Modulename:Cardiovascular and Lymphatic Systems

Content title: Microbes affecting the Cardiovascular

and Lymphatic Systems
Program: Medicine
Academic level: Year-II, Semester I
Academic year: 2015/16
Instructor: Dessie T. (BSc in MLT; MSc, Microbiology)
E-mail: desstegegne100@gmail.com

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 LEARNING OBJECTIVES

At the end of this session, students will be able to:

List the signs and symptoms of septicemia
Differentiate common gram-negative sepsis, gram-positive sepsis, and puerperal
sepsis.
Describe bacterial endocarditis and rheumatic fever.
Discuss the infection with, brucellosis, anthrax, gas gangrene.
Compare and contrast the causative agents, vectors, reservoirs, symptoms, and
preventive measures for plague, Lyme disease, and Rocky Mountain Spotted
Fever.
Describe infectious mononucleosis (EBV and CMV).
Compare and contrast the causative agents, vectors, reservoirs, and symptoms for
yellow fever,
Compare and contrast the causative agents, modes of transmission, reservoirs, and
symptoms for Ebola and other hemorrhagic fever

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Introduction
The heart, blood, and blood vessels make up the
cardiovascular system.
Lymph, lymph vessels, lymph nodes and lymphoid
organs constitute the lymphatic system.
Bacteria, virus, fungi and parasites may affect these
systems

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Discussion points:
What is the difference between bacteremia, septicemia and
sepsis?
What is infective endocarditis and rheumatoid fever mean?
Which microorganisms cause cardiac infection?
How/ the mechanism/ cardiac infection and cardiac failure is
caused?
How dental problems are associated with cardiac problem
What is the most diagnostic method for bacterial cardiac
infection? What about for viral cardiac infection?

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 Bacterial Diseases of the Cardiovascular and
Lymphatic Systems
Sepsis and Septic Shock
o Bacteremia : The presence of bacteria in the blood
o Septicemia: Sepsis involving proliferation of pathogens in
the blood.
o Sepsis: The growth of microorganisms with the release of toxin in
blood is called sepsis.
Gram-negative sepsis can lead to septic shock, characterized by
decreased blood pressure. Endotoxin causes the symptoms.
S. aures (septic shock syndrome), antibiotic-resistant enterococci
and group B streptococci cause gram-positive sepsis.
Puerperal sepsis begins as a focal infection of the uterus following
childbirth or abortion; it can progress to peritonitis or septicemia.
Streptococcus pyogenes is the most frequent cause.

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Bacterial Infections of the Cardiovascular
and Lymphatic Systems
Pericarditis (Streptococci, TB)
Subacute Bacterial Endocarditis (slower onset)-
alpha hemolytic streptococci including viridians
Acute bacterial endocarditis: usually caused by
S. aureus; S. pyognes
Rheumatic Fever (S. pyognes)
Brucellosis
Anthrax
Clostridium perfringes/Gas Gangrene/
Vector born bacteria

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 Subacute and acute Bacterial
Endocarditis:
Sub acute endocarditis: usually caused by alpha-hemolytic
streptococci from mouth (dentist!)
They have slow onset
Preexisting heart abnormalities are predisposing factors.
Signs include fever, anemia, and heart murmur.

Acute bacterial
endocarditis: usually
caused by S. aureus
rapid destruction of
heart valves.
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Endocarditis

Fig 23.4
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 Rheumatic Fever
Autoimmune complication of S. pyogenes infections.
Expressed as arthritis or heart inflammation. Can
result in permanent heart damage.
Antibodies against group A -hemolytic streptococci
react with streptococcal antigens deposited in joints
or heart valves or cross-react with heart tissue.
Rheumatic fever can follow
strep throat. Bacteria might
not be present at time of
rheumatic fever.
Prompt treatment of
streptococcal infections can
reduce the incidence of
rheumatic fever.
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Staphylococcus aureus
General characteristics
It is the most known cause of nosocomial infection
Structure& gram reaction: Staphylococci are Gram-positive
cocci about 0.5 1.0 m in diameter. They grow in clusters, pairs
and occasionally in short chains
Culture: Grow on most bacteriological media under (blood agar,
tryptic soy agar or heart infusion agar), B-hemolytic
Aerobic & micro aerophilic conditions; Grow rapidly at 35 - 37C0
Colonies on solid media are round, smooth & raised gray to deep
golden yellow colonies
Biochemical reaction: Catalase, coagulase positive
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Exotoxins
Several toxins that are lethal
Cause necrosis in skin
Contain soluble hemolysin (alpha - toxin)
Lyse RBCs, damage platelets &vascular smooth muscle
- toxin is toxic for human RBCs

