Micro of blood_compressed

Dr. Nabil A.
ElAila
Associate Professor of Molecular Microbiology
Al Aqsa University - Gaza , Palestine
1
The Cardiovascular System and
Lymphatics System
 Blood, heart, vessels = cardiovascular system
 Lymph, lymph vessels, lymph nodes and lymphoid
organs = lymphatic system
 Blood—Transports nutrients to and wastes from cells
 WBCs—Defend against infection
 Lymphatics—Transport interstitial fluid to blood
 Lymph nodes—Contain fixed macrophages
The Cardiovascular System
 Blood = mixture of plasma and
cells
 Plasma transports dissolved
substances; RBC carry oxygen;
WBC mediate body’s defenses
against infection
 Interstitial fluid – fluid that
filters out of capillaries into
spaces between tissue cells;
enters lymph capillaries as
lymph
 Lymph nodes contain fixed
macrophages, B and T cells
Figure 23.1
Relationship between Cardiovascular and Lymphatic System
The cardiovascular and lymphatic systems work closely to maintain fluid balance and support
immune function. The cardiovascular system circulates blood, while the lymphatic system drains
excess tissue fluid and returns it to the bloodstream, aiding in waste removal and immune
defense.
How Bacteria Enter the Circulatory and
Lymphatic Systems
•Entry Points for Bacteria:

•Acute infections, skin breaches, or mucosa ruptures.
•Common sources include insect bites, small wounds, and
even tooth brushing.
•Transient Bacteremia:
•Often brief and below detection levels.
•Typically harmless in healthy individuals.
•Severe Cases of Bacteremia Can progress to septicemia,
leading to complications like toxemia, sepsis, and septic
shock.
•Role of Immune Response:
•Often, the body’s immune reaction to infection causes
symptoms, not the bacteria directly.
Microbial Diseases of the Circulatory and Lymphatic System - - Dr. Nabil Elaila 5
Differences between bacteremia & septicemia
Bacteremia Septicemia
 Is the simple presence of  Is the presence & multiplication of
bacteria in the blood. bacteria in the blood.
 Is not as dangerous as  Is a potentially life-threatening
Septicemia. infection.
 Less amount of bacteria are  Large amounts of bacteria are
present in blood. present in the blood.
 This may occur through a wound  It can arise from infections
or infection, or through a throughout the body, including
surgical procedure or injection. infections in the lungs, abdomen,
 Toxins are not produced. & urinary tract.
 Bacteremia usually causes no  Toxins may be produced by
symptoms or it may produce bacteria.
mild fever.  It shows symptoms like chills,
fever, prostration, very fast
respiration &/or heart rate.
Differences between bacteremia & septicemia
Bacteremia Septicemia
 It can resolve without treatment.  Untreated septicemia can quickly
 Rapidly removed from the progress to sepsis.
bloodstream by the immune  Antibiotics will be used to treat
system. the bacterial infection th
 Caused by Staphylococcus,  Staphylococci, are thought to
Streptococcus, Pseudomonas, cause more than 50% of cases of
Haemophilus, E. coli, dental sepsis. Other commonly
procedures, UTI, implicated bacteria
peritonitis, Clostridium include Streptococcus pyogenes,
difficile colitis, IV drug use, & E. coli, Pseudomonas aeruginosa,
colorectal cancer. & Klebsiella species
Bacterial Sepsis and Septic Shock
 Sepsis: A severe immune response to infection, potentially
leading to life-threatening complications.
 Key Cytokines Involved: IL-1 and TNF-α play crucial roles
in immune defense but can cause harm when excessively
released.
 Vasodilation and Blood Pressure: IL-1 causes blood
vessel widening and fluid leakage, leading to low blood
pressure, a key feature of septic shock
 High cytokine levels cause vasodilation, edema, and blood
clots.
 Low blood pressure can impair kidney and respiratory
functions, potentially leading to multiple organ failure.
 Septic Shock Risks: Severe cases can cause organ failure
and death ifMicrobial
untreated.
Diseases of the Circulator and Lymphatic System - - Dr. Nabil Elaila 8
Causes and Bacteria Associated with Sepsis
Common Infections:
•Bacterial Pneumonia (50% of cases)
•Intra-abdominal Infections
•Urinary Tract Infections
•Pathogens Involved: Staphylococcus, Streptococcus,
•Pseudomonas, Pasteurella, Acinetobacter,
Enterobacteriaceae.
•Progression: Without treatment, localized infections
can advance to sepsis and septic shock.
Toxic Shock Syndrome (TSS)
 TSS is a severe toxemia associated with infections caused by
Staphylococcus aureus.
 S. aureus can produce toxic shock syndrome toxin-1 (TSST-
1), a superantigen.
 Risk factors include tampon use, contraceptive sponges,
diaphragms, or other devices left in the vagina longer than
recommended.
 Commonly occurs as a complication of infections like
pneumonia, osteomyelitis, and skin wounds.
Symptoms and Characteristics of
Staphylococcal TSS
 Symptoms include sudden vomiting, diarrhea, muscle pain,
fever (above 38.9°C / 102°F), and hypotension (low blood
pressure).
 A diffuse red rash appears, leading to skin peeling 1-2 weeks
after onset.
 Three or more organ systems are usually affected.
 The mortality rate is less than 3%.
Diagnosis and Treatment of
Staphylococcal TSS
 Diagnosed by clinical signs, symptoms, and toxin detection
from S. aureus cultures.
 Cultures often yield negative results; only 5% of skin and
blood cultures are positive.
 Treatment includes decontamination, debridement, blood
pressure support, and antibiotics (clindamycin +
vancomycin or daptomycin).
Streptococcal Toxic Shock-Like
Syndrome (STSS)
 Caused by Streptococcus pyogenes, more severe than
staphylococcal TSS.
 High risk of bacteremia (50%) and necrotizing fasciitis;
ARDS and hypoxemia are common.
 Mortality rate is 20%–60%, even with aggressive treatment.
 STSS often follows soft-tissue infections, such as cellulitis or
necrotizing fasciitis, or after influenza A or chickenpox
infections.
Puerperal Sepsis
 Puerperal sepsis, also known as childbed fever, is a
nosocomial infection following childbirth.
 Occurs during the puerperium, as the mother’s
reproductive system returns to its nonpregnant state.
 Infection sources include the genital tract, breast, urinary
tract, or surgical wounds.
 Can start in the uterus but may spread, causing peritonitis,
septicemia, and death.
 A major cause of maternal mortality before the germ theory
was established.
Causative Agents of Puerperal Sepsis
 Commonly associated with Streptococcus pyogenes.
 Other bacteria include Streptococcus spp., Staphylococcus
spp., Enterococcus spp.
 Gram-negative bacteria involved include Chlamydia spp., E.
coli, Klebsiella spp., and Proteus spp.
 Anaerobes such as Peptostreptococcus spp., Bacteroides
spp., and Clostridium spp.
 S. pyogenes uses M protein and a capsule to evade immune
response and produces exotoxins.
Symptoms and Diagnosis of
Puerperal Sepsis
 Symptoms include fever shortly after childbirth.
 Infection can be localized or spread throughout the body.
 Diagnosed by fever timing, infection extent, and identifying
bacteria in blood or urine.
 Bacterial cultures aid in determining the causative
organism.
 Antimicrobial susceptibility testing is essential for effective
treatment.
Prevention and Reduction of
Puerperal Sepsis
 Use of antiseptics during childbirth reduces infection risk.
 Strict handwashing by healthcare staff is critical.
 Hygiene protocols apply to doctors, midwives, and nurses.
 Adhering to aseptic techniques can prevent nosocomial
infections.
 Proper identification and treatment of infections lower
mortality risks.
Bacterial Endocarditis
 Endocarditis is an infection of the heart’s inner lining
(endocardium).
 Caused by bacteria such as Staphylococcus aureus, viridans
streptococci, Enterococcus faecalis, and HACEK group.
 Bacteria enter bloodstream through breaches (e.g., dental
procedures, body piercings).
 Higher risk for those with preexisting heart damage,
prosthetic valves, or rheumatic fever.
 Untreated endocarditis can rapidly damage heart valves and
be fatal.
Figure 25.2.1
: The heart of an individual who had subacute bacterial endocarditis of the mitral valve.
Bacterial vegetations are visible on the valve tissues. (credit: modification of work by
Centers for Disease Control and Prevention)
Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 19
Types of Endocarditis - Acute vs. Subacute
 Acute endocarditis is aggressive and can destroy heart
valves in days.
 Subacute endocarditis progresses slowly, damaging valves
over months.
 Blood clots (vegetations) form, protecting bacteria from
immune defenses.
 Vegetations contribute to fibrosis and long-term heart valve
damage.
 Subacute endocarditis may present with mild symptoms,
like fever.
Diagnosis and Treatment of Endocarditis
 Diagnosed using blood cultures, echocardiograms, and
clinical signs.
 Both acute and subacute endocarditis require high-dose IV
antibiotics.
 Acute endocarditis is treated with ampicillin, nafcillin, and
gentamicin.
 Prosthetic-valve endocarditis treated with vancomycin,
rifampin, and gentamicin.
 Rifampin helps penetrate biofilms on prosthetic devices.
Pericarditis
 Pericarditis is inflammation of the tissues surrounding the
heart.
 Caused by infections from Staphylococcus spp.,
Streptococcus spp., or other pathogens.
 Symptoms include chest pain, difficulty breathing, and dry
cough.
 Most cases of pericarditis are self-limiting.
 Rarely requires clinical intervention unless symptoms are
severe.
Diagnosis and Treatment of Pericarditis
 Diagnosed with chest radiographs, ECG, echocardiogram,
or fluid/biopsy tests.
 Antibacterial medications may be prescribed if caused by
bacterial infection.
 Pericarditis can also be caused by viruses (e.g., echovirus,
influenza).
 Fungi like Histoplasma spp. and Coccidioides spp. can also
cause pericarditis.
 In rare cases, parasitic infections like Toxoplasma spp. are
culprits.
Key Points Summary
 Endocarditis and pericarditis are serious infections
impacting heart tissue.
 Risk factors include heart damage, foreign devices, and
certain procedures.
 Endocarditis requires prompt diagnosis and aggressive IV
antibiotic treatment.
 Pericarditis is generally self-limiting but may need
treatment if bacterial.
 Accurate diagnosis is essential to target and manage these
infections effectively.
Rheumatic Fever (RF)
 RF is a nonsuppurative sequela of Streptococcus pyogenes
infection, especially after untreated pharyngitis.
 Typically affects children, occurring 2–3 weeks after a strep
throat infection.
 Was once a major cause of child mortality in the US, now
rare due to antibiotic treatment.
 Still a significant cause of child mortality in areas lacking
healthcare access. rheumatic heart disease, affecting the
heart and circulatory system.
 Can lead to Can lead to serious complications,
particularly if not treated promptly
Symptoms and Immune Response in
Rheumatic Fever
 RF is an immune-mediated condition; Antibodies against
group A beta-hemolytic streptococci react with antigens
deposited in joints or heart valves
 Symptoms include joint pain and swelling (reversible), and
nervous tissue damage.
 Heart valve damage from repeated RF episodes can lead to
scarring and stiffness.
 Irreversible damage to heart valves may cause a
characteristic heart murmur.
 Recurrent S. pyogenes infections increase risk of further RF
episodes and heart damage.
Treatment and Prevention of Rheumatic Fever
 The American Heart Association advises benzathine
benzylpenicillin every 3–4 weeks.
 Prophylactic antibiotics are recommended based on age
and reinfection risk.
 Preventive treatment aims to avoid recurrent S. pyogenes
infections.
 Early diagnosis and treatment of strep throat are key to
preventing RF.
 Consistent treatment helps reduce the likelihood of
rheumatic heart disease.
Tularemia
 Tularemia, or rabbit fever, is caused by Francisella
tularensis, a gram-negative bacterium.
 Zoonotic infection mainly affects rabbits but can infect
various animals and humans.
 Humans can contract it by handling infected animal tissues
or eating contaminated meat.
 Transmission also occurs through bites from infected ticks
and deer flies.
 Highly contagious and potentially fatal; classified as a BSL-3
organism and biowarfare agent.
Pathogenesis of F. tularensis
 Bacteria enter through skin breaks and travel to lymph
nodes.
 Phagocytes ingest F. tularensis, which then escapes into
their cytoplasm to multiply.
 Can disseminate to organs like liver, lungs, and spleen,
forming granulomas.
 Incubation is around 3 days, followed by skin lesions at
infection sites.
 Symptoms include fever, chills, headache, and painful,
swollen lymph nodes.
Tularemia lymphadenopathy

