bloodlytmphatic disease
TRANSCRIPT
23Microbial Diseases of the Cardiovascular and Lymphatic Systems
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.
The Cardiovascular System
Figure 23.1
The Lymphatic System
Figure 23.2
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
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
Sepsis Puerperal sepsis (childbirth fever)
Streptococcus pyogenes Transmitted to mother during childbirth by
attending physicians and midwives.
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
Bacterial Infections of the Heart
Figure 23.4
Rheumatic Fever Inflammation of heart valves Autoimmune complication of
Streptococcus pyogenes infections
Figure 23.5
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.
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
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.
Tularemia Francisella
tularensis, gram-negative rod
Transmitted from rabbits and deer by deer flies.
Bacteria reproduce in phagocytes.
Figure 23.6
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.
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
Anthrax Gastrointestinal
anthrax Ingestion of
undercooked food contaminated food
50% mortality. Inhalational
anthrax Inhalation of
endospores. 100% mortality.
Figure 23.7
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
Bacteria Viruses
Bacillus anthracis “Eradicated” polio and measles
Brucella spp. Encephalitis viruses
Chlamydophila psittaci Hermorrhagic fever viruses
Clostridium botulinum toxin Influenza A (1918 strain)
Coxiella burnetti Monkeypox
Francisella tularensis Nipah virus
Rickettsia prowazekii Smallpox
Shigella spp. Yellow fever
Vibrio cholerae
Yersinia pestis
Biological Weapons
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.
Animal Bites and Scratches
Pasteurella multocida Clostridium Bacteroides Fusobacterium Bartonella hensellae: Cat-scratch disease
Plague Yersinia pestis, gram-negative rod Reservoir: Rats, ground squirrels, and prairie
dogs Vector: Xenopsylla cheopsis Bubonic plague: Bacterial growth in blood and
lymph Septicemia plague: Septic shock Pneumonic plague: Bacteria in the lungs
Plague
Figures 23.10, 23.11
Relapsing Fever Borrelia spp., spirochete Reservoir: Rodents Vector: Ticks Successive relapses are less severe
Lyme Disease Borrelia burgdorferi Reservoir: Deer Vector: Ticks
Figures 23.13b–c
Lyme Disease
Figure 23.13a
Lyme Disease First symptom:
Bull's eye rash Second phase:
Irregular heartbeat, encephalitis
Third phase: Arthritis
Figure 23.14
Figure 23.12
Ehrlichiosis
Ehrlichia, gram-negative, obligately intracellular (in white blood cells)
Reservoir: Deer, rodents
Vector: Ticks
Figure 23.15
Typhus Epidemic typhus
Rickettsia prowazekii Reservoir: Rodents Vector: Pediculus humanus corporis Transmitted when louse feces rubbed into bite
wound
Typhus Epidemic murine typhus:
Rickettsia typhi Reservoir: Rodents Vector: Xenopsylla cheopsis
Spotted Fevers (Rocky Mountain Spotted Fever)
Rickettsia rickettsii Measles-like rash
except that the rash appears on palms and soles too.
Figure 23.18
Spotted Fevers (Rocky Mountain Spotted Fever)
Figure 23.16
Tick Life Cycle
Figure 23.17
Human Herpes Virus 4 Infections
Ebstein Barr Virus EBVInfectious 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
Infectious Mononucleosis
Figure 23.20
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
Pathogen Portal of entry
Reservoir Method of transmission
Yellow fever Arbovirus Skin Monkeys Aedes aegypti
Dengue Arbovirus Skin Humans Aedes aegypti;
A. Albopictus
Marburg, Ebola, Lassa
Filovirus, arenavirus
Mucous membranes
Probably fruit bats; other mammals
Contact with blood
Hantavirus pulmonary syndrome
Bunyavirus Respiratorytract
Field mice Inhalation
Viral Hemorrhagic Fevers
Ebola Virus
Figure 23.21
American Trypanosomiasis (Chagas’ Disease) Trypanosoma cruzi Reservoir: Rodents,
opossums, armadillos
Vector: Reduviid bug
Figures 23.22, 12.33d
Toxoplasmosis Toxoplas
ma gondii
Figure 23.23
Malaria Plasmodium vivax, P. ovale, P. malariae, P.
falciparum Anopheles mosquito
Figure 12.31b
Malaria
Figure 23.25
Malaria
Figure 23.24
Malaria
Figure 12.19
OTHER PROTOZOA
BLOOD and TISSUE PROTOZOA Plasmodium Babesia Trypanosoma brucei Trypanosoma cruzi Toxoplasma gondii Leishmania
PROTOZOA FROM OTHER BODY SITES Free-living Amebae
Naegleria Acanthamoeba
Trichomonas vaginalis
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
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
P. falciparum: Blood Stage ParasitesThin 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).
Gametocytes of P. falciparum in thin blood smears. Note the presence of a “Laveran’s bib”, which is not always visible.
