Q

Selective IgA deficiency

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

Most common - slight raised risk of autoimmune conditions
90% of patients are asymptomatic
prevalence 1:100 to 1:1000

41
Q

Hyper-IgM syndrome

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

no type switching in B cells= IgG is not produced. IgM continues to be produced leading to unusually high levels in serum

42
Q

Severe combined immunodeficiency (SCID)

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

T cells are defective. B cells are not activated

43
Q

Di George syndrome (thymus)

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

5-10% of all PID
deletion syndrome on chr22p11.2
absence of hypoplastic thymus= no T cell maturation

44
Q

Chronic granulomatous disease (CGD)

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

~10% of all PIDs

45
Q

Chronic granulomatous disease (CGD)

A

Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components

~10% of all PIDs
phagocytes lack killing machinery and are ineffective as a result

46
Q

Describe the serological antigensof E.coli

A
Capsule (K)
LPS (O)
Cell membrane
Fimbriae (F)
Flagella (H)
production of toxins
47
Q

Describe E. coli as a cause of diarrhoea including its pathogenesis, role of
toxins and clinical features

A

Enterotoxigenic E.coli (ETEC) is the most important cause of bacterial diarrohoeal illness

Faeco-oral transmission

ETEC produces two toxins, a heat-stable toxin (ST) and heat-labile toxin (LT)

Toxins stimulate the lining of the intestines to secreted excessive fluid =watery diarrhoea and abdominal cramping

other less common features: fever, nausea, chills, loss of appetite, headache, muscle aches and bloating

48
Q

Cystistis

A

Lower UTI

Risk factors: female, history UTI, secual activity, vaginal infection, diabetes, obesity, genetic susceptibilyt

Clinical features: frequent and urgent urination, dysuria, suprapubic pain, nocturia, hematuria, malaise

Causative organisms: Uropathogenic E.coli (UPEC)

Virulence factors:
Adhesins (type 1 & other chaperone-usher pili_
toxins (HIyA, CNF1)
Siderophores (aerobactin, enterobactin, yersinabactin)
capsule

49
Q

Pyelonephritis

A

Upper UTI

Risk factors: diabetes, HIV/AIDS, iatrogenic immunosuppression

Clinical symptoms: back and/or flank pain
fever, chills, malaise, nausea, vomiting, anorexia

Causative organisms: Uropathogenic E.coli (UPEC)

Virulence factors:
Adhesins (type 1 & P pili)
toxins (HIyA, CNF1)
Siderophores
flagella
50
Q

Describe UPEC virulence factors

A

Adhesins:
Type 1 fimbriae have adhesive tips that bind to alpha-D-mannosylated proteins on uroepithelium= adhesion, invasion of uroepitheilum and the formation of intracellular bacterial communities (IBCs)

Toxins:
Lipopolysaccharide (LPS)
alpha-Hameolysin (HIyA) is a secreted, pore-forming toxin, cytotoic towards epithelial cells in the urinary tract

bacteria produce their own iron-complexing proteins (siderophores) to acquire iron

51
Q

Describe E. coli as a cause of blood stream infections and sepsis

A

E.coli are the commonest cause of bacterial bloodstream infection in England

~50% of E.coli bloodstream infections occur in patients older than 75 years

52
Q

Describe the management of E. coli infections - Diarrhoea

A

Prevention:
avoid contaminated food and water
eating raw fruits, veg, seafood or undercooked meat or poultry in areas lacking adequate chlorinate

Treatment: most recover without any specific treatments,
clear liquids to prevent deydration
oral rehydration solutions
avoid antibiotics

53
Q

Describe the management of E. coli infections - UTI

A

Antibiotics: trimethoprim and nitrofurantoin

54
Q

Describe the management of E. coli infections - bloodstream infections

A

increasing resistance to a wide range of antibiotic classes

55
Q

Describe the management of E. coli infections - bloodstream infections

A

increasing resistance to a wide range of antibiotic classes

56
Q

Describe the structure of the Influenza virus

A

orthomyxovirus- spherical, enveloped viruses containing a segmented, negative strand RNA genome

Genetic material:
• (-) ssRNA – 8 genes
• encoding 11 proteins
• include 3 RNA polymerases (high error rates)
Two surface antigens:
• Haemagglutinin (H) – 18 types – binds to cells
of the infected person
• Neuraminidase (N) – 11 types - releases the
virus from the host cell surface

57
Q

Define the concept of an animal reservoir for type A influenza (including
poultry, horses, pigs, and other animals) and its major surface antigens -
hemagglutinin (HA) and neuraminidase (NA)

A

a) influenza type A viruses in many animals, including horses, pigs, and wild migrating waterfowl.

b) reassortment can occur between influenza A viruses that
infect different animal and avian species, e.g., pigs can be infected by human- and avian-specific influenza viruses

c) In environments where pigs, birds and humans coexist,
it is possible for a pig to be simultaneously infected with
multiple influenza subtypes.

d) “Reassortants” can, therefore, be produced within one
host animal (the pig), in which the mRNAs encoding the H
and N antigens have been reassorted into unique
combinations.

e)The reassortant virus then has the potential to
spread among humans, birds, and pigs.