Diagnosis and Laboratory Safety
 Tularemia diagnosis is challenging due to high
contagiousness and non-specific symptoms.
 Handling of specimens requires BSL-2 or BSL-3 labs with
strict biosafety protocols.
 DFA tests can confirm F. tularensis quickly using specific
antibodies.
 Culture requires cysteine-supplemented media, and PCR
can identify the bacterium.
 Serological tests with acute and convalescent sera can
confirm active infections.
Treatment and Epidemiology
 Tularemia is rare in the US but has symptoms similar to
other infections.
 Antibiotics like streptomycin, gentamycin, doxycycline, and
ciprofloxacin are effective.
 Diagnosis is often based on clinical signs and potential
exposure history.
 Protective equipment and biosafety measures prevent lab
infections.
 Early diagnosis and treatment are critical to prevent serious
outcomes.
Brucellosis
 Brucellosis is caused by Brucella species, gram-negative
coccobacilli.
 Major human pathogens: B. abortus (cattle), B. canis
(dogs), B. suis (swine), B. melitensis (goats/sheep).
 Known as undulant fever, Mediterranean fever, or Malta
fever.
 Common in regions like the Mediterranean, South/Central
Asia, and South America.
 Humans are infected through consumption of
contaminated meat/dairy or direct animal contact.
Transmission and High-Risk Groups
 Infection occurs via ingestion, inhalation, or direct skin
contact with infected animals.
 High-risk groups: slaughterhouse workers, veterinarians,
and those handling animal products.
 Brucella can survive stomach acid due to urease, and within
phagocytes due to LPS.
 Bacteria spread via macrophages, reaching organs like liver,
spleen, lungs, and brain.
 Leads to granuloma formation in various organs.
Symptoms and Disease Progression
 Symptoms include undulant (relapsing) fever, flu-like signs,
and chronic illness if untreated.
 Fever can reach 40–41°C (104–105.8°F) with recurrent
symptoms.
 Acute stage infections may become chronic without
treatment.
 Brucella is found in blood only during acute fever stage.
 Chronic brucellosis leads to granulomas in multiple organ
systems.
 Osteomyelitis is the most frequent complication
Diagnosis and Treatment
 Diagnosed using agglutination tests and ELISAs to detect
antibodies.
 Culturing Brucella is challenging and requires BSL-3
precautions.
 Doxycycline or ciprofloxacin combined with rifampin is
standard treatment.
 Gentamicin, streptomycin, and TMP-SMZ are alternative
antibiotics.
 Protective measures necessary in labs to avoid laboratory-
acquired infections.
 Prevention via: Pasteurization of milk, Immunization of
animals, Slaughtering of infected animals.
 There is no human vaccine
Anthrax
 Bacillus anthracis, gram-positive, endospore-forming aerobic
rod
 Diagnosis based upon isolation and identification
 Found in soil, lasting up to 60 years
 Grazing animals ingest endospores
 Cattle are routinely vaccinated
 Treated with ciprofloxacin or doxycycline
 Cutaneous anthrax (handling hides)
 Endospores enter through minor cut (pustule), respiratory
tract (septic shock), mouth
 20% mortality
Anthrax – cutaneous pustule
 Gastrointestinal anthrax
 Ingestion of
undercooked food
contaminated food
 50% mortality
 Inhalational anthrax
 Inhalation of
endospores
 100% mortality, hence
fear of terrorist
activities!
Figure 23.7
Potential Biological Weapons
Diagnosis of Infectious Diseases Dr. Nabil El Aila

Gas Gangrene
 Gas gangrene occurs when blood flow is interrupted,
causing tissue ischemia.
 Clostridium perfringens endospores germinate in ischemic,
anaerobic tissues.
 Common in traumatic injuries or conditions like diabetes
that disrupt blood supply.
 Infection leads to rapid muscle tissue death (myonecrosis).
 Gas gangrene can spread quickly, leading to severe
complications.
Symptoms and Signs
 Excruciating pain and foul-smelling wound with gas
bubbles.
 Thin, yellowish discharge with a small amount of blood at
infection site.
 Edema, blisters with bluish-purple fluid, and tissue
liquefaction.
 Necrotic tissue can spread several inches per hour.
 Septic shock and organ failure are common, with a high
mortality rate when sepsis develops.
Figure 25.2.2
: (a) In this image of a patient with gas gangrene, note the bluish-purple discoloration
around the bicep and the irregular margin of the discolored tissue indicating the spread of
infection. (b) A radiograph of the arm shows a darkening in the tissue, which indicates the
presence of gas. (credit a, b: modification of work by Aggelidakis J, Lasithiotakis K, Topalidou
A, Koutroumpas J, Kouvidis G, and Katonis P)

Virulence Factors and Pathophysiology
 α-Toxin: a lipase that destroys cell membranes and causes
blood clots.
 θ-Toxin: forms pores in cell membranes, leading to cell
lysis.
 Gas production from bacterial fermentation of butyric acid.
 Hydrogen and carbon dioxide gases form pockets in tissues.
 Toxins and gas facilitate the rapid spread of infection.
.
 Treatment often involves surgical debridement; severe cases
may need amputation.
 Vacuum-assisted closure (VAC) is used to drain wounds and
aid recovery.
 Common antibiotics: penicillin G and clindamycin.
 Hyperbaric oxygen therapy may be used as Clostridium
cannot survive in oxygen-rich environments.
Cat-Scratch Disease (CSD)
 Cat-scratch disease (CSD) is a bacterial infection caused by
Bartonella henselae.
 Transmitted to humans via scratches or bites from infected
cats.
 Cats contract B. henselae from flea feces during grooming.
 Bacteria enter human lymph nodes at bite/scratch site.
 B. henselae infects red blood cells, leading to localized
infection.
Symptoms and Complications
 Small nodule with pus forms at injury site within 1–3 weeks.
 Swollen, painful lymph nodes near infection site.
 Additional symptoms: fever, chills, and fatigue.
 Generally mild, self-limiting in healthy individuals.
 In immunocompromised patients, can lead to serious
conditions like bacillary angiomatosis and bacillary peliosis.
 Diagnosis is challenging; B. henselae is hard to grow in labs.
 Diagnostic tools: immunofluorescence, serology, PCR, and
gene sequencing.
 Most cases are self-limiting; antibiotics not usually needed.
 For immunocompromised: effective antibiotics include
rifampin, azithromycin, and ciprofloxacin.
 Prevention: keep cats flea-free and clean scratches
promptly.
Plague
 Caused by Yersinia pestis, a gram-negative bacterium.
 Zoonotic infection, commonly affecting rodents and small
mammals.
 Transmitted to humans, leading to acute febrile disease.
 Known for causing historical pandemics with high
mortality.
 Three forms: Bubonic, Septicemic, and Pneumonic plague.
Bubonic Plague
 Transmitted by bites from infected fleas, usually on lower
extremities.
 Symptoms appear after a 2-6 day incubation period: high
fever, headache, chills.
 Causes swollen, inflamed lymph nodes ("buboes"), often in
groin area.
 Mortality rate ~55% untreated; ~10% with antibiotics.
 Infection can spread through lymphatic system, forming
buboes throughout body.
Septicemic Plague
 Occurs when Y. pestis enters bloodstream through a cut or
wound.
 Rapid onset within 1-3 days: fever, chills, weakness,
abdominal pain, shock.
 Leads to disseminated intravascular coagulation (DIC),
causing necrosis.
 High mortality rate: ~100% untreated; ~50% with
treatment.
 Necrosis primarily affects extremities, leading to blackened
fingers/toes.
Pneumonic Plague
 Lung infection from inhaled droplets or spread from other
plague forms.
 Symptoms after 1-3 days: fever, headache, respiratory
distress, bloody mucus.
 Rapidly leads to respiratory failure and shock.
 Only form that spreads person-to-person via aerosolized
droplets.
 Mortality rate ~100% untreated; ~50% with antibiotics.
Plague
Bubonic plague (above) by