Toxic shock syndrome toxin

Associated with: fever, shock and skin rash

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Diseases Clinical symptoms Pathogenicity factors
Gastroenteritis (food 2-6 hours after ingesting toxin: Enterotoxins A-E preformed in food
poisoning) - toxin nausea, abdominal pain, vomiting,
ingested preformed in followed by diarrhea
food
Infective endocarditis Fever, malaise, leukocytosis, heart Fibrin-platelet mesh, cytolytic toxins
murmur (may be absent initially)

Abscesses/furuncles/car Subcutaneous tenderness, redness Coagulase, probably the cytolysins

buncles and swelling; hot
Toxic Shock Syndrome Fever, hypotension, scarlatiniform TSST-1
rash which desquamates (particularly
on palms and soles, multiorgan
failure

Impetigo Erythematous papules to bullae Coagulase, exfoliatins

Pneumonia Productive pneumonia with rapid
onset, high rate of necrosis and high
fatality; nosocomial, ventilator,

Surgical infections Fever with cellulitis and/or abscesses Coagulase, exfoliatins, TSST's
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Ways of cardiac system infection: through the
blood/hematophagus
Prevention & control
Early detection & treatment (especially MRSA
Personal hygiene
Proper storage of foods
Prevention of nosocomial infection

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Lab diagnosis
Gram stain for microscope Bacteria stain strongly
gram-positive, and are frequently seen in grapelike clusters.
Serological methods
Culture: Identification of an isolate as a
staphylococcus relies largely on microscopic and
colony morphology, and catalase positivity.
S. aureus is distinguished from the coagulase-negative
staphylococci primarily by coagulase positivity.
In addition, S. aureus colonies tend to be yellow and -
hemolytic, rather than gray and non hemolytic like the
coagulase-negative staphylococci.
S. aureus is also distinguished from most coagulase-
negative staphylococci by being mannitol-positive.

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Streptococcal cardiac infection
General characteristics
Gram-positive spherical/ovoid cocci arranged in long chains;
commonly in pairs
Non-spore-forming, nonmotile
Can form capsules and slime layers
Facultative anaerobes
Do not form catalase, but have a peroxidase system
Most parasitic forms are fastidious and require enriched
media.
Small, nonpigmented colonies
Sensitive to drying, heat and disinfectants
25 species
-hemolysis A,B,C,G and some D strains
a hemolysis S. pneumoniae and others collectively
called viridans
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Group A beta -Hemolytic Streptococci
(Streptococcus pyogens)
General characterstics
S. pyogenes are gram+ cocci, occur as long chains when recovered
from liquid culture, but may appear as individual cocci, pairs, or
clusters of cells in Gram stains of samples from infected tissue.
On culture, are B-hemolytic
Virulence factors
- Hyaluronic acid capsule (a polysaccharide) inhibits phagocytic
uptake
- M-protein: virulence factor, antiphagocytic,

Streptolysin O: Immunogenic, hemolysin/cytolysin

Exotoxins A-C (Pyrogenic or erythrogenic exotoxins)

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 Toxin production: these bacteria
produce the following toxins
Streptolysin O (oxygne labile)
Streptolysin S (oxygne stable)
Streptokinase
Hyaluronidase etc

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Clinical significance
S. pyogenes is a major cause of cellulitis. Acute pharyngitis
or pharyngotonsilitis: Impetigo, Erysipelas, Puerperal sepsis
(a new born), and some times acute endocardiaties
Acute rheumatic fever: (This autoimmune disease occurs
two to three weeks after the initiation of pharyngitis. It is
caused by cross-reactions between antigens of the heart and
joint tissues, and the streptococcal antibody).

Streptococcal toxic shock syndrome.

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Laboratory identification
Rapid latex antigen kits for direct detection of group A
streptococci in patient samples are widely used.
routine culturing for streptococcal identification.
Depending on the form of the disease, specimens for laboratory
analysis can be obtained from throat swabs, pus and lesion
samples, sputum, blood, or spinal fluid.
Serologic tests detect a patient's antibody titer to streptolysin-O
(ASO test) after group A streptococcal infection.

