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Module Title
Cardiovascular module
 Course code: IMP-07-203 17
 Phase: I
 Year/ semester: 2nd
year / Semester (3)
 Credit hours: 8 Hr.
 Course duration: 7 weeks.
2019-2020

2019-2020
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Prepared by: Dr. Azza Ali
Lecturer of microbiology
Date of tutorial 30/9/2019 - 1/ 10/2019
Pericarditis and myocarditis

2019-2020
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Intended Learning Outcomes (ILOs)
 On completion of this lecture, the student will be
able to:
1- Define Pericarditis and myocarditis.
2- Mention causes, viral, bacterial or fungal.
3- Describe pathogenesis, clinical picture and lab.
diagnosis.
4- Outline prevention and treatment.

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 Myocarditis
 Definition:
 It is inflammation of the heart muscle.
 The etiology is thought to be caused by a variety of
infectious and non-infectious causes.

MicroT1 myocarditis and pericarditis modified - Copy.pptx

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 Causative organisms: -
a- Viral pathogens:
 Enteroviruses including Coxsackie viruses are the most common cause.
 Cytomegalovirus, Epstein–Barr virus, parvovirus B19, herpesvirus 6 and
influenza have been implicated.
 b- Other pathogens
 that have been implicated include various bacteria, fungi, protozoa,
and helminths.
 c- Non-infectious causes
 include autoimmune disorders such as systemic lupus
erythematosus (SLE), Wegener’s granulomatosis, and giant cell arteritis.

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 Pathogenesis:
It occurs most commonly following hematogenous
spread of virus or other pathogen to the heart
muscle, although direct spread from adjacent
structures can occur.
 It may result in cardiac dysfunction leading to heart
failure.

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 Clinical manifestations:
Patients with myocarditis present with signs and
symptoms of heart failure.
 Patients may have signs and symptoms of a systemic
infection as well (fever, constitutional symptoms )
 Those with associated pericarditis often have chest
pain.

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 Diagnosis:
A definitive diagnosis requires cardiac muscle biopsy revealing myocardial
inflammation and necrosis.
 Most cases are diagnosed in a patient presenting with heart failure, cardiac
dysfunction on echocardiogram and elevated cardiac enzymes.
 Cardiac markers, such as troponin, may be elevated, but during which course of
the disease process is mostly unknown. Higher levels of troponin likely correlate
with more myocardial damage as it is indicative of myonecrosis, but negative
values do not rule out the diagnosis.
 Other tests that should be ordered include complete blood count
(CBC), erythrocyte sedimentation rate (ESR), and c-reactive protein (CRP). The
white count, ESR, and CRP may be elevated but are not diagnostic in any way.

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 Viral antibody titers should also be ordered and should include coxsackievirus
group B, HIV, CMV, Ebstein-Barr virus, hepatitis and influenza viruses. Titers will
typically increase by four-fold during the acute phase with gradual fall with the
progression of the disease process. Serial titers may be helpful.
 Cardiac ECHO should be ordered and may show nonspecific findings such as
reduced left ventricular function, global hypokinesis, and even regional wall
motion abnormalities.
 Contrast MRI or nuclear studies can show the extent of inflammation and
cellular edema, although this may still be non-specific.
Treatment:
Treatment of the cause of myocarditis if possible, and supportive care is most often
given.

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2-Pericarditis
 Definition:
 It is inflammation of the pericardium, which can be
due to infection, autoimmune diseases, trauma, or
malignancy.

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 Causative organisms:
 Viral infections, Coxsackie virus and echovirus are most common.
 Non pecific bacteria: Staph. aureus and Strept . pneumoniae are most
common.
 Specific bacterial infection: Mycobacterium tuberculosis is one of the
most common infectious causes of pericarditis worldwide.
 Fungi such as Histoplasma capsulatum and Coccidioides immitis can
cause pericarditis, which clinically presents similarly to tuberculous
pericarditis

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 Pathogenesis
 Pathogens reach the pericardium by either :
 Hematogenous spread through the blood or
 Direct spread from adjacent intrathoracic structures or,
rarely
 Directly from infected myocardium.
 Inflammation of the pericardium can result in the
formation of pericardial effusion.

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 Clinical Manifestations:
 Chest pain is the most common manifestation of
pericarditis. Pain often worsens with inspiration or
coughing
Diagnosis:
 Culture of pericardial fluid or pericardial tissue
may reveal causative bacteria.
 Viruses are rarely isolated.