Yersinia pestis
Bubo – swollen lymph
node (systemic
infection)
Antibiotics effective, but
must be given promptly
after exposure Figure 23.10, 11
 Diagnosis: sample fluid from buboes, blood, or sputum;
shows "safety pin" staining.
 Confirmation tests: direct fluorescent antibody, serology,
bacteriophage lysis.
 Antibiotics: gentamicin, fluoroquinolones, streptomycin,
levofloxacin, ciprofloxacin, doxycycline.
 Effective treatment depends on early diagnosis.
 Virulence factors: F1 capsule component avoids
phagocytosis, aiding dissemination.
Figure 25.2.5
: (a) Yersinia pestis infection can cause inflamed and swollen lymph nodes (buboes), like
these in the groin of an infected patient. (b) Septicemic plague caused necrotic toes in this
patient. Vascular damage at the extremities causes ischemia and tissue death. (credit a:
modification of work by American Society for Microbiology; credit b: modification of work by
Zoonotic Febrile Diseases
 A wide variety of zoonotic febrile diseases (diseases that
cause fever) are caused by pathogenic bacteria that require
arthropod vectors.
 These pathogens are either obligate intracellular species of
Anaplasma, Bartonella, Ehrlichia, Orientia, and Rickettsia,
or spirochetes in the genus Borrelia.
 Isolation and identification of pathogens in this group are
best performed in BSL-3 laboratories because of the low
infective dose associated with the diseases.
Five diseases transmitted by ticks
• Relapsing fever – Borrelia transmitted by soft ticks,

reservoir is rodents, fever/jaundice/rose-colored spots
• Lyme disease – Borrelia burgdorferi, field mice
reservoir
• Ehrlichiosis – Ehrlichia transmitted by Ixodes ticks
• Typhus – rickettsias, obligate intracellular parasites
(epidemic typhus by body louse, murine typhus by rat
flea)
• Spotted fevers (Rocky Mountain spotted fever)
Relapsing Fever
 Caused by Borrelia species, primarily B. recurrentis
(louseborne) and B. hermsii (tickborne).
 Transmitted by body louse (Pediculus humanus) and soft-
bodied tick (Ornithodoros hermsi).
 Lice acquire Borrelia from humans; ticks from rodents.
 Infection occurs when Borrelia in vector’s saliva or excreta
enters skin through bites.
 Characterized by cycles of fever and symptoms, giving it the
name "relapsing" fever.
Symptoms and Disease Cycle
 Initial symptoms: high fever (39–43 °C), headache, and
muscle aches.
 Symptoms last about 3 days, then subside but return after a
week.
 The cycle of fever/symptoms can repeat several times if
untreated.
 Caused by antigenic variation of Borrelia, allowing immune
evasion.
 Cyclical nature requires early intervention to disrupt
repeated relapses.
Figure 25.2.11
: A peripheral blood smear from a patient with tickborne relapsing fever. Borrelia appears
as thin spirochetes among the larger red blood cells. (credit: modification of work by
 Diagnosed by observing spirochetes in blood using
darkfield microscopy.
 First-line antibiotics for louseborne relapsing fever:
doxycycline or erythromycin.
 First-line antibiotics for tickborne relapsing fever:
tetracycline or erythromycin.
 Early treatment disrupts the cyclical fever pattern and clears
infection
 .Prompt diagnosis and antibiotic therapy are key to
managing relapsing fever.
Lyme Disease
 Caused by the spirochete Borrelia burgdorferi.
 Transmitted by the bite of hard-bodied, black-legged
Ixodes ticks.
 In the US, I. scapularis transmits B. burgdorferi in the east
and north-central regions; I. pacificus in the west.
 Most commonly reported vector-borne illness in the US.
 Fifth most common Nationally Notifiable disease in 2014.
Tick Life Cycle and Reservoirs
 Ixodes ticks have a 2-year life cycle with four developmental
stages.
 Deer, mice, and birds can serve as reservoirs for B.
burgdorferi.
 Ticks require a blood meal at each stage: larvae, nymph,
and adult.
 Larvae may acquire B. burgdorferi from their first blood
meal, typically from mice.
 Nymphs can feed on humans and are the primary stage for
transmission.
Lyme Disease
Figure 23.13a
Lyme Disease
Figure 23.13b, c
Lyme Disease
 First symptom
 bull's eye rash
 Second phase
 Irregular heartbeat,
encephalitis
 Third phase
 Arthritis
Figure 23.14
Transmission and Infection Process
 Nymphs feed on small rodents, humans, or other animals,
burrowing into the skin.
 Feeding period lasts several days to a week, with
transmission usually requiring 24 hours.
 Adults primarily feed on larger animals, like deer, and
occasionally humans.
 Ticks mate and produce eggs, continuing the transmission
cycle.
 Infection risk is highest in late spring and summer when
nymphs are most active.
Symptoms of Lyme Disease
 Early Localized Stage: Bull's-eye rash (erythema migrans)
at the tick bite site (70-80% of cases).
 Rash forms 3 to 30 days after the bite, average is 7 days, and
may be warm to the touch.
 Other early symptoms: flu-like symptoms, malaise,
headache, fever, and muscle stiffness.
 Early Disseminated Stage: Severe headache, neck
stiffness, facial paralysis, arthritis, and carditis (days to
weeks later).
 Late Stage: Chronic inflammation leading to arthritis,
meningitis, encephalitis, and altered mental states,
potentially fatal if untreated.
 Presumptive Diagnosis: Bull’s-eye rash combined with other
symptoms.
 Indirect immunofluorescent antibody (IFA) and skin biopsy
can visualize bacteria.
 Serological Tests: ELISA to detect serum antibodies.
 Early Stage Treatment: Amoxicillin or doxycycline effective.
 Late Stage Treatment: Penicillin G, chloramphenicol, or
ceftriaxone
Figure 25.2.10
: (a) A characteristic bull’s eye rash of Lyme disease forms at the site of a tick bite. (b) A
darkfield micrograph shows Borrelia burgdorferi, the causative agent of Lyme disease. (credit a:
modification of work by Centers for Disease Control and Prevention; credit b: modification of
work by American Society for Microbiology)
Anaplasmosis
 Cause: Zoonotic tickborne disease caused by Anaplasma
phagocytophilum.
 Geographic Distribution: Primarily in the central and
northeastern US, Europe, and Asia.
 Symptoms: Mild flu-like illness; severe in 50% of cases,
with <1% mortality rate.
 Reservoirs: Small mammals like white-footed mice,
chipmunks, and voles.
 Vector: Transmitted by the bite of an Ixodes tick.
Diagnosis and Treatment of Anaplasmosis
•Virulence Factors: Includes adherence factors and
immune-evading mechanisms.
•Diagnostic Methods:
•Microscopic examination of neutrophils/eosinophils
(Giemsa/Wright stain).
•PCR for A. phagocytophilum detection.
•Serological tests for antibody titers.
•First-Line Treatment: Doxycycline.
•Hospitalization: Required for at least 50% of cases.
•Outcome: Rare fatalities (<1%) with proper treatment.
Ehrlichiosis
 Cause: Zoonotic tickborne disease caused by Ehrlichia
chaffeensis.
 Geographic Distribution: Primarily in the eastern US, with
occasional cases in the West.
 Vector: Transmitted by the lone star tick (Amblyomma
americanum).
 Symptoms: Flu-like symptoms, with a rash more common
in children (60%) and adults
(less than 30%).
 Rash Types: Petechial, maculopapular
, and macular rashes.
Diagnosis and Treatment of Ehrlichiosis
 Virulence: E. chaffeensis infects monocytes, forming
intracellular microcolonies.
 Diagnosis: Confirmed through PCR and serological tests.
 First-Line Treatment: Doxycycline for adults and children.
 Key Diagnostic Feature: Intracellular microcolonies in
monocytes.
 Similarities to Anaplasmosis: Symptoms overlap, but rash is
more common in HME.
Epidemic Typhus
 Cause: Epidemic typhus is caused by Rickettsia prowazekii.
 Transmission: Spread by body lice (Pediculus humanus)
and flying squirrels as animal reservoirs.
 Symptoms: High fever, body aches, and a rash starting on
the abdomen and chest, radiating to extremities.
 Severity: Severe cases can lead to shock, heart damage,
brain tissue damage, and death.
 Chronic Carrier State: Infected humans
can become carriers of R. prowazekii.
Historical Significance and Global Impact
 Historical Role: Epidemic typhus caused millions of deaths
during times of war (e.g., WWI).
 Mortality Rate: Can reach up to 40% in the absence of
treatment, especially in developing countries.
 Recent Outbreaks: Notable outbreaks in Burundi, Ethiopia,
and Rwanda in recent years.
 1997 Outbreak: In Burundi refugee camps, 45,000 cases in a
population of 760,000.
 Decline in the US: Rare in the US due to improved hygiene
and insecticides.
 Challenges in Diagnosis: Symptoms overlap with other
diseases, making rapid diagnosis difficult.
 Diagnostic Methods: PCR for R. prowazekii genes,
immunofluorescent staining of tissue biopsies, and
serology.
 Serology Limitation: Antibody titers take up to 10 days to
develop, delaying diagnosis.
 First-Line Treatment: Antibiotics, typically doxycycline or
chloramphenicol.
 Early Treatment: Treatment is usually started before a
complete diagnosis to prevent severe outcomes.
Murine Typhus
 Cause: Caused by Rickettsia typhi.
 Transmission: Spread by the bite of the rat flea (Xenopsylla
cheopis) from infected rats.
 Symptoms: Includes rash, chills, headache, and fever
lasting about 12 days.
 Additional Symptoms: Some patients experience cough and
pneumonia-like symptoms.
 Severe Illness: Can lead to seizures, coma, renal and
respiratory failure in immunocompromised individuals.
 Diagnosis Methods: Biopsy from rash, indirect
immunofluorescent antibody (IFA) staining, PCR, and
serologic testing.
 Serology: Acute and convalescent serologic testing to
confirm infection.
 Primary Treatment: Doxycycline is the first-line treatment.
 Alternative Treatment: Chloramphenicol as a second choice
for therapy.
 Prognosis: Severe cases can develop in vulnerable
populations, requiring prompt treatment.
Rocky Mountain Spotted Fever (RMSF)
 Cause: Caused by Rickettsia rickettsii.
 Transmission: Spread by hard-bodied ticks (e.g., American
dog tick, Rocky Mountain wood tick, brown dog tick).
 Geographic Range: Endemic in North and South America,
especially in Southeast US (North Carolina, Oklahoma,
Arkansas, Tennessee, Missouri).
 Symptoms: Includes high fever, headache, body aches,
nausea, and vomiting.
 Rash: Petechial rash (similar to measles) starts on
hands/wrists, spreading to trunk, face, and extremities.
Figure 25.2.7
: In the US, Rocky Mountain spotted fever is most prevalent in the southeastern
states. (credit: modification of work by Centers for Disease Control and Prevention)