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a-Hemolytic Streptococci:
(Viridians Group)
Large complex group
Streptococcus mutans, S. oralis, S. salivarus,
S. sanguis, S. milleri, S. mitis
Are gram positive cocci
Most numerous and widespread residents of the gums
and teeth, oral cavity and also found in nasopharynx,
genital tract, skin
Not very invasive; dental or surgical procedures
facilitate entrance to the cardiac system
S.mutans- Tooth decay
 Viridans Streptococci
Pathogenesis for cardiac infection:
The viridans streptococci are relatively avirulent, but
Streptococcus mutans and other members of the
viridans group cause dental caries.
S. mutans produce slime layers that adhere to teeth,
basis for plaque that are the causes of dental caries
In patients with abnormal or damaged heart valves,
they can also infect these valves during a
bacteremia/dental origion, causing serious subacute
bacterial endocarditis.
Persons with preexisting heart disease are at high risk.
Colonization of heart by forming biofilms
Also cause Bacteremia, meningitis, abdominal infection,
tooth abscesses
Route of infection for endocarditis: through blood
circulation from the dental procedures
Prevention and control
Persons with preexisting heart conditions should
receive prophylactic antibiotics before surgery or
dental procedures.
Lab diagnosis:
Microscopic with gram stain (gram+ cocci in
chains),
Serologic
Culture- B-hemolytic
 Pericardial Tuberculosis (TB pericarditis):
What are the general c-xs of TB? (discussion point)
TB pericarditis
It is frequently seen in patients with HIV.
Patients usually present with fever, retro-sternal pain,
cough, dyspnea and generalized edema because of
pericardial effusion.
Cardiac tamponade/accumulation of fluid/may appear
later
Constrictive pericarditis may develop as a complication
of TB pericarditis even after treatment and patients can
present with symptoms and signs of right sided heart
failure.
Pericardial Tuberculosis (TB pericarditis):
Diagnosis: is usually reached by analyzing the
pericardial effusion, which is always done in
hospitals.
It may show lymphocytosis, but yield for AFB is low.
Chest x-ray may show enlarged heart shadow, which
suggests effusion.
Ultrasound should be done when available and it
demonstrates effusion.
 Genus Brucella
Gram negative, short rods, coccobacilli
Non-motile, non-spore forming, non-capsulated
Aerobic, require complex media (amino acid, thiamine,
nicotinamide)
Growth enhanced (serum/blood)
Catalase +ve, oxidase +ve
Many require CO2 for growth
characteristically located intracellularly
Cause disease primarily in animals
Bacteremia and septicaemia in humans
characteristically located intracellularly
Species of medical importance
B. abortus,
B. melitensis, and B.suis causes human brucellosis
Natural habitats
Animals main reservoir

Transmit from Animal to humans through

Milk products
Handling of animals and cultures

Inhalation of aerosols
Virulence factor
Ability to resist phagocytosis
Ability of intracellular survival
Pathogenesis and clinical manifestation
Brucellae are intracellular organisms infecting Red blood
cells of the spleen, liver, kidneys and bone marrow. From
these sites, the bacteria pass into the blood.
Disease- brucellosis (undulant fever, Malta fever), is
characterized by an acute bacteremic phase followed by a
chronic stage.
Characterized by fever which may be continuous,
intermittent, undulating or irregular.
headache, sweating (especially at night) and generalized
pains associated with fatigue and depression.
anaemic and leukopenic with a relative lymphocytosis.
musculoskeletal symptoms (back pain, arthritis, arthralgia).
 Lab. Diagnosis
Specimens:
Blood, bone marrow aspirates, biopsy specimen (lymph nodes,
bone, etc), serum
Microscopy-
tiny gram-negative coccobacilli
Culture
Tryptone soya (tryptic soy) diphasic medium
chocolate agar.
Serum dextrose agar
Blood culture media
Serological diagnosis
Many cases of brucellae infection are diagnosed by serological test
which include the standard agglutination test and an ELISA
procedure for detection of brucella-specific IgM/IgG
Prevention and control
limitation of spread and possible eradication of animal
infection,
pasteurization of milk and milk products, and

reduction of occupational hazards wherever possible.

