Viral Infections of Muscle :

Myocarditis and Pericarditis

Efrida Warganegara
Aetiology and Transmission
Group B, and to a lesser extend group A
coxsackieviruses and certain
enteroviruses, are the main viral
causes of myocarditis & pericarditis

Bothcondition are seen principally in

adult male and are important
because they can be mistaken for
myocardial infarction, yet the
prognoses is good and complete
recovery is rule
 Aetiology and Transmission
Spreadby fecal-oral and occasionally
from pharyngeal sectretion

Mumps and influenzae are less

common causes of myocarditis or
pericarditis

Rubella can causes myocardiris and

associated congenital lesion in the
foetus
 Clinical Features and Pahogenesis
Ingested coxsackievirus spread from the
pharynx or gut wall to the lymphatics
and then to the blood

Invasion of heart or pericardium takes

place across blood vessels and result in
acute inflamation.

In the heart and pericardium this gives rise

to dyspnoe, pain in the chest, and
sometimes mimics a myocardial
infarction
Diagnosis, treatment and prevention
Coxsackievirus may be isolated from
throat swab, fecal specimens or pericardial
fluid

Rising titres of neutralizing antibody may

be demonstrable, or the presence of IgM
antibodies in ELISA test

There are no spesific treatments and

no vaccine for coxsackievirus infection
JOINT AND BONE INFECTIONS :

1. Reactive Arthritis, Arthralgia,

and Septic Arthritis

2. Osteomyelitis
 Reactive Arthritis, Arthralgia,
and Septic Arthritis
Aetiology, pathogenesis, diagnosis, and treatment
Joints and bones will be considered separately for
convinience, but joint lesions often spread to
involved neighbouring bone, and vice versa
Joints can become infected by the hematogenous
route or directly following trauma or surgery, but in
many cases the condition is immunologically
mediated rather than due to microbial invasion of the
joints
The microbe responsible is at a distant site in the
body, and it is a reactive arthritis
Aetiology, pathogenesis, diagnosis, and treatment

Reactive Arthritis and Arthralgia occur

after certain enteric bacterial infections, and
Arthralgia in rubella & hepatitis B infection
is of similar origin
In this type of arthritis more than one joints is
usually affected
Ankylosing Spondylitis is ssociated with
Klebsiella infection
There is no evidence that rheumatoid arthritis is
caused by either viruses or mikrobes.
Circulating bacteria sometimes localized in
joints, especially following trauma can cause
supurative (septic) arthritis generally a single
joint is involved
Aetiology, pathogenesis, diagnosis, and treatment

Joints are very susceptible, particularly if they are

already damaged for instance by rheumatoid
arthritis, or if prothesis has been inserted
Knee are most commonly affected, followed by
hips, ankle and elbows
Patients show fever, joint paint, limitation of
movement, swelling, and usually a joint effusion.
Bacteria can be isolated from the joint fluid
(seen in the centrifuged deposites), and the
commonest organism is Stapylococcus aureus.
`
 Osteomyelitis
Aetiology & Pathogenesis
As with Joint, infection can be by direct route (from a
nearby focus of infection, after fracture, after
orthopedic surgery) or from circulating microbes
The commonest cause of hematogenous osteomyelitis
is Staphylococcus aureus, but when infection is from
a neighbouring site it is generally mixed with Gram
(-) rod and occasionally anaerobes also present
Accute osteomyelitis typically involves the growing
end of a long bone, where sprouting capillary loops
adjacent to epiphysial growth plat
romote the localization of circulating bacteria
tends to be a disease of children and adolescent
 Osteomyelitis
Clinical features, diagnosis, and treatment
There is a painful tender bone lesion and
generally febril illness.
Diagnosis is from blood culture taken before
start of antimicrobial therapy or when there
is an open lesion, from a bone biopsi
Periosteal reaction and bone loss maybe visible
radiologically
Treatment is begun on a most likely basis
cloxacillin for penicillinase-producing S. aureus,
as soos as microbiological sample have been
taken
 Osteomyelitis
Clinical features, diagnosis, and treatment
Osteomyelitis become chronic, especially when
there are necrotic bone fragments to act as a
continued source of infection
Surgical intervention fot the debridement and
drainage, as well as prolonged courses of antibiotics
may be necessary
Tuberculosis may affect the spine, the hop, the
knee, or the bones of the hands and feet
Constitutional disturbances are often absent, but
the site is generally painful and pressure from
a tuberculous abscess in the spine can cause
paraplegi.
INFECTIVE ENDOCARDITIS