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 Treatment:
 It is dependent on the pathogen.
 Most viral etiologies are treated with symptomatic management
and supportive care
 Bacterial, mycobacterial, and fungal infections will require directed
antimicrobial therapy.
Prevention:
 Immunization against Strept . pneumoniae may be effective.
 Treatment of early or latent stages of infections (e.g., tuberculosis)
may prevent development of pericarditis in some cases.

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Non Specific bacterial infection :
Common bacterial infection include: Staph. aureus and Strept. Pnuemonae
Laboratory diagnosis:
Specimen: sputum, pleural fluid, pericardial effusion aspirate, blood…
Microscopic examination:
Gram stained film: shows pus cells, Gram positive cocci arranged in clusters (Staph), or Gram positive diplococci
surrounded by hallo (Pnuemo).
Culture: on blood agar, blood culture, the resulting colonies are identified morphologically and by biochemical
reactions.
Antibiotic sensitivity testing to choose the proper antibiotic for treatment.
Prevention:
Vaccination: pnuemococcal conjugate vaccine.

Pneumococci in tissue, stained by Gram stain.
(Gram-positive capsulated diplococci )
Growth of Strept. viridans or Strept. pneumo on blood agar
showing partial or alpha-haemolysis
Fig. : Blood culture for diagnosis of :
• Acute bacterial endocarditis
• Puerperal sepsis
• Subacute bacterial endocarditis

Fig. 2.7:Pneumococci by Quellung reaction
(capsule swelling with specific antisera)
Fig. 2.8: Optochin sensitivity test
Strept. pneumo is sensitive
Strept. viridans is resistant
Fig. 2.7:, Inulin fermentation test
Strept. pneumo ferment inulin…..pink
Strept. viridans not ferment inulin....colorless
Fig. 2.7:, Bile solubility test
Strept. pneumo soluble in bile (transparent tube)
Strept. viridans not soluble in bile (turbid tube)

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 Some important fungi
1- Histoplasma capsulatum
{ both cause Systemic mycosis
2-Coccidioides immitis
General characters:
 Immunity mainly CMI
 Restricted in specific area ( specific areas in american desert )
 Infection is by Inhalation of spores
 not transmitted among human
 Lung
 Acute & chronic pulmonary & disseminated infections
 Dimorphic form hyphi at 25o
C , and yeast at 37o
C
 cultured on (inhibitory mold agar or Sabourauds agar ( chloramphenicol & cyclohexamide) (1 – 3 days).
 TTT: systemic antifungal

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 (1) H. capsulatum (Not capsulated)
 Path.: Inhalation  conidia  yeast  lung MQ  RES(reticulo-endothelial system) granuloma
In 95% of cases CMI  cytokine (-) intracellular growth.
Disease: (1) acute pulmonary: flu like (2) chronic pulmonary histoplasmosis
(3) Disseminated (fatal form): in immuno suppressed (hepatosplenomegally), enlareged LN &
anemia)
Diagnosis
Direct
1- Specimen: Sputum, BM (bone marrow)
2- Film stained with a)Giemsa (for BM)
b)Gomori methenamine silver (GMS) [histological section]
Oval cell in side MQ
3-Isolation and Identification on fungal media…. See above
4- detect Ag
5-DNA probe
Indirect
1) Serology: detect IgG by CFT ( titre > 1: 32 = dissemination)
2) ID skin test ( histoplasmin )

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(2) Coccidioides immitis:
 C/P: (1) Asymptomatic (60%)
(2) Valley fever: a) Flu like
b) Rash, pneumonia and pleural effusion
(3) Disseminated: Bone, meninges
 Diagnosis:
specimen: Sputum , CSF
Microscopy with (KOH): show spherules
containing endospores
(3) As Histoplasma

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 Some important viruses
 -EBV
 It infects B-lymphocytes and reticuloendothelial system (liver,
spleen).
 It causes Latent infection in B-lymphocytes and or pharyngeal
epithelial cells.
 It causes Burkett's lymphoma.
 -CMV
 It remains dominant in mononuclear cells to be reactivated in
immune compromised patients causing serious disease.