Tick Life Cycle
Figure 23.17
Pathogenesis and Severity
 Severity: RMSF can be fatal within 8 days if untreated.
 Rash Timing: Rash usually appears on day 6 or later;
petechiae indicate progression to severe disease.
 Fatalities: Due to increased vascular permeability,
hypotension, cardiac arrest, or ischemia following blood
coagulation.
 Mortality Rate: 3% or higher, even with clinical support if
untreated.
 Prognosis: Early treatment is critical before petechiae
formation to reduce mortality.
Spotted Fevers (Rocky Mountain spotted fever)
 Rickettsia rickettsii
 Measles-like rash except that
the rash appears on palms and
soles too
 Prognosis: Early treatment is
critical before petechiae
formation to reduce mortality.
Figure 23.18
 Diagnosis Methods: Based on symptoms, fluorescent
antibody staining of biopsy, PCR, and serologic tests.
 Challenges: RMSF can mimic other diseases, making
diagnosis difficult.
 First-Line Treatment: Doxycycline is the primary treatment.
 Alternative Treatment: Chloramphenicol is used if
doxycycline is unavailable.
 Clinical Support: Early treatment is essential to reduce
complications and improve survival rates.
End of Lecture

Dr. Nabil A. ElAila
1
Epstein-Barr Virus (EBV)
Epstein-Barr Virus (EBV)
 Belong to the gammaherpesvirus subfamily of
herpesviruses (Human Herpesvirus 4 (HHV-4)
 Nucleocapsid 100 nm in diameter, with 162 capsomers
 Membrane is derived by budding of immature particles
through cell membrane and is required for infectivity.
 Genome is a linear double stranded DNA molecule with
172 kbp
 The viral genome does not normally integrate into the
cellular DNA but forms circular episomes which reside in
the nucleus.
 The genome is large enough to code for 100 - 200 proteins
but only a few have been identified.
Dr. Nabil El Aila Med. Virology

Epidemiology
 EBV infects over 90% of the world's population, often
acquired during childhood or adolescence.
 Spread primarily through saliva ("kissing disease"), but also
via blood, organ transplants, and perinatal exposure.
 In developing countries, primary infection occurs in early
childhood; in developed regions, it’s more common during
adolescence
 Linked to Burkitt lymphoma, Hodgkin lymphoma,
nasopharyngeal carcinoma, and other malignancies,
especially in immunocompromised individuals.
 Disease associations vary; e.g., Burkitt lymphoma is
common in malaria-endemic areas, while nasopharyngeal
carcinoma is prevalent in East Asia.
Antigenic components of the virus
 Viral capsid antigen (VCA)
 Early antigens (EAs)
 Epstein-Barr nuclear antigen (EBNA).

Pathogenesis
 The infection first occurs in the oropharynx and then spreads to
the blood, where it infects B lymphocytes.
 Cytotoxic T lymphocytes react against the infected B cells. The T
cells are the "atypical lymphs" seen in the blood smear. EBV
remains latent within B lymphocytes.
 A few copies of EBV DNA are integrated into the cell genome;
many copies of circular EBV DNA are found in the cytoplasm.
 The immune response to EBV infection consists first of IgM
antibody to the VCA. IgG antibody to the VCA follows and
persists for life.
Pathogenesis
 The IgM response is therefore useful for diagnosing acute
infection, whereas the IgG response is best for revealing prior
infection.
 Lifetime immunity against second episodes of infectious
mononucleosis is based on antibody to the viral membrane
antigen.
 In addition to the EBV-specific antibodies, nonspecific heterophil
antibodies are found.
 The term "heterophil" refers to antibodies that are detected by
tests using antigens different from the antigens that induced them.
 The heterophil antibodies formed in infectious mononucleosis
agglutinate sheep or horse red blood cells in the laboratory.
Disease Association
1. Infectious Mononucleosis
2. Burkitt's lymphoma
3. Nasopharyngeal carcinoma
4. Lymphoproliferative disease and lymphoma in the
immunosuppressed.
5. X-linked lymphoproliferative syndrome
6. Chronic infectious mononucleosis
7. Oral leukoplakia in AIDS patients
8. Chronic interstitial pneumonitis in AIDS patients.

Infectious Mononucleosis
 Illness results from primary infection with EBV. A clinically apparent
illness usually only develops when primary infection occurs in
adolescence or adulthood.
Clinical Features:
incubation period - 4 to 7 weeks
route of infection - close contact, kissing. Virus is secreted intermittently
in the saliva of asymptomatic carriers.
Signs and symptoms - fever, generalised lymphadenopathy, sore throat,
malaise, tiredness, splenomegaly, hepatomegaly, abnormal liver function
tests and atypical lymphocytosis in the peripheral blood. The disease is
self limiting, but convalescence may be prolonged in some cases.
 Diagnosis of IM is usually made by the heterophil antibody test and/or
detection of EBV IgM.
 There is no specific treatment.
Infectious mononucleosis
Burkitt’s Lymphoma
 A fast-growing cancer of B cells caused by EBV, often in
malaria or HIV patients.
 Burkitt's lymphoma (BL) occurs endemically in parts of
Africa (where it is the commonest childhood tumour) and
Papua New Guinea.
 It usually occurs in children aged 3-14 years.
 It responds favorably to chemotherapy.
 It is restricted to areas with holoendemic malaria. Therefore it
appears that malaria infection is a cofactor.

Burkitt Lymphoma (BL)
 Targeted Cells: BL involves solid tumors primarily made of
abnormal B cells.
 HIV and Malaria: Lead to polyclonal B-cell activation and
uncontrolled EBV+ B-cell proliferation, causing lymphoma.
 Multiple copies of EBV genome and some EBV antigens can be
found in BL cells and patients with BL have high titres of
antibodies against various EBV antigens.
Figure 1. (a) Burkitt lymphoma can cause large tumors. (b) Characteristic irregularly shaped
abnormal lymphocytes (large purple cells) with vacuoles (white spots) from a fine-needle
aspirate of a tumor from a patient with Burkitt lymphoma. (credit a: modification of work by
Bi CF, Tang Y, Zhang WY, Zhao S, Wang XQ, Yang QP, Li GD, and Liu WP; credit b: modification
of work by Ed Uthman)
Cancers Associated with EBV
 Nasopharyngeal Carcinoma (China)
 Burkitt's Lymphoma (Africa)!!