(Caution: Brucellae are highly infectious (Hazard Risk

Group 3) pathogens. Laboratory-acquired infections can
occur following accidental inoculation or inhalation of the
organisms. Collect blood with great care, minimize the
creation of aerosols and whenever possible, carry out
procedures which may produce aerosols in a safety cabinet)

 Anthrax
Bacillus anthracis G+ rod, aerobic,
virulence factors: Capsule, plasmid encoded toxins
Anthrax toxin consists three
components/Edema factor (EF), Lethal factor (LF)
and Protective antigen (PA)
Zoonosis; found in soil with its spores of long lasting

In human
Pulmonary anthrax (woolsorters disease), Inhalation of
endospores; 100% mortality
Cutaneous anthrax, most common, endospores enter
through minor cut; 20% mortality
Gastrointestinal anthrax: Ingestion of undercooked
contaminated food; 50% mortality
Treated with ciprofloxacin or doxycycline
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 Pathogenesis
The virulence factors of B anthraces are its capsule and three-
component toxin, both encoded on plasmids.
The principal virulence factors are a necrotizing enterotoxin and a
potent hemolysin.
Released toxin causes breakdown of organs probably of the spleen
and lymphnodes in particular.
This causes the sudden onset of hyperacute illness with dyspnea,
cyanosis, high fever, and disorientation, which progress in a few hours
to shock, coma, and death
 Laboratory Diagnosis

Specimen: fluid or pus from a local lesion, blood, and

sputum.
Microscopic
- Gram stain- large gram-positive rods.
- Loefflers polychrome (McFadyean) methylene blue
stained smear- Square ended blue-black bacilli
surrounded by a pink/purple capsule
Immunofluorescence staining
Culture
- BA- non-hemolytic gray to white mucoid colonies with a
rough texture and a ground-glass appearance
Biochemical test
- Ferment glucose, maltose, sucrose, trehalose, and
dextrose, with acid production but not gas
Serological test
- ELISA measure antibodies against edema and lethal
toxins
Animal pathogenicity test
- kill mice or guinea pigs upon intraperitoneal injection.
Gas Gangrene (Clostridial Myonecrosis)
Gangrene: Soft tissue death from ischemia especially susceptible to
growth of anaerobic bacteria /Clostridium perfringens/:
General C-xs:
C. perfringens: Large gram-positive, spore-forming rods (spores rare in
tissue), non-motile
Anaerobic: stormy fermentation in milk media
Double zone of beta hemolysis
Reservoir: Soil/dust and human colon
- There are five sero groups(A-E) of C.perfringens based on; surface
antigens and major lethal toxins (a,,,) produced,
Types A and C cause disease in humans
C. perfringens can invade the wall of the uterus during improperly
performed abortions
Death due to toxemia
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generally occurs at wound
or surgical site painful
swelling and tissue
destruction. Rapidly
progressive, often fatal.
 Lab diagnosis
Specimen: wound exudate, pus, and tissue.
Microscopic examination
The presence of large gram-positive rods in Gram-stained smears
suggests gas gangrene clostridia; spores are not regularly present.
Culture
- lactose egg yolk medium- red, opeaque colonies
surrounded by clear area
Serology
- Nagler reaction- inhibition of opacity by anti-toxin
Prevention of gas gangrene: early cleansing of wound, Extensive
debridement of the wound, administration of penicillin
Treatment of gas gangrene:- clindamycin and penicillin; polyvalent
antitoxin
Vector-Transmitted Diseases

Plague
Relapsing Fever
Lyme Disease
Ehrlichiosis
Typhus
Epidemic Typhus
Spotted Fevers

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 Plague
Black death: Yersinia pestis,
G- rod, bipolar staining
Reservoir: Rats, ground
squirrels, and prairie dogs
Vector: infected fleas
Bubonic plague:
Bacterial growth in blood
and lymph
Plague suit
Septicemia plague:
Septic shock
Pneumonic plague:
Bacteria in the lungs

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Bipolar staining: Dark
stained bipolar ends in
Wright's stain (blood from
plague victim)
 Lyme Disease
Lyme disease is a Zoonosis caused by Borrelia
burgdorferi
Reservoir: mice, deer; Vector: Ixodes ticks
3 stages with various symptoms
1. Early localized stage: Bulls eye rash
= erythema (chronicum) migrans
ECM; flu-like symptoms
2. Early disseminated stage: Heart and
Nervous system symptoms; also skin
and joints affected
3. Late stage: Chronic arthritis
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Clinical manifestations:
The most common early indication of Lyme disease in
humans is a rash, followed by fever, flu-like symptoms,
chills, headache and fatigue.
Later symptoms may include joint pain, headache, facial
paralysis, myocarditis (inflammation of the heart muscle),
and heart block