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Coxsackie viruses
It belonges to Picorna viridae family, Enteroviruses genera
 CapsidIcosahedral
 Core SS RNA [+ve] sense
 Envelop Naked
 Coxsackie virus A  23 Serotypes (1 – 22 , 24 serotypes)
 Coxsackie virus B  6 Serotypes

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Group [A] 23 serotypes Group [B] 6 serotype
Fecal -oral  Mode  Fecal –oral
 Acute hemorrhagic conjunctivitis  Disease   Pleurodynia (Bornholm disease
 Herpangina Pharynx (the Devil's Grippe): sudden Sharp
 Vesicle in Palate pain on one side of chest (self
limited)
 Fever Tonsil  Myocarditis: arrhythmia
 Children & self limited  generalized disease in infants
 Hand, foot & mouth disease [Vesicles]  Type 1 DM
Both causes:  Aseptic meningitis
 Common colds

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 Diagnosis
 Specimen: Throat swab (1st
few days), Stool (for weeks), CSF...)
1- Direct demonstration of the virus by E.M.
2-Tissue culture :[C P E] appear in group A within (3 – 8 days) while grpup B within
(5 – 14 days)
3- Serology detection of specific antibody by ELISA
 PCR is the rapid method for diagnosis (2 – 5 hr)
Prevention  No vaccine

Fixed cell culture slide showing CPE of
enterovirus e.g. coxsackie, and polio
(Cell rounding & shrinking, nuclear pyknosis and cell destruction)

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ECHO viruses
[Enteric Cytopathic Human Orphan]
 Morph.  as Coxsackie
It belonges to Picorna viridae family, Enteroviruses genera
 C SS RNA [+ve] sense
 C Icosahedral
 E Naked
34 serotypes
 Mode  Feco-oral
Disease
 A septic meningitis
 Febrile illness with or without rash.
 Diagnosis  ...................................
 Prevention  No vaccine

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Parvovirus B19
 Mode of Transmission
 Transmission is by respiratory secretions, blood, and blood products of infected patients.
 The virus can be also transmitted vertically from mother to fetus.
 Pathogenesis
 It infects primarily two types of cells:
 -Red blood cell precursors (erythroblasts) in the bone marrow, which accounts for the aplastic
anemia,
 -Endothelial cells in the blood vessels, which accounts, in part, for the
 rash associated with erythema infectiosum.
 Clinical manifestation:
 Transient Aplastic Crisis (TAC):
 There is temporary arrest of RBCs production. This becomes apparent only in patients with chronic
hemolytic anemia.

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 Pure Red Cell Aplasia (PRCA):
 B19 may establish a persistent infection in immunocompromised patients causing severe
chronic aplastic anemia and the patients are dependent on blood transfusions.
 Laboratory Diagnosis:
 Specimens: Serum, blood cells.
 Direct detection:
 ELISA: for direct detection of viral antigen.
ELISA is used to detect B 19 IgM antibodies, which indicates recent infection.
 PCR: for detection of viral DNA. It is the most sensitive assay.
 Treatment
 Symptomatic treatment.

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 Prevention and Control:
Screening of blood donors.
 Standard infection control precautions should be followed to
prevent transmission of B19 to healthcare workers from
patients with TAC or immunodeficient patients with chronic
B 19 infection.
 There is recombinant vaccine available under evaluation
against human parvovirsus for people with chronic anaemia.

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Intended Learning Outcomes (ILOs)
 On completion of this lecture, the student abled to:
1- Define Pericarditis and myocarditis.
2- Mention causes, viral, bacterial or fungal.
3- Describe pathogenesis, clinical picture and lab.
diagnosis.
4- Outline prevention and treatment.

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Questions:
1-What is the most common cause of myocarditis in adolescents?
a. Drugs
b. Coxsackie virus
c. Tuberculosis
d. Post myocardial infarction
2-Which of the following family of viruses are the most common cause of viral cardiomyopathy?
a. Adenoviridae
b. Hepadnaviridae
c.Picornaviridae
d. Reoviridae

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3-A 17-year-old male, previously healthy, presents with an acute flu-like illness, malaise, fever and
chest pain. During his work up he is found to have sinus tachycardia on ECG and an elevated
troponin. He is admitted to the hospital for suspected acute myocarditis. Which clinical
finding is most concerning for having a poor prognosis in this patient?
 Fever
 Tachypnea
 Elevated troponin
 Congestive heart failure
4-Which of the following is most likely to have purulent pericarditis as a possible complication?
 Coxsackievirus infection
 Sepsis
 Myocardial infarction
 Tuberculosis

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5-Select the virus that most often causes acute viral
pericarditis.
a. Rhinovirus
b. Epstein-Barr virus
c. Coxsackie B virus
d. Adenovirus

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Learning Resources:
References
1- https://www.ncbi.nlm.nih.gov/books/NBK431080/
2- https://www.ncbi.nlm.nih.gov/books/NBK459259/
3- Medical microbiology (department book), Ragaa Awad, Laila
Saleh, Azza-Elsalakawi.
4- Medical microbiology (Ain Shams department book).

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