Diagnosis
 In the hematologic approach, absolute lymphocytosis occurs and as many
as 30% abnormal lymphocytes are seen on a smear.
 These atypical lymphs are large and have a lobulated nucleus and a
vacuolated, basophilic cytoplasm.
 They are cytotoxic T cells that are reacting against the EBV-infected B cells.
 Specific serological tests:
Antibody to the viral capsid and nuclear antigens are useful for confirming
the diagnosis of acute IM:
IgG and IgM to Viral capsid antigen (VCA): detectable early during the
acute phase
VCA IgM: only present during acute phase
IgG to EBV nuclear antigens (EBNA): detectable late in convalescence (>
6 months post infection)
Normal Lymphocyte
Atypical lymphocytes
Diagnosis
 Acute EBV infection is usually made by the heterophil antibody
test and/or detection of anti-EBV VCA IgM.
 Cases of Burkitt’s lymphoma should be diagnosed by histology.
The tumour can be stained with antibodies to lambda light chains
which should reveal a monoclonal tumour of B-cell origin. In
over 90% of cases, the cells express IgM at the cell surface.
 Cases of Naso Pharyngeal Carcinoma should be diagnosed by
histology.
 The determination of the titre of anti-EBV VCA IgA in screening
for early lesions of NPC and also for monitoring treatment.
 A patient with non-specific ENT symptoms who have elevated
titres of EBV IgA should be given a thorough examination.

Heterophile antibody test (Paul-Bunnell)
 Secreted by infected B cells.
 Can agglutinate cells from other species (sheep RBCs).
 Not directed against EBV.
 A titer of 1:40 is considered positive for acute IM.
 Positivity: 50% 1st week of illness, and 60-90% in the 2nd or
3rd weeks.

Treatment of Burkitt Lymphoma
 Treatment Regimen: Intensive chemotherapy (CODOX-
M/IVAC) plus rituximab.
 Chemotherapy Drugs: Includes cyclophosphamide,
vincristine, doxorubicin, methotrexate, etc.
 High Cure Rate: Greater than 90% cure rate in both
children and adults.
 Fast Growing Tumors: Rapid treatment initiation is critical
due to the speed of tumor growth.
 Immunodeficiency-Associated: Burkitt lymphoma is more
common in HIV-infected patients.
Treatment
 No antiviral therapy is necessary for uncomplicated infectious
mononucleosis.
 Acyclovir has little activity against EBV, but administration of
high doses may be useful in life-threatening EBV infections.

 Prevention
 There is no EBV vaccine.

Cytomegalovirus

Properties
 Belong to the betaherpesvirus subfamily of herpesviruses
 double stranded DNA enveloped virus
 Nucleocapsid 105nm in diameter, 162 capsomers
 The structure of the genome of CMV is similar to other
herpesviruses, consisting of long and short segments which
may be orientated in either direction, giving a total of 4
isomers.
 A large no. of proteins are encoded for, the precise number
is unknown.

CMV Transmission
 Body Fluid Contact: Transmitted via saliva, urine, blood,
and other fluids.
 Common Modes: Spread through sexual contact, nursing,
transfusions, and organ transplants.
 Congenital Transmission: Can cross the placenta, leading to
congenital CMV in infants.
 Infection in Newborns: Possible during birth or through
breastfeeding.
 Frequency: Occurs in about 1 in 150 US infants.
Epidemiology
 CMV is one of the most successful human pathogens, it can be
transmitted vertically or horizontally usually with little effect on
the host.
 Transmission may occur in utero, perinatally or postnatally. Once
infected, the person carries the virus for life which may be
activated from time to time, during which infectious virions appear
in the urine and the saliva.
 Reactivation can also lead to vertical transmission. It is also
possible for people who have experienced primary infection to be
reinfected with another or the same strain of CMV, this reinfection
does not differ clinically from reactivation.
 In developed countries with a high standard of hygiene, 40% of
adolescents are infected and ultimately 70% of the population is
infected. In developing countries, over 90% of people are ultimately
infected.
Pathogenesis
 The virus may be transmitted in utero, perinatally, or postnatally.
Perinatal transmission occurs.
 Perinatal infection is acquired mainly through infected genital
secretions, or breast milk. Overall, 2 - 10% of infants are infected
by the age of 6 months worldwide.
 Postnatal infection mainly occurs through saliva.
 Sexual transmission may occur as well as through blood and
blood products and transplanted organ.

Clinical Manifestations
 Congenital infection - may result in cytomegalic inclusion
disease
 Perinatal infection - usually asymptomatic
 Postnatal infection - usually asymptomatic. However, in a
minority of cases, the syndrome of infectious mononucleosis may
develop which consists of fever, lymphadenopathy, and
splenomegaly. The heterophil antibody test is negative although
atypical lymphocytes may be found in the blood.
 Immunocompromised patients such as transplant recipients and
AIDS patients are prone to severe CMV disease such as
pneumonitis, retinitis, colitis, and encephalopathy.
 Reactivation or reinfection with CMV is usually asymptomatic
except in immunocompromised patients.

Congenital Infection
 Defined as the isolation of CMV from the saliva or urine
within 3 weeks of birth.
 Commonest congenital viral infection, affects 0.3 - 1% of all live
births. The second most common cause of mental handicap
after Down's syndrome and is responsible for more cases of
congenital damage than rubella.
 Transmission to the fetus may occur following primary or
recurrent CMV infection. 40% chance of transmission to the
fetus following a primary infection.
 May be transmitted to the fetus during all stages of pregnancy.

Cytomegalic Inclusion Disease
 CNS abnormalities - microcephaly, mental retardation,
spasticity, epilepsy, periventricular calcification.
 Eye - choroidoretinitis and optic atrophy
 Ear - sensorineural deafness
 Liver - hepatosplenomegaly and jaundice which is due to
hepatitis.
 Lung - pneumonitis
 Heart - myocarditis
 Thrombocytopenic purpura, Haemolytic anaemia
 Late sequelae in individuals asymptomatic at birth - hearing
defects and reduced intelligence.
Laboratory Diagnosis (1)
 Direct detection
 biopsy specimens may be examined histologically for
CMV inclusion bodies or for the presence of CMV
antigens. However, the sensitivity may be low.
 The pp65 CMV antigenaemia test is now routinely used
for the rapid diagnosis of CMV infection in
immunocompromised patients.
 PCR for CMV-DNA is used in some centers but there
may be problems with interpretation.

CMV pp65 antigenaemia test
(Virology Laboratory, New-Yale Haven Hospital)

Laboratory Diagnosis (2)
 Virus Isolation
 conventional cell culture is regarded as gold standard but requires
up to 4 weeks for result.
 More useful are rapid culture methods such as the DEAFF Detection
of early antigen fluorescent foci
 test which can provide a result in 24-48 hours.
 Characteristic Cell Sign: CMV cells show an “owl’s eye”
inclusion on staining
 Serology
 Prenatal Screening: CMV is included in TORCH testing during
pregnancy.
 the presence of CMV IgG antibody indicates past infection.
 The detection of IgM is indicative of primary infection although it
may also be found in immunocompromised patients with
reactivation.
Figure 2. Cells infected with CMV become enlarged and have a characteristic
“owl’s eye” nucleus. This micrograph shows kidney cells from a patient with
CMV. (credit: modification of work by Centers for Disease Control and
Prevention)
Cytopathic Effect of CMV
(Courtesy of Linda Stannard, University of Cape Town, S.A.)

DEAFF test for CMV
(Virology Laboratory, New-Yale Haven Hospital)

Specimens for Laboratory Diagnosis
Site for virus culture Serology
Urine Saliva Blood Tissue affected IgG IgM
Neonates + + - - - +
Adults + - + - + +
Pregnant women - - - - + +
Immunocompromised + + + + + -

CMV Treatment
 Antiviral Treatments:
 Ganciclovir, valganciclovir, foscarnet, and cidofovir for
severe cases.
Arthropod-Borne Viral Diseases
 There are a number of arthropod-borne viruses, or
arboviruses, that can cause human disease.
 Among these are several important hemorrhagic fevers
transmitted by mosquitoes.
 Three that pose serious threats: yellow fever, chikungunya
fever, and dengue fever.
Viral Hemorrhagic Fevers
Yellow Fever Virus

Yellow Fever
 Yellow fever is an acute, febrile illness; severe cases are
characterized by liver dysfunction which leads to jaundice
(hence the naine yellow fever), Renal dysfunction and
hemorrhage with high mortality
Structure
 Yellow fever Virus is an arbovirus
 Family:- Flaviviridae, Genus:- Flavivirus
 Enveloped, spherical particles 50nm in diameter with
icosahedral nucleocapsid symmetry and surface projections
 Nucleic acid:- Linear, positive-sense, single-stranded RNA,
11kb long
 Seven genotypes have been identified based on the
genomic sequence
 2 genotypes in South America (South America I and II)and
 5 genotypes in Africa, namely,
Transmission
 Vector:- Aedes aegypti or the tiger mosquito
 Transntission Cycle:-
 1. Jungle cycle - between monkeys and forest mosquito
 2. Urban Cycle- between humans and urban mosquito
(Aedes aegypti)
Clinical Manifestation
 Incubation period- 3-6 days
 Febrile illness occurs in the early stages of the disease and is
characterized by
 Presence of fever, chills, headache, dizziness, myalgia and
back ache - followed by nausea, vomiting and relative
bradycardia
 Around 15% progress to severe symptoms like jaundice and
vomiting.
 Symptoms in Severe Cases: Includes petechial rash,
mucosal hemorrhages, and epigastric tenderness.
 Severe Complications: Includes delirium, seizures, shock,
and multi-organ failure.
.
Clinical Manifestation
Severe cases are characterize by
 Hemorrhagic manifestations
 Platelet dysfunction
 Features of Liver involvement (Hepatitis)
 Mid-Zonal necrosis and presence of councilman bodies
 Intranuclear inclusion may be seen inside the
hepatocytes called Torres bodies
 Appearance of jaundice
 Renal dysfunction
 Encephalitis occurs very rarely
 Morality rate is high (>20%), especially among children and
elderly.
Lab Diagnosis
 Serology:- IgM ELISA can be done after 3 days of onset of
symptoms.
 Gives false positive results in other flavivirus infections
(Dengue, West Nile and Zika virus)
 People who are vaccinated within 30 days Positive test
confirmed by Plaque-reduction neutralization test. -
More specific
 Molecular Method:-
 RT-PCR detecting specific viral RNA (NS 5 region) in blood
are more confirmatory than serology.
 It should be performed within 10 days of onset of
symptoms.
Yellow fever Vaccine
 Ye11ow fever 17D Vaccine
 Live attenuated vaccine (Contra indicated in people having
allergic to egg)
 Strict cold chain has to be maintained during the transport
(+5C to -30 C).
 Available in Lyophilized form, once reconstituted it should
be used within 1/2 hour
 Vaccine is effective within 7 days of administration, the
efficacy lasts for upto 35 years
 Cholera and yellow fever vaccine interact with each other;
hence should not given together (3 weeks gap to be
maintained).
Treatment
 No Specific Treatment: Treatment is limited to supportive
care.
 Hospitalization: Patients often hospitalized for observation
and care.
 Symptom Management: Focuses on supportive care to
manage symptoms.
 Preventive Care: Use of mosquito control measures like
insect repellents and netting.
Dengue fever Virus
Dengue Fever Virus (DENV)
 Nickname: "Breakbone fever" due to extreme joint and
muscle pain.
 RNA Virus
 Family: Flaviviridae
 Genus: Flavivirus
 Enveloped virus
 3 major proteins
 SS positive sense RNA
 Transmission
 Arthropods (mosquitoes or ticks)
 Arbovirus (arthropod-borne virus)
Dengue Fever Virus (DENV)
 Transmitted by: Aedes aegypti and Aedes albopictus

