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Bloodlytmphatic diusease
1. 23
Microbial Diseases of the Cardiovascular
and Lymphatic Systems
2.
3. The Cardiovascular System
and Lymphatics System
Blood: Transports nutrients to and wastes from
cells.
WBCs: Defend against infection.
Lymphatics: Transport interstitial fluid to blood.
Lymph nodes: Contain fixed macrophages.
6. Sepsis and Septic Shock
Sepsis: Bacteria
growing in the blood
Severe sepsis:
Decrease in blood
pressure
Septic shock: Low
blood pressure cannot
be controlled
Figure 23.3
7. Sepsis
Gram-negative sepsis
Endotoxins caused blood pressure decrease.
Antibiotics can worsen condition by killing bacteria.
Gram-positive sepsis
Nosocomial infections
Staphylococcus aureus
Streptococcus pyogenes
Group B streptococcus
Enterococcus faecium and E. faecalis
8. Sepsis
Puerperal sepsis (childbirth fever)
Streptococcus pyogenes
Transmitted to mother during childbirth by attending
physicians and midwives.
9. Bacterial Infections of the
Heart
Endocarditis: Inflammation of the endocardium
Subacute bacterial endocarditis: Alpha-hemolytic
streptococci from mouth
Acute bacterial endocarditis: Staphylococcus aureus
from mouth
Pericarditis: Streptococci
11. Rheumatic Fever
Inflammation of heart valves
Autoimmune complication of Streptococcus
pyogenes infections
Figure 23.5
12.
13. RF
RF is characterized by a constellation of findings
major manifestations
(1) migratory polyarthritis of the large joints
(2) carditis,
(3) subcutaneous nodules
(4) erythema marginatum of the skin
(5) Sydenham chorea, a neurologic disorder with
involuntary purposeless, rapid movements.
14. RF
minor manifestations (nonspecific signs and
symptoms)
fever, arthralgia
elevated blood levels of acute phase reactants
CRP, ESR, ASO
The diagnosis is established by the so-called Jones
criteria:
evidence of a preceding group A streptococcal infection,
with the presence of two of the major manifestations
listed above or one major and two minor manifestations
15. RF
After an initial attack, there is increased vulnerability to
reactivation of the disease with subsequent pharyngeal
infections, and the same manifestations are likely to
appear with each recurrent attack.
Carditis is likely to worsen with each recurrence, and
damage is cumulative.
valvular disease
cardiac murmurs, cardiac hypertrophy and dilation, and heart
failure, arrhythmias (particularly atrial fibrillation in the
setting of mitral stenosis), thromboembolic complications,
and infective endocarditis.
16. Tularemia
Francisella tularensis,
gram-negative rod
Transmitted from
rabbits and deer by
deer flies.
Bacteria reproduce in
phagocytes.
Figure 23.6
17. Brucellosis (Undulant Fever)
Brucella, gram-negative rods that grow in
phagocytes.
B. abortus (elk, bison, cows)
B. suis (swine)
B. melitensis (goats, sheep, camels)
Undulating fever that spikes to 40°C each evening.
Transmitted via milk from infected animals or
contact with infected animals.
18. Anthrax
Bacillus anthracis, gram-positive, endospore-
forming aerobic rod
Is found in soil.
Cattle are routinely vaccinated.
Treated with ciprofloxacin or doxycycline.
Cutaneous anthrax
Endospores enter through minor cut
20% mortality
20. Biological Weapons
1346: Plague-ridden bodies used by Tartar army against Kaffa.
1925: Plaque-carrying flea bombs used in the Sino-Japanese War.
1950s: U.S. Army spraying of S. marcescens to test weapons dispersal.
1972: International agreement to not possess biological weapons.
1979: B. anthracis weapons plant explosion in the Soviet Union.
1984: S. enterica used against the people of The Dalles.
2001: B. anthracis distributed in the United States
22. Gangrene
Ischemia: Loss of blood supply to tissue.
Necrosis: Death of tissue.
Gangrene : Death of soft tissue.
Gas gangrene
Clostridium perfringens, gram-positive, endospore-
forming anaerobic rod, grows in necrotic tissue
Treatment includes surgical removal of necrotic tissue
and/or hyperbaric chamber.
34. Spotted Fevers (Rocky Mountain
Spotted Fever)
Rickettsia rickettsii
Measles-like rash
except that the rash
appears on palms and
soles too.
Figure 23.18
37. Human Herpes Virus 4 Infections
Ebstein Barr Virus EBV
Infectious Mononucleosis
Childhood infections are asymptomatic.