EFRIDA WARGANEGARA
INTRODUCTION
Infective endocarditis is an uncommon
disease that often present as a Pyrexia of
Unknown Origin (PUO), and is fatal if
untreated

Infection involves the endothelial lining of

the heart, including the heart valves

Occurs as an acute, rapidly progressive

disease or subaccute form
Introduction - continue
In about 1/3 of patient, there is a pre-
existing : - heart defect (congenital;
acquired : result of rheumatic fever) or a
prosthetic heart valve insitu

However, the patient may be unaware of

any defect prior to the infection
 Etioloic Agent in Infective Endocarditis
Percentage of
Agent Cases
Streptococci 60-80
Viridans streptococci 30-40
Enterococci 5-18
Other streptococci 15-25
Staphylococci 20-35
Coagulase-positive 10-27
Coagulase-negattive 1-3
Gram-negative aerobic bacilli 1.5-13
Fungi 2-4
Miscellaneous bacteria <5
Mixed-infection 1-2
"culture negative" <5-24
Aetiology
Almost any organism can cause endocarditis,
but infection of native valves is caused most
commonly by species of Oral Streptococci :
Viridans streptococcus (Strep. sanguis,
Strept. oralis, Strept. mitis)

Alfa-hemolytic (but they may be

nonhemolytic), most prevalent members of
the normal flora of the URT and important
for the healthy state of the mucous
membranes there
 About 1/4 - 1/3 of cases are caused
by Staphylococcus, alhough this
fraction is higher in intravenous drug
abusers. have a higher incidence of
Gram (-) and fungal endocarditis
arising from m.o. that they inject into
themeselves
 Coagulase-negative Staphylococcus
are common causes of early prosthetic-
valves endocarditis and are probably
acquired at the time of surgery

The species causing late infection (>3

months) after cardiac surgery resemble
more closely those seen in native valve
endocarditis
Pathogenesis
Endocarditis is an endogenous infection
acquired when m.o. entering the
bloodstream establish themselves on the
heart valves. Thus any bacteriemia may
potentially result in endocarditis

Most commonly streptococcus from the oral

flora enter the bloodstream (during dental
procedure or vigourus teeth cleaning or
flossing), and adhere to damaged heart
valves
 In the course of the bacteriemia, viridans
streptococci, penumococci, or enterococci may
settle on normal or previously deformed heart
valves producing Accute Endocarditis

Subaccute endocarditis often involves

abnormal valves (congenital deformities and
rheumatic, or atherosclerotic lesion).
Subaccute endocarditis, most frequently due to
members of the normal flora of the resp. or
intestinal tract that have accidently reached the
blood
Subaccute Bacterial Endocarditis (SBE)

Viridans streptococcus ordinarily the most

prevalen members of the upper resp trac flora,
are also the most frequent cause of SBE

Group D streptococcus (enterococcus

and S. bovis) also are common causes SBE,
that 5-10% cases are due to enterococcus
originating in the gut or urinary trac.
 The lesion is slowly progressive, and a
certain amount of healing accompanies
the active inflammation : vegetation
consist of fibrin, platelet, blood cells,
and bacteria adherent to the valve
leaflets multiplication attract
further deposition of fibrin and
platelet they are protected from
the host defences and vegetation can
grow to several centimeters in size
 Theclinical course is gradual,
quite slow process and
correspondingly the time period
between the initial bacteriemia and
the onset of symptom is around 5
weeks