mosquitoes.
 Global Distribution: Primarily tropical regions, affecting
millions yearly.
 There are four Serotypes of the virus: DENV-1, DENV-2,
DENV-3, DENV-4,
 All serotypes can cause the full spectrum of disease.
 Immunity: Lifelong immunity to the infecting serotype.
Short-term protection against other serotypes
Epidemiology
 Mortality:
 Without treatment: 1-5%
 With adequate treatment: Less than 1%
 Severe disease: 26%
 Global Impact:
 Endemic in over 110 countries
 50-100 million infections annually
 500,000 hospitalizations annually
 12,500-25,000 deaths annually
Dengue Infection
Clinically significant Dengue infection may be
1. Simple dengue fever (DF)
2. Dengue hemorrhagic fever (DHF)

(plasma leak <5%)
3. Dengue Shock Syndrome (DSS)

(plasma leak >5%)
Characteristic Symptoms:
• Fever > 2 and < 10 days (essential criterion)

• Headache (behind the eyes)
• Muscle and joint pain, Rash (similar to measles)
• Skin rash
• Severe Symptoms (in a small proportion of cases):
•Dengue Hemorrhagic Fever
•Bleeding
•Low blood platelets
•Blood plasma leakage
•Dengue Shock Syndrome
•Dangerously low blood pressure
Clinical course of Dengue fever virus
 The course of dengue infection is divided into three
phases:
• Febrile phase
• Critical phase
• Recovery phase
Febrile Phase
• High fever (over 40°C/104°F), often biphasic (breaks and
returns)
• Generalized pain
• Headache (lasts 2-7 days)
• Early Rash: Flushed skin (days 1-2)
• Late Rash: Measles-like rash (days 4-7)
• Petechiae: Small red spots that do not disappear when
pressed, caused by broken capillaries
• Bleeding: Mild bleeding from mucous membranes (mouth
and nose)
•People generally don’t die during this stage
Critical phase
 Follows the resolution of high fever
 Typically lasts one to two days
 Is associated with plasma leak – volume depletion & shock
 Fluid Accumulation: Significant fluid accumulation in the
chest and abdominal cavity due to increased capillary
permeability and leakage
 This lead to the Depletion of fluid from circulation and
decreased blood supply to vital organs
 Organ dysfunction and severe bleeding typically from the
gastrointestinal tract)
 Dengue shock syndrome and dengue hemorrhagic fever
occur in less than 5% of all cases of dengue
 This is the phase where management is critical
58
Recovery phase
 Resorption of leaked fluid into the bloodstream
 This usually lasts two to three days
 Severe itching and slow heart rate
 During this stage, a fluid overload state may occur. If it
affects the brain, it may cause a reduced level of
consciousness or seizures
 This is the phase where people die because of the problems
faced during the critical stage
Diagnosis
•Clinical Diagnosis:
•Based on reported symptoms and physical examination
•It is especially common in endemic areas
•Early Disease: Can be difficult to differentiate from other
viral infections
•Laboratory Tests:
•Diagnostic value during the acute phase
•Serology can be used in later stages
•Antibody Tests: IgG and IgM antibodies can confirm
diagnosis in later stages
•IgG Detection: Not diagnostic unless blood samples are
collected 14 days apart and a fourfold increase in IgG levels is
detected
• RT-PCR of blood.
IgG antibody - specific to
the initial infecting DV
serotype + cross reacting
antibody
IgM antibody to the