58
Q

Describe the clinical symptoms and complications of influenza
infection

A

headache, high fever, sore throat, runny nose, muscle aches and pains

complications of influenza:
viral pneumonia, secondary (bacterial) pneumonia,
central nervous system syndromes, or Reye syndrome

59
Q

Describe how you would diagnose flu in a clinical setting

A

sample from a nasopharyngeal swab

60
Q

Briefly outline the management of influenza including treatment options
and prevention Treatment and prevention
including vaccination and how this is determined by WHO each year

A

antivirals

NA inhibitors- Tamiflu

Prevention: formalin-activated vaccine by injection influenza A&B
live, attenuated, cold-adapted vaccine by nasal spray Influenza A&B

61
Q

Define the concepts of antigenic shift (acquisition of a novel HA and NA by
the virus) and antigenic drift (yearly accumulation of mutations in the HA
and NA)

A

antigenic shift= acquisition of a novel HA and NA by the virus

antigenic drift =yearly accumulation of natural mutations in the HA and NA - this causes seasonal epidemics

62
Q

Define the concepts of antigenic shift (acquisition of a novel HA and NA by
the virus) and antigenic drift (yearly accumulation of mutations in the HA
and NA)

A

antigenic shift= major changes in the genes of flu vruses that occur suddenly when two or more different strains combine. Acquisition of a novel HA and NA by the virus- cause widespread epidemics/pandemics

antigenic drift =yearly accumulation of natural mutations in the HA and NA - this causes seasonal epidemics

63
Q

Define the concepts of pandemics and epidemics (seasonality) and how
these may arise in relation to influenza.

A

Antigentic shift phenomenon can
be easily explained by the reassortment of different RNA segments from each species in a new capsid.

Occurs infrequently - maybe every 10 or 20 years

Only influenza type A viruses show antigenic shift

May not have been seen in circulation in population for
many years

Immune systems of many individuals have no defence
against this new subtype

Epidemic - Prevalent among a people or a community at a special time, and produced by some special causes not generally present in the affected locality

Pandemic - epidemic over a very large area;
affecting a large proportion of a population – often the world

64
Q

Suppurative complications of streptococcal

pharyngitis

A
  • Peritonsillar cellulitis/abscess
  • Retropharyngeal abscess
  • Mastoiditis, sinusitis, otitis media
  • Meningitis, brain abscess
65
Q

Acute rheumatic fever

A

Complications of streptococcal pharyngitis

Inflammation of heart, joints, CNS
• Follows on from pharyngitis
• Rheumatogenic M types
• Possible mechanisms:
– Auto-immune
– Serum sickness
– Binding of M protein to collagen
– ASO, ASS induced tissue injury
66
Q

Acute post-streptococcal

glomerulonephritis

A

Complications of streptococcal
pharyngitis

Acute inflammation of renal glomerulus
• M type specific but NOT same as ARF M types
• Antigen-antibody complexes in glomerulus

67
Q

Impetigo

A

Streptococcus pyogenes skin infections

Childhood infection, 2-5 years
– Initial skin colonisation, followed by intradermal innoculation
– No ARF but impetigo is most common cause of glomeruonephritis

68
Q

Erysipelas

A

Streptococcus pyogenes skin infections

– Dermis infection with lymphatic involvement
– Face, lower limbs
– Facial lesions frequently preceded by pharyngitis
– Lower limb infection usually secondary to invasion of skin via trauma, skin disease or local fungal infection

69
Q

Cellulitis

A

Streptococcus pyogenes skin infections

Skin and subcutaneous tissue infection
– Impaired lymphatic drainage and illicit injecting drug use important risk factors

70
Q

Necrotising fasciitis

A

Streptococcus pyogenes skin infections

Infection of deeper
subcutaneous tissues and fascia.
– Rapid, extensive necrosis
– Usually secondary to skin break
– Severe pain, even before gross
clinical changes
– High fever, fulminant course, high
mortality (20-70%)
71
Q

Streptococcal toxic shock syndrome

A

Deep tissue infection with
Strep pyogenes AND Bacteraemia AND Vascular collapse AND Organ failure

From health to death in hours

Entry of group A strep into deeper tissues and
bloodstream

Streptococcal pyrogenic exotoxins stimulate T-cells
through binding to MHC class II antigen-presenting
cells and V-β region of T-cell receptor, inducing
monocyte cytokines (TNF-α, IL-1β, IL-6) and lymphokines (TNF-β, IL-2, IFN-γ).
M-protein fibrinogen complex formation