Thedisease is variably fatal in

untreated cases
 Clinical Feature
The patient almost always has a fever, anemia,
weakness, a heart murmur, embolic
phenomena, and enlarged spleen and renal
lesion
Also complain of nonspesific sympyom : anorexia,
weight loss, malaise, chills, nausea, vomiting, and night
sweats
Periheral manifestation may also be evident in the
form of splinter haemorrhages and Oslers nodes
Microscopic haematuria resulting from immune
complex deposition in the kidney is a characteristic
 Diagnosis
The blood culture is he single most
important laboratory test.
Ideally 3 separate samples of blood
should be collected within a 24-hour
periode and before antimicrobial
therapy
Isolation of the causative is essentially
to enable antibiotic susceptibility test
to be performed and optimal therapy
 Treatment and Prevention
To complete eradication takes several weeks
Penicillin for susceptibility streptococcus is
a choice, if allergy erythromycin
For enterococus : combination
penicillin/ampicillin with aminoglycoside
For staphylococcus : b-lactamase stable
penicillin (oxacillin, may be combination with
an aminoglycoside, rifampicin or fucidic acid.
For methycillin-resistance stapylococcus :
vancomycin or teicoplanin
Treatment and Prevention

Prevention : people with known

heart defect should be given
prophylactic antibiotic to protec
them during dental surgery and
any other invasive procedure
that is likely to cause a transient
bacteriemia
 Rheumatic Fever and
Rheumatic Heart Disease

Efrida Warganegara
 Rheumatic Fever
This is an indirect complication, most
serious sequele of Strep. Pyogenes because it
result in damage to heart muscle and valves

Pharyngeal infection with B-hemolytic

group A streptococci is followed frequently
by the development of antistreptococcal
antibodies, and if there is a hyperimmune
response the infection may be followed by
rheumatif fever
 Rheumatic Fever
Antibodies are formed to antigens in the
streptococcal cell wall which cross-react with
the sarcolemma of human heart, and with
tissues elsewhere
The onset of rheumatic fever is often
preceded by S. pyogenes infection 1-4 weeks
earlier, although the infection may be mild and
may not detected
In general, however, patients with more severe
strepyococcal sore throats have a greater
chance of developing rheumatic fever.
Symptom and Sign
Typical symptom and sign RF include fever,
malaise, a migratory nonsuppurative
polyarthritis, and evidence of inflamation of
all parts of the heart (endo-, myo-, peri-
cardium)

The carditis characteristically leads to

thickened and deformed valves and to small
perivascular granulomas in the myocardium
(Ashoffs bodies) that are finally replaced
by scar tissues
 Symptom and Sign
Granuloma are formed in the heart
(Aschoff s nodule) and 2-4 weeks after
the sore throat the patient (usually children)
develops myocarditis or pericarditis

Perhaps subcutanous nodules, polyarthritis and

rarely chorea, a disease of the central
nervous system (CNS) that can be caused
by anti-streptococcal antibodies reacting with
neurones
 Symptom and Sign
Erythrocyte sedimentation rates, serum
transminase levels, ECG, and other test are
use to estimate rheumatic activity
Rheumatic fever has a marked tendency to
be reactivated by recurrent streptococcal
infections.
The first attack of RF usually produces only
slight cardiac damage, which, however,
increases with each subsequent attack
 Rheumatic Heart Disease
Repeated attacks of Strep. pyogenes with different
M type can result in damage to the heart valves

Certain children have a genetic predisposition to

this immune-mediated disease.

If a primary attack is accompanied by rising or

high antistreptolysin O (ASO) antibody levels,
future attacks must be prevented by penicillin
prophylaxis throughout chilhood.

In many developing countries rheumatic heart

disease is the commonest type of heart disease
Terima Kasih