secondary infecting DV
serotype
Following primary infection –

Specific antibody response + CMI (memory T cells)
Cross reactive antibody response + CMI (memory T cells)
61
Dr. S Guanasena
Treatment, and Prevention
 Treatment:
 Supportive Care: Rest, hydration, and antipyretics (e.g.,
paracetamol for fever).
 Severe Cases: Hospitalization for intravenous fluids, blood
transfusion (if hemorrhage occurs), and monitoring for shock
syndrome.
 Prevention
 . Mosquito Control: Eliminate standing water, use insecticides,
and encourage use of mosquito nets and repellents.
 Vaccination: Dengvaxia is a type of chimeric vaccine,
specifically designed to protect against dengue virus.
 It is a live-attenuated recombinant vaccine created by
combining genetic material from the four serotypes of the
dengue virus (DENV-1 to DENV-4) with the yellow fever virus
backbone. Microbial Diseases of the Circulatory and Lymphatic System - - Dr. Nabil Elaila 62
Ebola Virus Disease (EVD)
 The Ebola virus is a severe infectious disease in humans and
primates.
 First appeared in 1976 at Nzara in Sudan and at Yambuku in
the Democratic Republic of Congo near the Ebola River in
Africa.
 Ebola is a negative RNA virus. a BSL-4 level filovirus
(species of Ebolavirus).
 There are different species of the Ebola virus.
 Reston ebolavirus was first discovered in laboratories in
Reston, United States of America (USA)
 Ebola virus is responsible for viral hemorrhagic fevers like:
Lassa fever, Yellow fever, Marburg, Dengue fever
 2014 Outbreak: Affected 10 countries, with over 28,000
cases and 11,000 deaths.
Modes of Transmission of the Ebola Virus
 Unsterilized needles
 Sub-optimal hospital conditions
 Personal contact
 Through blood-to-blood contact
 Human-to-human transmission
 Reusing needles and blood gloves in hospitals
 Ebola is introduced into the human population through
close contact with the blood, secretions, organs, or other
bodily fluids of infected animals
Mechanism of Action of the Ebola Virus
 Every tissue is affected, except bones and muscles.
 The virus creates blood clots.
 Clots go towards internal organs (lungs, eyeballs).
 It prevents oxygen from reaching tissues.
 The virus also destroys connective tissue (affinity with
collagen).
Early Symptoms of Ebola
 High temperature (at least 38.8°C)
 Muscle, joints, and abdominal pain
 Sore throat, fatigue, and general discomfort.
 Nausea
 Bloodstream slow down
 Loss of appetite
 Rashes
 Increased liver enzyme activity
Lab Diagnosis
 Antibody-capture enzyme-linked immunosorbent assay
(ELISA)
 Antigen-capture detection tests
 Serum neutralization test
 Reverse transcriptase polymerase chain reaction (RT-PCR)
assay
 Electron microscopy
 Virus isolation by cell culture
Treatment
 There are no licensed specific treatments.
 Patients are frequently dehydrated and require oral
rehydration with solutions containing electrolytes.
 New drug therapies are being evaluated.
 However, there have been very recent developments in
preventative medication.
Prevention and Control
 a. Hospitals must follow precautionary methods, such as:
 Wearing glovesIsolating infected individuals
 Practicing nurse barrier techniques
 Proper sterilization and disposal of all equipment
 b. Burials must be done correctly:
 No washing or touching the carcass
 Put into body bags and bury outside the city
 c. Report any questionable illness to officials
Hantavirus
 Hantavirus: A genus of over 20 known rodent-borne viruses
belonging to the Bunyaviridae family.
 Human Diseases: 11 species of hantavirus are associated
with human diseases.
 Syndromes: Two major forms of hantavirus syndromes:
 Hemorrhagic fever with renal syndrome (HFRS): Found in
the Old World.
 Hantavirus cardiopulmonary syndrome (HCPS, also called
HPS): Found in the New World.
Epidemiology of Hantavirus
 Hemorrhagic Fever with Renal Syndrome
 (HFRS):Approximately 150,000 to 200,000 cases
hospitalized annually worldwide.
 Most cases occur in developing countries.
 Case fatality rate ranges from <3% to 12% depending on the
virus.
 Geographic Distribution:
 Only one case reported from Africa.
 No cases reported in Rwanda.
Transmission of Hantavirus to Humans
 Contact with Rodent Excreta: Hantavirus can be
transmitted through contact with infected rodent excreta
(urine, saliva, feces, dead body, or blood).
 Inhalation, Mucosa Contact, or Bite: The virus can enter
the body through inhalation, contact with mucous
membranes, or a bite from an infected rodent.
Clinical Features
 A 2-3 weeks incubation period is followed by a protracted
clinical course
 Hantavirus pulmonary syndrome (HPS) initial Symptoms:
Flu-like signs—headache, fever, muscle aches, nausea,
vomiting.
 Progression of HPS: Leads to pulmonary edema,
pneumonia, shock, and high mortality (up to 50%).
Clinical Features
 The hallmark triad of HFRS comprises of fever, headache,
nausea, hemorrhage, and renal failure.
 Typical Phases:
 Febrile period
 Hypotension
 Oliguria
 Diuresis
 Convalescence phase
 Progression of HFRS: Can cause hemorrhaging, kidney
failure, shock, with a mortality rate up to 15%.
Differential Diagnosis of Hantavirus
 Viral hemorrhagic fevers (dengue fever, etc.)
 Leptospirosis
 DIC
 Malaria
 Hemolytic uremic syndrome
 Sepsis
 Scrub typhus
Lab Diagnosis
 A full blood count (FBC) , Liver function test (LFTS) (LDH,
Transaminases, coagulation factors, albumin)
 Renal function tests (urea, creatinine, electrolytes)
 Additional Tests:
 Cardiac enzymes (CK-MB, troponin)CXR (if respiratory signs)
 ELISA: Detects IgG and IgM antibodies against viral antigens.
 Western blot, rapid immunoblot strip assay (RIBA),
Immunochemistry
 IgM rises with symptom onset, peaks 7-11 days later.
 IgM declines, IgG increases in the convalescent phase.
 Plaque Reduction Neutralization Test: Gold standard for
serological diagnosis, distinguishes between Hantavirus
species. Requires BSL-3 laboratory.
 Other Tests: RT-PCR: Detects viral RNA in blood clots.
77
Management of Hantavirus
 No Specific Therapy: Currently, no specific therapy exists
for HFRS.
 Supportive Care: The cornerstone of treatment is
supportive management.
 ICU Admission: Early admission to an ICU for monitoring
vital signs (blood and tissue oxygenation, cardiac output,
central blood pressure, and cerebral pressure).
 Fluid Balance: Careful monitoring and management of
fluid balance based on patient status, urine output, and
kidney function.
 Haemodialysis: Usually one or two sessions are required
for HFRS treatment.
 Ribavirin shows antihantaviral effect invitro and invivo
Prevention of Hantavirus
 Rodent Control: Control of rodents in houses and
avoidance of exposure to rodent excreta in rural settings.
 Vaccines: Vaccines are being studied in animals, and some
countries like Korea are using them in military camps.
End of Lecture
81
Dr. Nabil A. ElAila
1
Chagas Disease
 Also known as American trypanosomiasis.
 A neglected tropical disease (NTD) caused by Trypanosoma
cruzi.
 Transmitted primarily by triatomine (kissing) bugs.
 The bug bites near the face, often defecating at the bite site.
 Fecal matter rubbed into bite or mucous membranes causes
infection.
Transmission & Prevalence
 Spread through infected bug bites, blood transfusions,
organ transplants, and congenital transmission.
 Endemic in Mexico, Central America, and South America.
 6–7 million people estimated to be infected (WHO).
 Bugs feed on humans and animals, defecating near the bite.
Phases of Chagas Disease
 Three stages: acute, intermediate, and chronic.
 Symptoms vary with patient immunocompetence.
 Acute phase: symptoms may resolve but infection can
persist.
 Intermediate phase: asymptomatic with low blood
parasite levels.
 Chronic phase: life-threatening complications may
develop.
Acute Phase Symptoms
 Symptoms: fever, headache, rash, vomiting, diarrhea.
 Enlarged spleen, liver, lymph nodes; chagoma at entry
point.
 Romaña's sign: swelling near bite (eyelids, face).
 Can spontaneously resolve, but untreated can harm heart or
brain.
 Rare cases of myocarditis or meningoencephalitis in
children
Chronic Phase Complications
 Often occurs decades after initial infection.
 Possible complications: swollen colon, bowel obstruction.
 Enlarged esophagus leads to dysphagia, malnutrition.
 Flaccid cardiomegaly can lead to heart failure, sudden
death.
 Chronic phase may be debilitating or fatal.
Diagnosis & Treatment
 Diagnosed through microscopy, IFA, EIAs, PCR, or
culturing.
 Xenodiagnosis in endemic areas (bugs feed on patient,
tested for T. cruzi).
 Medications: nifurtimox and benznidazole effective in
acute phase.
 Lower efficacy in chronic phase.
 Vector control is key to prevention.
Figure 25.4.6
: (a) Trypanosoma cruzi protozoan in a blood smear from a patient with Chagas disease. (b)
The triatomine bug (also known as the kissing bug or assassin bug) is the vector of Chagas
disease.

Toxoplasmosis
 Cause: Protozoan Toxoplasma gondii.
 Hosts: Birds, mammals, with domestic cats as the only
definitive hosts.
 Transmission to Humans: Through contact with infected
cat feces, litter, or contaminated environments.
 Prevalence: 22.5% of U.S. population (12+ years) infected;
often asymptomatic in immunocompetent people.
 Risk Groups: Immunocompromised individuals, pregnant
women, and fetuses.
Life Cycle of T. gondii
 Oocyst Shedding: Cats shed unsporulated oocysts in feces.
 Sporulation: Oocysts become infective 1–5 days after
shedding.
 Intermediate Hosts: Birds and rodents ingest oocysts,
forming tissue cysts.
 Behavioral Changes in Hosts: Infected mice lose fear of cats,
aiding parasite transmission.
 Transmission to Cats: Cats become infected by eating
infected birds or rodents.
Toxoplasmosis – Toxoplasma gondii
 Toxoplasma
gondii
Figure 23.23
Symptoms and Effects in Humans
 Asymptomatic in Most: Many infections go unnoticed or
cause mild symptoms.
 Behavioral Influence: Possible influence on human
personality and psychomotor skills.
 Severe Complications: In immunocompromised
individuals, reactivated cysts cause encephalitis, seizures,
and can be fatal.
 Organ Damage: Cysts can affect brain, lungs, and other
tissues.
 Treatment Needed: For severe cases, especially in
immunocompromised patients.
Risks During Pregnancy
 Transmission to Fetus: Tachyzoites can cross the placenta.
 Fetal Impact: Risk of fetal loss, CNS damage, blindness, or
mental retardation.
 Factors Affecting Severity: Maternal health, gestational age,
and parasite virulence.
 Precautions for Pregnant Women: Safe handling of meat,
gardening, and pet care.
 CDC Recommendations: Special care advised for pregnant
women to prevent infection.
Diagnosis of Toxoplasmosis
 Serology: TORCH testing (T stands for Toxoplasmosis) for
maternal infection.
 Fetal Diagnosis: PCR testing for T. gondii DNA in amniotic
fluid.
 Tissue Observation: Cysts can be seen in stained biopsy
specimens.
 Imaging: CT, MRI, and lumbar puncture for detection in
adults.
 Differentiating Symptoms: Important due to similarities
with other conditions.
Figure 25.4.4
: (a) Giemsa-stained Toxoplasma gondii tachyzoites from a smear of peritoneal fluid
obtained from a mouse inoculated with T. gondii. Tachyzoites are typically crescent shaped
with a prominent, centrally placed nucleus. (b) Microscopic cyst containing T. gondii from
mouse brain tissue. Thousands of resting parasites (stained red) are contained in a thin
parasite cyst wall.
Prevention and Treatment
 Preventive Measures: Handwashing, cooking meat
thoroughly, avoiding cat litter.
 Food Safety: Cook meat to 74-76°C to kill parasites.
 Treatment for High-Risk Groups: Pyrimethamine and
sulfadiazine for neonates, pregnant women, and
immunocompromised (except first trimester).
 First Trimester Caution: Spiramycin used to reduce fetal
transmission as it doesn’t cross the placenta.
 No Treatment for Most: Immunocompetent individuals
usually don’t need intervention.
Malaria
 Global Impact: Over 214 million cases and 438,000 deaths
in 2015, mainly in Africa.
 Population at Risk: More than half of the world’s
population.
 Cause: Protozoan parasites in the genus Plasmodium (e.g.,
P. falciparum, P. vivax).
 Transmission: Through bites of infected Anopheles
mosquitoes.
 Current Threats: Potential for reintroduction
in malaria-free regions.
Malaria
Figure 23.24
Common Species and Severity
 Most Lethal Species: P. falciparum (causes falciparum
malaria).
 Affected Regions: High prevalence in Africa and Asia.
 Other Species: P. knowlesi, P. malariae, P. ovale, and P.
vivax.
 Impact on Blood Cells: Plasmodium infects and destroys
red blood cells.
 Organ Damage: Infection can lead to severe damage to the
spleen, liver, and bone marrow
Symptoms and Disease Progression
 Classic Symptoms: Cycles of fever, chills, and sweating.
 Initial Symptoms: Malaise, chills, fever, headache, and
nausea.
 Hemolysis: Leads to “sludge blood,” causing oxygen
deprivation and organ failure.
 Severe Outcomes: Necrosis of blood vessels, organ failure,
and death.
 Cycle Frequency: Fever cycles every 2 days (tertian) or 3
days (quartan), varying by Plasmodium species.
Life Cycle of Plasmodium
 Sporozoite Stage: Injected by mosquito, travels to the liver.
 Schizont Formation: In the liver, produces merozoites.
 Merozoites: Infect red blood cells, causing symptoms upon
their release.
 Gametocyte Formation: Some parasites form gametocytes
taken up by mosquitoes.
 Mosquito Phase: Gametocytes develop into zygotes,
forming sporozoites to complete the cycle.
Malaria
Figure 23.25
Malaria
Figure 12.19
 Diagnosis: Blood smear microscopy and rapid EIA assays for
Plasmodium antigens.
 Treatment Drugs: Chloroquine, atovaquone, artemether,
lumefantrine.
 Drug Resistance: Some Plasmodium species are resistant to
antimalarial drugs.
 Prophylactic Measures: Medications can be prescribed for
prevention.
 No Vaccine: Efforts are ongoing, but no vaccine is available
yet.
Figure 25.4.2
: A blood smear (human blood stage) shows an early trophozoite in a delicate ring form (upper
left) and an early stage schizont form (center) of Plasmodium falciparum from a patient with
malaria. (credit: modification of work by Centers for Disease Control and Prevention)
Prevention and Control
 Insecticide Use: Reduces mosquito populations.
 Insecticide-Treated Bed Nets: Prevents bites during sleep.
 Vector Control: Essential to limiting disease spread.
 Public Health Initiatives: Focus on reducing exposure and
treating cases.
 Ongoing Research: Aims to develop an effective vaccine and
better treatments.
Leishmaniasis
 Leishmaniasis is a neglected tropical disease (NTD).
 Widespread in tropical and subtropical regions.
 Affects people in over 90 countries worldwide.
 Caused by around 20 species of Leishmania protozoan
parasites.
 Transmitted by sand fly vectors (e.g., Phlebotomus and
Lutzomyia).
Parasite Mechanism
 Leishmania protozoan is phagocytosed by macrophages.
 Uses virulence factors to survive inside phagolysosomes.
 Inhibits enzymes in the phagolysosome, preventing
destruction.
 Parasite replicates within macrophages.
 Infected macrophages burst, spreading the infection to new
cells.
Types of Leishmaniasis
 Three main clinical forms: cutaneous, visceral, and
mucosal.
 Cutaneous: sores form at bite sites, can develop into ulcers.
 Visceral: affects lymph nodes, liver, spleen, and bone
marrow.
 Mucosal: lesions in mouth, nose, or pharynx, often
disfiguring.
 Prompt treatment of cutaneous infection reduces mucosal
risk.
Visceral Leishmaniasis
 Develops over months or years, affecting major organs.
 Symptoms: fever, weight loss, spleen and liver swelling.
 Causes anemia, leukopenia, and thrombocytopenia.
 Leads to immunocompromised state.
 Increases risk of fatal lung and gastrointestinal infections.
Leishmaniasis
Diagnosis of Infectious Diseases Dr. Nabil El Aila