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.
P. falciparum schizonts: seldom seen in peripheral blood. Mature schizonts have 8 to 24 small merozoites; dark pigment, clumped in one mass.
Plasmodium malariae: Blood Stage ParasitesThin Blood Smears
Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (rings); Figs. 6-13: Trophozoites; Figs. 14-22: Schizonts; Fig. 23: Developing gametocyte; Fig. 24: Macrogametocyte (female); Fig. 25: Microgametocyte (male).
P. malariae gametocytes: round to oval with scattered brown pigment; may almost fill red blood cell (RBC). The RBCs are normal to smaller than normal (3/4 ×) in size.
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.
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.
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.
Plasmodium ovale: Blood Stage Parasites
Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (Rings); Figs. 6-15: Trophozoites; Figs. 16-23: Schizonts; Fig. 24: Macrogametocytes (female); Fig. 25: Microgametocyte (male).
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.
Plasmodium vivax: Blood Stage ParasitesThin 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).
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.
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.
P. vivax schizonts: large, have 12 to 24 merozoites, yellowish-brown, coalesced pigment, and may fill the red blood cell (RBC).
P. vivax trophozoites: show amoeboid cytoplasm, large chromatin dots, and have fine, yellowish-brown pigment.
Positive IFA result with P. malariae schizont antigen.
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)
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
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
A dividing parasite is seen at the right. Dividing forms are seen in African trypanosomiasis, but not in American trypanosomiasis (Chagas' disease)
Tsetse fly. The vector of African trypanosomiasis
Winterbottoms sign
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
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
Trypanosoma cruzi crithidia
Trypanosoma cruzi: Leishmanial form
Riduviid bug: the vector of American trypanosomiasis
Ramana's sign: unilateral conjunctivitis and orbital edema
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
- 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
T. gondii tachyzoites: crescentic to pyriform shaped with a prominent, centrally placed nucleus.
Toxoplasma gondii cyst in brain tissue stained with hematoxylin and eosin (100×).
T. gondii oocysts in a fecal floatation (100×).
A: Positive reaction (tachyzoites + human antibodies to Toxoplasma + FITC-labelled antihuman IgG = fluorescence.)
B: Negative IFA for antibodies to T. gondii.
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)
- 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
L. tropica amastigotes: ovoid in shape; large & eccentric nucleus; small, rodlike kinetoplast positioned opposite the nucleus; rodlike axoneme perpendicular to the kinetoplast
Disease Visceral leishmaniasis
Cutaneous leishmaniasis
Mucocutaneous leishmaniasis
Babesiosis
Fatal if untreated
Papule that ulcerates and scars
Disfiguring Replicates in RBCs
Causative agent
Leishmania donovani
L. Tropica L. Braziliensis Babesia microti
Vector Sandflies Sandflies Sandflies Ixodes ticks
Reservoir Small mammals
Small mammals Small mammals
Rodents
Treatment Amphotericin B or miltefosine
Amphotericin B or miltefosine
Amphotericin B or miltefosine
Atovaquone + azithromycin
Geographic distribution
Asia, Africa, Southeast Asia
Asia, Africa, Mediterranean, Central America, South America
Rain forests of Yucatan, South America
United States
Leishmaniasis
BABESIA Disease: Babesiosis Lab Dx: Giemsa stained thick and
thin blood smears
Babesiosis
Figures 23.26, 12.32
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.
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.
Schistosomiasis
Figure 23.28
S. haemotobium Granulomas in urinary bladder wall
Africa, Middle East
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 cercariae
U.S. parasite of wildfowl
Schistosomiasis
Tissue damage (granulomas) in response to eggs lodging in tissues
Schistosomiasis
Figure 23.27a
SCHISTOSOMA MANSONI- Disease: Schistosomiasis, intestinal
schistosomiasis, bilharziasis “snail fever”- Site in host: veins of LI- Portal of entry: skin- Definitive host: humans, baboons &
rodents- Intermediate host: snail (Biomphalaria sp
& Tropicorbis sp)- Infective stage: cercariae - Lab Dx: eggs in stool; rectal or liver biopsy
Biomphalaria spp.
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
Male and female schistosomes.
SCHISTOSOMA HAEMATOBIUM- Disease: Urinary schistosomiasis,
schistosomal hematuria, urinary bilharziasis
- Site in host: veins of urinary bladder- Portal of entry: skin- Definitive host: humans, monkeys &
baboons- Intermediate host: snail (Bulinus,
Physopsis, and Biomphalaria sp)- Infective stage: cercariae - Lab Dx: eggs in stool; cystoscopy
Bulinus spp.
S. haematobium eggs: large and have a prominent terminal spine at the posterior end
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.
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
Onchomelania, hupensis spp.
S. japonicum egg: typically oval or subspherical, and has a vestigial spine (smaller than those of the other species)
Cercaria
Schistosomiasis
Figure 23.27b