Transmitted via saliva
Characterized by proliferation of monocytes
Burkitt’s lymphoma
Nasopharyngeal carcinoma
Cancer in immunosuppressed individuals, and malaria
and AIDS patients
40. Cytomegalovirus Infections
Cytomegalovirus (Human herpesvirus 5)
Infected cells swell (cyto-, mega-)
Latent in white blood cells
May be asymptomatic or mild
Transmitted across the placenta; may cause mental
retardation
Transmitted sexually, by blood, or by transplanted
tissue
41. Viral Hemorrhagic Fevers
Pathogen Portal of Reservoir Method of
entry transmission
Yellow fever Arbovirus Skin Monkeys Aedes
aegypti
Dengue Arbovirus Skin Humans Aedes
aegypti;
A. Albopictus
Marburg, Filovirus, Mucous Probably Contact with
Ebola, arenavirus membranes fruit bats; blood
Lassa other
mammals
Hantavirus Bunyavirus Respiratory Field mice Inhalation
pulmonary tract
syndrome
50. PROTOZOA FROM OTHER BODY SITES
Free-living Amebae
Naegleria
Acanthamoeba
Trichomonas vaginalis
51. PLASMODIUM
Disease: Malaria
P. vivax: Benign tertian malaria
P. malariae: Quartan malaria
P. falciparum: Malignant tertian malaria
P. ovale: Ovale tertian malaria
Lab Dx: Giemsa stained thick and thin
blood smears; IFA; PCR
52. Infected RBC:
P. vivax and P. ovale: reticulocytes
P. malariae: senescent erythrocytes
P. falciparum: erythrocytes of all ages
Cyclic paroxysm of fever:
P. vivax and P. ovale: every 48 hours
P. malariae: every 72 hours
P. falciparum: every 36-48 hours
53.
54. P. falciparum: Blood
Stage Parasites
Thin Blood Smears
Fig. 1: Normal red cell;
Figs. 2-18: Trophozoites
(among these, Figs. 2-10
correspond to ring-stage
trophozoites);
Figs. 19-26: Schizonts (Fig.
26 is a ruptured schizont);
Figs. 27, 28: Mature
macrogametocytes (female);
Figs. 29, 30: Mature
microgametocytes (male).
55. Gametocytes of P. falciparum in thin blood
smears. Note the presence of a “Laveran’s bib”,
which is not always visible.
56. P. falciparum rings have delicate cytoplasm and 1 or 2 small
chromatin dots. Red blood cells (RBCs) that are infected are not
enlarged; multiple infection of RBCs more common in P. falciparum
than in other species. Occasional appliqué forms (rings appearing
on the periphery of the RBC) can be present.
57. P. falciparum schizonts: seldom seen in peripheral
blood. Mature schizonts have 8 to 24 small merozoites;
dark pigment, clumped in one mass.
60. P. malariae rings: have sturdy cytoplasm and a large
chromatin dot. The red blood cells (RBCs) are normal
to smaller than normal (3/4 ×) in size.
61. P. malariae schizonts: have 6 to 12 merozoites with large
nuclei, clustered around a mass of coarse, dark-brown
pigment. Merozoites can occasionally be arranged as a
rosette pattern.
62. P. malariae trophozoites: have compact cytoplasm and a
large chromatin dot. Occasional band forms and/or
"basket" forms with coarse, dark-brown pigment can be
seen.
64. P. ovale gametocytes: round to oval, and may almost fill
the red blood cells (RBCs). Pigment is brown and more
coarse than that of P. vivax. RBCs are normal to slightly
enlarged (1 1/4 ×), may be round to oval, and are
sometimes fimbriated. Schüffner's dots are visible
under optimal conditions.
65. Plasmodium
vivax: Blood Stage
Parasites
Thin Blood Smears
Fig. 1: Normal red cell;
Figs. 2-6: Young
trophozoites (ring stage
parasites);
Figs. 7-18:
Trophozoites;
Figs. 19-27: Schizonts;
Figs. 28 and
29: Macrogametocytes
(female);
Fig. 30:
Microgametocyte (male).
66. P. vivax gametocytes: round to oval with scattered
brown pigment and may almost fill the red blood cell
(RBC). RBCs are enlarged 1 1/2 to 2 × and may be
distorted. Under optimal conditions, Schüffner's dots
may appear more fine than those seen in P. ovale.
67. P. vivax rings: have large chromatin dots and can show
amoeboid cytoplasm as they develop. RBCs can be normal
to enlarged up to 1 1/2 × and may be distorted. Under
optimal conditions, Schüffner's dots may be seen.
68. P. vivax schizonts: large, have 12 to 24 merozoites,
yellowish-brown, coalesced pigment, and may fill the
red blood cell (RBC).
69. P. vivax trophozoites: show amoeboid cytoplasm, large
chromatin dots, and have fine, yellowish-brown pigment.
71. TRYPANOSOMA BRUCEI
Disease: African trypanosomiasis
T. b. gambiense: Gambian trypanosomiasis,
West & Mid-African sleeping sickness
T. b. rhodesiense: Rhodesian
trypanosomiasis, East African sleeping
sickness
Lab Dx: Giemsa stained thick and thin blood
smears or lymph exudate (early stage); Giemsa
stained smears of CSF (late stage)
72. Site in host: lymph glands, blood stream, brain
Portal of entry: skin
Source of infection: tsetse fly
Winterbottom’s sign: enlargement of
posterior cervical LNs
73.
74. Trypomastigote: slender to fat and stumpy forms; in
Giemsa stained films – C or U shaped forms NOT seen;
small, oval kinetoplast located posterior to the nucleus; a
centrally located nucleus, an undulating membrane, and an
anterior flagellum. The trypanosomes length range is 14-
33 µm
75. A dividing parasite is seen at the right. Dividing forms
are seen in African trypanosomiasis, but not in American
trypanosomiasis (Chagas' disease)
79. TRYPANOSOMA CRUZI
Disease: American trypanosomiasis, Chaga’s
disease
Lab Dx: Giemsa stained thick and thin blood
smears for the trypomastigote; histopath
exam for the amastigote
Site in host: Tissues – heart; blood
Portal of entry: skin
Source of infection: Kissing bug Triatomidae
80. Trypomastigote: shape is short & stubby to long &
slender; in Giemsa stained blood films – C or U shaped;
kinetoplast is large, oval & located posterior to the
nucleus; anterior long free flagellum
85. TOXOPLASMA GONDII
Disease: Toxoplasmosis
Site in host: All organs
Portal of entry:
Ingestion of oocyst contaminated water
Aerosolization of oocyst contaminated dust or
litter
Consumption of raw or undercooked cyst
infected meat
Transplacental passage of the tachyzoite
86. - Definitive host: domestic cats
- Intermediate host: infected rodents
Accidental intermediate host: humans
Lab Dx: IFAT and ELISA; Giemsa-stained
smears of exudates, aspirates or tissues
87.
88. T. gondii tachyzoites: crescentic to pyriform
shaped with a prominent, centrally placed nucleus.
91. A: Positive reaction (tachyzoites + human antibodies to
Toxoplasma + FITC-labelled antihuman IgG = fluorescence.)
B: Negative IFA for antibodies to T. gondii.
92. LEISHMANIA
- Disease:
- L. tropica complex: Old Word Cutaneous
leishmaniasis (oriental sore, Aleppo boil, Delhi
ulcer, Baghdad boil)
- L. mexicana complex: New Word Cutaneous
leishmaniasis (chiclero ulcer, bay sore)
- L. braziliensis complex: Mucocutaneus
leishmaniasis (espundia, uta)
- L. donovani: Visceral leishmaniasis (kala-azar or
black disease, Dumdum fever)
93. - Lab Dx: Giemsa stained tissue sections or
impression smears
- Site in host: Monocytes/macrophages of
skin & mucosa
- Portal of entry: Skin
- Source of infection: Phlebotomus or
Lutzomiya fly
94.
95. L. tropica amastigotes: ovoid in shape; large & eccentric
nucleus; small, rodlike kinetoplast positioned opposite
the nucleus; rodlike axoneme perpendicular to the
kinetoplast
96. Leishmaniasis
Disease Visceral Cutaneous Mucocutaneous Babesiosis
leishmaniasis leishmaniasis leishmaniasis
Fatal if Papule that Disfiguring Replicates in
untreated ulcerates and RBCs
scars
Causative Leishmania L. Tropica L. Braziliensis Babesia
agent donovani microti
Vector Sandflies Sandflies Sandflies Ixodes ticks
Reservoir Small Small mammals Small Rodents
mammals mammals
Treatment Amphotericin Amphotericin B Amphotericin B Atovaquone +
B or or miltefosine or miltefosine azithromycin
miltefosine
Geographic Asia, Africa, Asia, Africa, Rain forests of United States
distribution Southeast Mediterranean, Yucatan, South
Asia Central America, America
South America
100. Babesia microti infection, Giemsa stained thin smear. The
organisms resemble P. falciparum; however Babesia
parasites present several distinguishing features: they
vary more in shape and in size; and they do not produce
pigment.
101. Infection with Babesia. Giemsa stained thin smears
showing the tetrad, a dividing form pathognomonic for
Babesia. Note also the variation in size and shape of the
ring stage parasites and the absence of pigment.
103. Schistosomiasis
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 East Asia
wall
S. mansoni Granulomas in intestinal African, Middle East,
wall South American,
Caribbean
Swimmer’s itch Cutaneous allergic U.S. parasite of
reaction to cercariae wildfowl
108. Schistosoma mansoni eggs: large (length 114 to 180 µm)
and have a characteristic shape, with a prominent lateral
spine near the posterior end. The anterior end is tapered
and slightly curved. When the eggs are excreted, they
contain a mature miracidium
116. S. haematobium eggs: large and have a prominent
terminal spine at the posterior end
117.
118. S.haematobium: adult schistosomes live in pairs in the pelvic veins
(especially in the venous plexus surrounding the bladder); males are
10-15 mm in lenght by 0,8-1 mm in diameter, and have a ventral
infolding from the ventral sucker to the posterior end forming the
gynecophoric canal. Adult male with female in the copulatory groove.
119. SCHISTOSOMA JAPONICUM
- Disease: Schistosomiasis, Katayama fever
- Site in host: veins of SI
- Portal of entry: skin
- Definitive host: humans, dogs, cats,
horses, pigs, cattle, deer, caribou &
rodents
- Intermediate host: snail (Oncomelania)
- Infective stage: cercariae
- Lab Dx: eggs in stool; liver biopsy