Cutaneous leishmanioasis – 20 spp.
Tick vector for Babesiosis
Figure 12.32
Diagnosis of Leishmaniasis
 Identified by Giemsa-stained smears or cultured samples.
 PCR-based assays can detect infection from tissue samples.
 DNA probes help identify specific Leishmania species.
 Differentiates between cutaneous and mucosal forms.
 Accurate diagnosis is crucial for appropriate treatment.
Figure 25.4.7
: (a) A micrograph of a tissue sample from a patient with localized cutaneous
leishmaniasis. Parasitic Leishmania mexicana (black arrow) are visible in and around
the host cells. (b) Large skin ulcers are associated with cutaneous leishmaniasis.
Treatment Options
 Cutaneous leishmaniasis usually heals on its own.
 Lesions may scar, but recurrence rates are low.
 Severe cases are treated with stibogluconate, amphotericin
B, or miltefosine.
 Prompt treatment is essential to prevent progression.
 Treatment depends on the form and severity of the disease.
Babesiosis
 Babesiosis is a rare zoonotic disease caused by Babesia spp.
 Parasitic protozoans that infect wild and domestic animals.
 Transmitted to humans by black-legged Ixodes ticks.
 Babesia infects and replicates inside red blood cells.
 Cycle continues as infected cells rupture and release more
parasites.
Symptoms and High-Risk Cases
 Many patients are asymptomatic.
 Symptomatic cases: malaise, fatigue, chills, fever, headache,
muscle and joint pain.
 Severe cases in asplenic patients, the elderly, and
immunocompromised individuals.
 Severe symptoms: high fever, hemolytic anemia, blood in
urine, jaundice, and kidney failure.
 Previously asymptomatic infection can worsen after
splenectomy.
 Diagnosed through microscopic observation in blood
smears.
 Serologic (IFA) and PCR tests also available for
confirmation.
 Many cases do not need treatment; mild infections often
resolve on their own.
 Severe infections treated with atovaquone and
azithromycin or clindamycin and quinine.
 Prompt diagnosis and treatment are crucial for high-risk
patients.
Figure 25.4.5
: In this blood smear from a patient with babesiosis, Babesia parasites can be
observed in the red blood cells.
Schistosomiasis
 Schistosomiasis, also known as bilharzia, is a neglected
tropical disease (NTD).
 Caused by Schistosoma blood flukes, primarily S. mansoni,
S. haematobium, and S. japonicum.
 Endemic to Caribbean, South America, Middle East, Asia,
and Africa.
 Only trematodes that infect humans through skin
penetration.
 WHO estimates 258 million people needed preventive
treatment in 2014
Schistosomiasis
 Blood fluke Schistosoma
 Snail is intermediate host, free-swimming cercariae penetrate
human skin
 Live in veins of liver or urinary bladder
 Tissue damage (granulomas) in response to eggs lodging in
tissues
• S. haemotobium Granulomas in urinary Africa, Middle East

bladder wall
• S. japonicum Granulomas in intestinal wall East Asia
• S. mansoni Granulomas in intestinal wall African, Middle East,
South American,
Caribbean
• Swimmer’s itch Cutaneous allergic reaction to U.S. parasite of wildfowl
cercariae
Schitstosomasis
(a) Male and female schitosomes.

Figure 23.27a
Life Cycle of Schistosoma
 Eggs are shed in human urine or feces, contaminating
freshwater habitats.
 Eggs hatch into miracidia, which infect snails as
intermediate hosts.
 Inside snails, miracidia mature and transform into
cercariae.
 Cercariae exit snails and penetrate human skin in water.
 Cercariae mature in the bloodstream, mate, and release
eggs.
Schitstosomasis
 Sanitation and snail
eradication help
prevent it
 Chemotherapy
treats disease
Figure 23.27b
Transmission Cycle
 Eggs released by adult worms travel to bladder or intestine.
 Eggs are excreted in urine or stool, continuing the cycle.
 Eggs that remain in the body cause inflammation and
scarring.
 Intermediate snail hosts are essential for parasite
development.
 Cycles can perpetuate in contaminated water sources.
Early Symptoms of Schistosomiasis
 Initial symptoms: rash or itchy skin at cercariae entry site.
 Within 1–2 months: fever, chills, cough, and muscle aches.
 Symptoms result from immune response to circulating
eggs.
 Eggs trapped in tissues cause ongoing inflammation.
 Severity varies by infection intensity and immune response.
Long-Term Complications
 Chronic infection leads to tissue inflammation and
scarring.
 Damage can affect liver, CNS, intestines, spleen, lungs, and
bladder.
 Symptoms: abdominal pain, liver enlargement, blood in
urine/stool.
 Chronic infections in children can cause malnutrition and
anemia.
 Increased risk of bladder cancer with prolonged infections.
Diagnosis and Control
 Diagnosis: microscopic egg observation in feces/urine,
tissue samples, or serologic tests.
 Treated effectively with praziquantel for all Schistosoma
species.
 Prevention: improved wastewater management and
education.
 Limiting contact with contaminated water is key to control.
 Public health efforts aim to reduce exposure and
transmission.
Schistosomiasis – granuloma (scar-like
tissue)
Figure 23.28
Swimmer’s Itch
 Swimmer’s itch is a skin rash caused by certain Schistosoma
species.
 It occurs when cercariae (larval form) of bird/mammal
schistosomes penetrate human skin.
 Common in freshwater bodies like lakes and ponds,
especially in summer.
 Schistosoma species involved do not mature in humans;
humans are accidental hosts.
 Primarily found in areas where infected birds or mammals
release parasite eggs into water.
Symptoms and Prevention of
Swimmer’s Itch
 Symptoms: itchy, red rash at the site of cercariae
penetration; may develop blisters.
 Rash appears within minutes to days and may last a week or
more.
 Not a serious infection; symptoms are usually self-limiting.
 Prevention: avoid swimming in contaminated freshwater or
dry off immediately after swimming.
 Control: reducing bird/mammal presence and managing
snail populations in recreational waters.
End of Lecture

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Dr. Nabil A.

•Entry Points for Bacteria:

Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 30

Diagnosis of Infectious Diseases Dr. Nabil El Aila

Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 42

Bubonic plague (above) by

• Relapsing fever – Borrelia transmitted by soft ticks,

Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 82

Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 91

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

(Virology Laboratory, New-Yale Haven Hospital)

(Courtesy of Linda Stannard, University of Cape Town, S.A.)

Dr. Nabil El Aila Med. Virology

(Virology Laboratory, New-Yale Haven Hospital)

Dr. Nabil El Aila Med. Virology

Dr. Nabil El Aila Med. Virology

 Transmitted by: Aedes aegypti and Aedes albopictus

1. Simple dengue fever (DF)

2. Dengue hemorrhagic fever (DHF)

3. Dengue Shock Syndrome (DSS)

• Fever > 2 and < 10 days (essential criterion)

IgM antibody to the

Following primary infection –

Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 8

Diagnosis of Infectious Diseases Dr. Nabil El Aila

Tick vector for Babesiosis

• S. haemotobium Granulomas in urinary Africa, Middle East

(a) Male and female schitosomes.

Microbiology of Gastrointestinal Sydtem - Dr. Nabil Elaila 55

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