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Diagnosis
Symptoms alone: often misdiagnosis
In most cases not possible to isolate and
culture B. burgdorferi indirect
serological tests (ELISA and Western
blot)
PCR
Prevention: Vector control; early diagnosis and
treatment

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Life Cycle
of the Tick
 Ehrlichiosis
First described in 1986
Caused by Ehrlichia species and
transmitted by Ixodes ticks
diseases of animals and
humans
Obligately intracellular (in white
blood cells)
Monocytic Ehrlichiosis (HME)
granulocytic Ehrlichiosis (HGE)
Nonspecific symptoms (similar to
other diseases)
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 Rocky Mountain Spotted
Fever (RMSF)

Rickettsia rickettsii
Zoonosis
Reservoir: mammals
Vector: ticks
Characteristic hemorrhagic
rash maculopapular
starts on palms and soles
(unlike measles!)
Can damage vital organs
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Table. Summary of Rickettsial and Ehrlichial Diseases
Laboratory diagnosis

Specimen: Serum for serological tests

The serological tests to diagnose typhus are:

1. Indirect fluorescent antibody test

2. Complement fixation test

3. Weil felix reaction: Some of the antigen of Proteus strain

(OX-19, OX-2,OX-K) agglutinates with sera from patients with

rickettsial diseases.
Table. Weil-Felix Reactions
Treatment

Drug of choice: tetracycline and chloramphenicol.

Prevention and Control

Personal hygiene.

Delousing with insecticide.

Removing of vegetations in which rates and mites live.

Tick repellents.
VIRAL DISEASES OF THE CARDIOVASCULAR
AND LYMPHATIC SYSTEMS

Infectious Mononucleosis
Viral Hemorrhagic Fevers

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 Infectious Mononucleosis
Epstein-Barr virus (EBV)
The EBV DNA genome contains about 172 kbp, has a G +
C content of 59%, and encodes about 100 genes.
is a ubiquitous herpesvirus that is the causative agent of
acute infectious mononucleosis

is associated with nasopharyngeal carcinoma, Burkitt's

lymphoma, Hodgkin's disease, and other
lymphoproliferative disorders in immunodeficient
individuals

EBV is common in all parts of the world, with over 90% of

adults being seropositive.
In developing areas, infections occur early in life; more
than 90% of children are infected by age 6.

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 These infections in early childhood usually occur
without any recognizable disease.
Also known as Kissing disease Virus multiplies in parotid
glands and is present in saliva. It causes the proliferation of
atypical lymphocytes (life-long infection) Transmission via
saliva

Most people (~95%) infected. It is however usually

asymptomatic.

Characteristic triad: fever, pharyngitis, and lymphadenopathy

(+spleno- and hepatomegaly) lasting for 1 to 4 weeks.

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 Triad

Swollen lymph nodes, sore throat, fatigue and headache are some of the
symptoms of mononucleosis. It is generally self-limiting and most patients
can recover in 4 to 6 weeks without medications.
 Proliferation of infected B cells results in massive
activation and proliferation of Tc cells (CD8 cells)
characteristic lymphoid hyperplasia.

Transformation of B cells to immortal plasmacytoid

cells secrete a wide variety of IgMs = heterophile
antibodies (Monospot test)
Commercially-available test kits are 70-92% sensitive
and 96-100% specific

"Downy cell: lymphocytes infected

by EBV or CMV in infectious
mononucleosis. Cytoplasmic rim is
intensely blue and has tendency to
"stream" around adjacent red cells.
Pathogenesis of infectious mononucleosis
Laboratory diagnosis
Laboratory studies of EBV are hampered by the lack of a
fully permissive cell system able to propagate the virus.
EBV can be isolated from saliva, peripheral blood, or
lymphoid tissue by immortalization of normal human
lymphocytes, usually obtained from umbilical cord blood.
Molecular methods: Nucleic acid hybridization is the most
sensitive means of detecting EBV in patient materials.
Serologic tests (ELISA, IgG-for latent/past infection and or
immunity, IgM for current infection antibody detection)

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Cytomegalovirus
Cytomegaloviruses are ubiquitous herpesviruses that are
common causes of human disease.
The name for the classic cytomegalic inclusion disease
derives from the propensity for massive enlargement of
cytomegalovirus-infected cells
Cytomegalovirus has the largest genetic content of the human
herpesviruses.
Its DNA genome is significantly larger than that of HSV.
Cytomegalovirus produces a characteristic cytopathic effect
Cytomegalovirus may be transmitted person-to-person in
several different ways, all requiring close contact
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 There is a 4- to 8-week incubation period in normal older children
and adults after viral exposure.
Primary cytomegalovirus infections in immunosuppressed hosts
are much more severe than in normal hosts.
Individuals at greatest risk for cytomegalovirus disease are those
receiving organ transplants, those with malignant tumors who are
receiving chemotherapy, and those with AIDS.
Viral excretion is increased and prolonged, and the infection is
more apt to become disseminated.
A high percentage of babies with this disease will exhibit
developmental defects and mental retardation.
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Lab diagnosis
Culture: Human fibroblasts are used for virus isolation
attempts (with in 2-4 weeks).
The virus can be recovered most readily from throat
washings and urine.
Molecular methods: Nucleic acid hybridization is
the most sensitive means of detecting EBV in
patient materials.
Serologic tests (ELISA, IgG-for latent/past
infection and or immunity, IgM for current infection
antibody detection)
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Treatment and control
Specific control measures are not available to prevent
cytomegalovirus spread.
Isolation of newborns with cytomegalic inclusion
Screening of transplant donors.
Ganciclovir also controls progressive hearing loss in neonates
with congenital infections.
Foscarnet, an analog of inorganic pyrophosphate, is
recommended for treatment of cytomegalovirus retinitis.
Acyclovir and valacyclovir have shown some benefits in
bone marrow and renal transplant patients.
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 Viral Hemorrhagic Fevers

Enveloped RNA viruses: Arenaviruses,

filoviruses, bunyaviruses, and flaviviruses
Viruses geographically restricted to where
their host species live
For some viruses, after accidental transmission
from host, humans to human transmission may
occur
Human cases or outbreaks sporadic and
irregular. Not easily predictable
Marburg VHF: 1967 outbreak in Marburg (D)
imported from Africa; Mortality rate 25%
Ebola HF: 1995 major outbreaks in Zaire and
Sudan; Mortality rate 50 90%, and in 2014/15 in
some African countries
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Ebola virus
It was first discuvered in 1976 near Ebola river in Zaire
Found mostly in west Africa
Ebola is an acute infectious, hemorrhagic viral fever (fever
and severe internal bleeding), conjunctivitis, headache,
myalgia, diarrhea
It is an enveloped single stranded, un segmented, single
stranded RNA virus with a thread/6 like structure
Death rate is : 50-100%
Transmission: Ebola is transmitted with direct contact with
body fluids of symptomatic person
Incubation period: 2-21 days
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 Examples of Hemorrhagic Signs
Hematemesis
Gingival bleeding

Bleeding at IV Site

66
Prevention, treatment and control

Currently there are no approved vaccines and

treatment/except supportive and isolation & or care.
a. Hospitals must follow precautionary methods,
1. wearing gloves
2. isolating infected individuals
3. practicing nurse barrier techniques
4. proper sterilization and disposal of all
equipment
b. Burials must be done correctly
1. no washing or touching carcass
2. put into body bags and bury outside city
c. Report any questionable illness to
officials
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 Currently two vaccines are on trial (cAd3-EBPZ vaccine and
VSV-EBOV)
Lab diagnosis: Serological, PCR, Cell culture (the process
require high safety cabinate/level-4/
Other lab results:
Thrombocytopenia (50,000-100,000/mL range)
Leukopenia followed by neutrophilia
Transaminase elevation: elevation serum aspartate amino-transferase
(AST) > alanine transferase (ALT)
Electrolyte abnormalities from fluid shifts
Coagulation: PT and PTT prolonged
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 Marburg virus is identical with Ebola virus in
form and structure except antigenically (reading
assignment; Including Candidia and
Aspergilous infection of the cardiovascular
system)

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 Classic Viral Hemorrhagic Fevers: Yellow Fever
Caused by arbovirus (flaviviridae) transmitted
by mosquitoes
Direct damage to liver and heart jaundice,
hemorrhaging, weak heart function
circulatory and kidney failure
African and American tropical jungles
No treatment
Can be prevented by highly effective
attenuated vaccine

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 AGENT
Genus :Flavivirus fibricus,
Group B Arbovirus
Family : Toga virus
The yellow fever virus is 35-40 nm in size.
It consists of a single strand of RNA virus

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Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings