BIO 3372 Chapter 23-1 - gsau

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Invisible InvadersInvisible InvadersInvisible InvadersInvisible InvadersAmazing AlliesAmazing AlliesAmazing AlliesAmazing Allies

Chapter 23 Microbial Diseases of the Cardiovascular and Lymphatic System

Structure and Function of the Cardiovascular and Lymphatic Systems

Learning Objective

Identify the role of the cardiovascular and lymphatic systems in spreading and eliminating infections.


• Cardiovascular system: circulates blood th h th b d ' tithrough the body's tissues– Includes the heart and associated arteries,

veins, and capillaries– Delivers substances to and removes

substances from the cells

The human cardiovascular system and related structures

Superior vena cava(main upper vein)

Lung

Aorta(main artery)

Capillaries in lungInferior vena cava (main lower vein)

Liver Stomach

Heart

Spleen

Kidneys

Capillariesto intestines

K y

Intestines

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• Blood: consists of – Fluid called plasma– Formed elements: cells and cell fragments

suspended in plasma• Red blood cells - transports O2 and CO2

Whit bl d ll i it• White blood cells - immunity• Platlets – blood clotting

Insert Table 16.1If possible, break into multiple slides

Insert Table 16.1If possible, break into multiple slides

An overview of the body’s defenses

First line of defense

•Intact skin•Mucous membranesand their secretions

•Normal microbiota

Second line of defense Third line of defense

•Specialized lymphocytes:T cells and B cells

•Antibodies

•Phagocytes, such as neutrophils, eosinophils, dendritic cells, andmacrophages

•InflammationInflammation•Fever•Antimicrobial substances

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Phagocytosis

• Phago: from Greek, meaning eat• Cyte: from Greek, meaning cell• Ingestion of microbes or particles by a

cell, performed by phagocytes

Phases of Phagocytosis

Macrophage

Macrophage engulfing rod-shaped bacteria

Pseudopods

Bacterium


• Lymphatic system– Plasma leaves blood capillaries to become interstitial

fluid fluid – Lymphatic system provides an accessory return route

for the interstitial fluid to the blood– Lymph capillaries transport interstitial fluid (now

called lymph) to lymph vessels (lymphatics) and lymph nodes

• Very permeable• Picks up microorganisms and infectious agents

– Lymph nodes (a component of the immune system) contain fixed macrophages, B cells, and T cells

• Buboes: swollen lymph nodes

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Relationship between cardiovascular and lymphatic systems

To lymphatic systemVenule

To heartInterstitialfluid

To lymphatic system

Valve to

Lymphocytesand macrophages

Tissuecells

Lymphcapillaries

Blood From heartArteriole

preventbackflow

From lymphaticill tcapillaries capillary system

b) Lymph nodea) Capillary system in lung

a) From the capillaries, some blood plasma filters into the surrounding tissue where it is called interstitial fluid and enters the lymph capillaries. This fluid, now called lymph, returns to the heart through the lymphatic circulatory system (green).

b) All lymph returning to the heart must pass through at least one lymph node

Bacterial Diseases of the Cardiovascular and Lymphatic Systems

Learning Objectives

List the signs and symptoms of sepsis, and explain the importance of infections that develop into septic shock.

Differentiate gram-negative sepsis, gram-positive sepsis and puerperal sepsispositive sepsis, and puerperal sepsis.

Describe the epidemiologies of endocarditis and rheumatic fever.

Discuss the epidemiology of tularemia.


Learning Objectives

Discuss the epidemiology of brucellosis.Discuss the epidemiology of anthrax.Discuss the epidemiology of gas gangrene.Identify pathogens and the diseases that Identify pathogens and the diseases that

are transmitted by animal bites and scratches.


Learning ObjectivesCompare and contrast the causative agents,

vectors, reservoirs, symptoms, treatments, and preventive measures for plague, Lyme disease, and Rocky Mountain spotted fever.

Describe the epidemiologies of epidemic typhus, endemic murine typhus, and spotted fevers.

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• Blood is normally sterile• Moderate numbers of bacteria

can enter the bloodstream, especially in hospital settings due especially in hospital settings due to invasive procedures

• Blood and lymph contain defensive phagocytic cells

• Blood is low in free ironO i th bl d b t i • Once in the blood, bacteria are widely disseminated and some can reproduce in the blood if the body’s defenses fail

Sepsis and Septic Shock• Septicemia

– Acute illness due to the presence of pathogens or their toxins in the blood

S i• Sepsis– Systemic inflammatory response syndrome (SIRS)– Caused by an infection that releases mediators of inflammation

into the bloodstream– Site of infection is not necessarily the blood

• Lymphangitis– Inflamed lymph vesselsInflamed lymph vessels– Visible as red streaks from the site of infection

• Severe sepsis – Decreased blood pressure and dysfunction of at least one organ

• Septic shock– Sepsis and uncontrollable decreased blood pressure

Lymphangitis, one sign of sepsis Gram-Negative Sepsis

• Also called endotoxin shock• Endotoxins (lipopolysaccharides [LPS]) cause a • Endotoxins (lipopolysaccharides [LPS]) cause a

severe drop in blood pressure• Antibiotics can worsen the condition by killing

bacteria• Treatment involves neutralizing the LPS g

components and inflammatory-causing cytokines• 750,000 cases of septic shock in the US

annually and 225,000 are fatal.

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Gram-Positive Sepsis• Most common cause of sepsis• Potent exotoxins that cause toxic shock syndrome• Bacterial components that lead to toxic shock are not

l t l k ibl iti ll ll completely known, possibly gram-positive cell wall components or even DNA

• Hospital-acquired infections– Enterococcus faecium and Enterococcus faecalis

• Inhabit the colon• Colonize wounds and the urinary tract• Resistant to many antibiotics

– Group B streptococci (GBS)• Streptococcus agalactiae

– Neonatal sepsis that is life-threatening– CDC recommends that pregnant women be tested for GBS

and those with GBS be offered antibiotics

Puerperal Sepsis

• Also called puerperal fever and hildbi th fchildbirth fever– Caused by Streptococcus pyogenes– Transmitted to the mother during

childbirth• Infects the uterus and progresses to an • Infects the uterus and progresses to an

infection of the abdominal cavity (peritonitis)• Modern hygienic practices have made this an

uncommon complication of childbirth.

Bacterial Infections of the Heart• Pathogen source usually an infection

elsewhere in the body• Endocarditis

– Inflammation of the endocardium

Heart wall consists of 3 layers

• Subacute bacterial endocarditis– Impairs the function of the heart

valves– Particularly in patients with heart

abnormalities– Alpha-hemolytic streptococci from an

oral or tonsil infection

• Acute bacterial endocarditis• Acute bacterial endocarditis– Rapid progression of the disease– Caused by Staphylococcus aureus

• Pericarditis– Inflammation of the sac around the

heart– Streptococci

Pericardium is a double-walled sac around the heart

Rheumatic Fever• Autoimmune complication of S. pyogenes infections• Ages 4-18; often following a case of streptococcal

sore throat• Arthritis and fever initially• Leads to inflammation of the heart valves

– Immune reaction against streptococcal M protein– Re-infection renews the immune attack

• Subcutaneous nodules at the jointsj• Sydenham's chorea

– 10% of rheumatic fever cases developcomplications

– Purposeless, involuntary movements during waking hours

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A nodule caused by rheumatic feverTularemia

• Caused by Francisella tularensis– Gram-negative rod

• Zoonotic disease

• Transmitted from rabbits, ticks, and deer flies– Entry via several routes, wound most

common– Creates an ulcer at the site of entry– Mortality usually <3%

• Bacteria reproduce in phagocytes– Enlarges the regional lymphg g y p– Makes chemotherapy more difficult

• A respiratory infection can occur via dust of dried urine or feces of infected animal– Infective dose is small– Mortality rate >30%

F. tularensis bacteria (blue) infecting a macrophage (yellow)

Tularemia cases in the United States (2001–2010) Brucellosis (Undulant Fever)• 500,000 new human cases annually• World’s most common bacterial zoonosis• Middle East and Mexico - endemic areas• Brucella spp.

– Aerobic gram-negative rods– Brucella abortus (elk, bison, cows)– Brucella suis (swine)– Brucella melitensis (goats, sheep, camels)

• Transmitted via milk from infected animals or contact with m m f m f m winfected animals

• Perisists in the reticuloendothelial (macrophage) system; evades phagocytes; becomes chronic and can affect any organ

• Undulant fever (malaise, night sweats, muscle aches)– Not usually fatal

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Anthrax• Caused by Bacillus anthracis– Gram-positive, endospore-forming

aerobic rod

• Found in soil; spores survive up to 60 years

• Primarily affects grazing animals; fatal sepsis

• Spores introduced into the body are taken up by macrophages and germinate

B t i t th bl d t d – Bacteria enter the bloodstream and release toxins

• Treated with ciprofloxacin or doxycycline

• Vaccination of livestock Bacillus anthracis spores in a murine macrophage

Anthrax• Bacteria produces virulence factors

– Protective antigen: binds the toxins to t t ll itti th i ttarget cells, permitting their entry

– Edema toxin: causes local swelling and interferes with phagocytosis

– Lethal toxin: targets and kills macrophages

– Amino acid capsule that avoids an immune response

Three Forms of Anthrax• Cutaneous anthrax

– Endospores enter through a minor cut– 90% of human form of anthrax– 20% mortality if enters the bloodstream – 20% mortality if enters the bloodstream

without treatment

• Gastrointestinal anthrax (rare)– Ingestion of undercooked, contaminated food– 50% mortality rate

• Inhalational (pulmonary) anthraxInhalational (pulmonary) anthrax– Inhalation of endospores– Bacteria enter the bloodstream; progresses

into septic shock– Near 100% mortality rate– Bioterrorism

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Applications of Microbiology: Protection against Bioterrorism

• 1346: plague-ridden bodies used by the Tartar army against Kaffa (Ukraine)against Kaffa (Ukraine)

• 1937–1945: plague-carrying flea bombs used in the Sino-Japanese War

• 1979: explosion of B. anthracis weapons plant in the Soviet Union

• 1984: Salmonella enterica used against the people of 1984 Salmonella enterica used against the people of The Dalles, Oregon

• 1996: Shigella dysenteriae used to contaminate food• 2001: B. anthracis distributed in the United States

Potential Biological Weapons Gangrene• Ischemia: loss of blood supply to tissue• Necrosis: death of tissue

Gangrene: death of soft tissue• Gangrene: death of soft tissue• Gas gangrene

– Caused by Clostridium perfringens, a gram-positive, endospore-forming anaerobic rod

• Grows in necrotic tissue; dead tissue provides t i t f t b h d t ith nutrients; ferments carbohydrates with gas

• Produces toxins that move along muscle bundles that kill the tissues

– Treatment includes the surgical removal of necrotic tissue and/or use of a hyperbaric chamber

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The toes of a patient with gangrene

H b i Ch b Hyperbaric Chamber: pressurized oxygen rich atmosphere

Systemic Diseases Caused by Bites and Scratches

• 1% of ER visits; 4.4 million annually in US• Dogs make up 80% of reported bites;

cats about 10%– Cat bites have higher infection rates

• Pasteurella multocida– Gram-negative rod; causes sepsis

• Staphylococcus, Streptococcus, Corynebacterium

Cat-Scratch Disease• Caused by Bartonella henselae

– Aerobic, gram-negativeInhabits cat red blood cells; carried in the – Inhabits cat red blood cells; carried in the blood of 50% of cats

– Multiplies in the digestive system of cat fleas• Cat claws contaminated with flea feces scratch

human

• Forms a papule at site of infection and • Forms a papule at site of infection and swollen lymph nodes

• Self-limiting• 22,000 cases annually in the US

Electron micrograph showing the location of Bartonella henselae within a red blood cell

Pore Red blood cell

B. henselaecell

Cat Scratch Disease

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Vector-Transmitted DiseasesPlague

• Caused by Yersinia pestis– Gram-negative rodGram negative rod– Transmitted by the rat flea (Xenopsylla cheopis)– Endemic to rats, ground squirrels, and prairie dogs

• Bacteria blocks the flea's digestive tract– Flea bites the host and ingested blood is

regurgitated into the host

• Bacteria enter the bloodstream and proliferate in the lymph tissue– Cause intense swellings called buboes

Plague• Bubonic plague

– Bacterial growth in the blood and lymph– Buboes form– Most common form; 50–75% mortality rate within a week

of initial infection

• Septicemic plague– Septic shock due to bacteria in the blood

• Pneumonic plaguep g– Bacteria in the lungs– Easily spread by airborne droplets– Near 100% mortality rate; need to diagnose within 15 hrs

• Antibiotic prophylaxis for exposure

Buboes of bubonic plague

Black Death

U.S. geographic distribution of human plague, 1970–2012

In areas where human proximity to rats is common

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Relapsing Fever

• Caused by Borrelia spp.– Spirochetep

• Transmitted by soft ticks that feed on rodents

• High fever, jaundice, rose-colored skin spots

• Successive relapses are less psevere

• Diagnosis: bacteria in the blood• Treated with tetracycline

Lyme Disease (Lyme Borreliosis)

• Caused by Borrelia burgdorferiM st c mm n tickb rn dis s in th Unit d • Most common tickborne disease in the United States

• Field mice are the most common reservoir– Nymphal stage of the Ixodes tick feeds on mice and

infects humans

• Ticks feed and mate on deer, but are not infected, important for maintaining the ticks

• Ticks must attach 2-3 days to transfer bacteria; 1% of tick bites result in Lyme disease

Lyme disease in the United States, reported cases by county, 2012

On Atlantic coast almost all ticks c rr th B rr licarry the Borrelia

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Life cycle of the tick vector of Lyme diseaseTicks have 3 feedings Lyme Disease (Lyme Borreliosis)

• First phase– Bull's-eye rash; flulike symptoms

d h• Second phase– Irregular heartbeat; encephalitis;

facial paralysis; memory loss

• Third phase– Arthritis due to an immune response

• Diagnosis via ELISA, indirect fluorescent-antibody (FA) test, or Western blot

• Treated with antibiotics– More difficult to treat in later stages

Typhus

• Caused by Rickettsia spp.– Obligate intracellular parasites– Infect the endothelial cells of the vascular

system• Block and rupture the small blood vessels

Spread by arthropod vectors– Spread by arthropod vectors

Typhus

• Typhus fever (epidemic louse borne typhus)– Caused by Rickettsia prowazekii– Carried by the body louse: Pediculus humanus

corporis– Transmitted when louse feces are rubbed into

the bite wound from the louseP l d f d h f d d – Prolonged fever and a rash of red spots due to subcutaneous hemorrhaging

– Rare but with high mortality rates– Treated with tetracycline and chloramphenicol

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Typhus

• Endemic murine typhusC d b Ri k i hi– Caused by Rickettsia typhi

– Transmitted by the rat flea: X. cheopis– Rodents (murine = mouse) are common hosts– Mortality rate less than 5%

Clinically indistinguishable from typhus – Clinically indistinguishable from typhus fever

– Treated with tetracycline and chloramphenicol

Typhus

• Rocky Mountain spotted f (ti kb t h )fever (tickborne typhus)– Caused by Rickettsia rickettsii– Spread by wood ticks (Dermacentor andersoni)

and dog ticks (Dermacentor variabilis)– Measles-like rash, except that the rash also M as s rash, c pt that th rash a so

appears on the palms and soles– Without early diagnosis, mortality rate is

approximately 20%– Treatment with tetracycline and chloramphenicol

U.S. geographic distribution of Rocky Mountain spotted fever (tickborne typhus), 2011 Life cycle of the tick

vector (Dermacentor spp.) of Rocky Mountain spotted fever

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Viral Diseases of the Cardiovascular and Lymphatic Systems

Learning ObjectivesDescribe the epidemiologies of Burkitt's lymphoma,

infectious mononucleosis, and CMV inclusion disease.

Compare and contrast the causative agents, vectors, reservoirs, and symptoms of yellow fever, dengue, and dengue hemorrhagic fever.

Compare and contrast the causative agents, reservoirs, and symptoms of Ebola hemorrhagic fever and Hantavirus pulmonary syndrome.

Burkitt's Lymphoma• Tumor of the jaw• Most common childhood cancer in Africa

– Due to Epstein-Barr virus (human herpesvirus 4)

– Cancer starts in immune cells – B cells– Rapidly fatal if left untreated

• In areas without malaria, it is rare and is abdominal

• Malaria infections foster development of the plymphoma by suppressing the immune system’s response to the virus

• EB virus establishes a lifelong infection in most people that is harmless and rarely causes disease

Infectious Mononucleosis• Caused by Epstein-Barr virus• In developing world, 95% of adults have antibodies. In the US,

20% of adults have antibodies.f• Childhood infections are often asymptomatic• Transmitted via saliva due to persistent infection of mouth

and throat; incubation of 4 to 7 weeks• Fever, sore throat, swollen lymph nodes, enlarged spleen• Peak incidence is age 15-25; no recommended therapyg ; py• Replicates in resting memory B cells

– Form unusual lobed nuclei– Produce heterophile antibodies

• Weak antibodies with multi-specific activities• Used in diagnosis of the disease

Lymphocyte with an unusual lobed nucleus characteristic of mononucleosis

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Other Diseases and Epstein-Barr Virus

• Epstein-Barr virus associated with:– Multiple sclerosis

• Autoimmune attack on the nervous system

– Hodgkin's lymphoma• Tumors of the spleen, lymph nodes, and liverm f p , ymp ,

– Nasopharyngeal cancer

Cytomegalovirus Infections• Cytomegalovirus (human herpesvirus 5)• Remains latent in white blood cells; replicates slowly;

evades antibodies by moving between cells• 80% of population in the US carry it• 80% of population in the US carry it• May be asymptomatic or mild in adults• Infected cells swell

– Form "owl's eyes" inclusions

• Cytomegalic inclusion disease (CID)– Transmitted across the placenta; causes mental

retardation or hearing loss in newbornsretardation or hearing loss in newborns– 40%-50% rate if initial infection occurs during pregnancy

• Immunocompromised – CMV may cause a life-threatening pneumonia

• Transmitted sexually, via blood, saliva, or by transplanted tissue

Typical U.S. prevalence of antibodies against Epstein-Barr virus (EB virus), cytomegalovirus (CMV), and

Toxoplasma gondii (TOXO) by ageViral hemorrhagic fevers are a group of illnesses caused by four families of viruses.

Viral Hemorrhagic Fevers

Ebola virusMarburg virusLassa fever virusesYellow fever viruses

C f t th ff t th Common features: they affect many organs, they damage the blood vessels (hemorrhage), and they affect the body's ability to regulate itself.

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Yellow Fever• Yellow fever virus is injected into the

skin from the Aedes aegypti mosquito• Fever, chills, headache, nausea, vomiting

d d l d• Jaundice due to liver damage- bile pigments deposited into the skin

• Endemic in tropical areas• No treatment; attenuated vaccine

available• Mortality rate 20%Mortality rate 20%• Local control of mosquitoes and

immunization are effective controls• Monkeys are a natural reservoir; human

to human transmission maintains the disease

Yellowing of skin gives the disease its name – Yellow Fever

Dengue and Severe Dengue

• Milder than yellow fever; transmitted by A. aegypti

• Endemic to the Caribbean and tropical environments

• Asymptomatic and mild (dengue) to severe bleeding and organ impairment (severe dengue)

• No animal reservoir• No vaccine or effective drug treatment• Vector control has NOT proven successful

50 million cases annually in at least 100 countriesLeading cause of death among southeast Asian childrenRecent cases in Florida raises concern for emergence of Dengue in the US

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Emerging Viral Hemorrhagic Fevers

• Marburg virus (green monkey virus)– Transmitted from African monkeys– Headache, high fever, vomiting blood,

profuse bleeding internally and externally– Death occurs from organ failure and shock

• Lassa fever– Arenavirus; found in rodent urineArenavirus; found in rodent urine– Found in West Africa– Similar to Argentine and Bolivian hemorrhagic fevers (South America) and Whitewater Arroyo virus (California)

Emerging Viral Hemorrhagic Fevers

• Ebola hemorrhagic fever– Caused by the Ebolavirus, a filovirus similar

t th M b ito the Marburg virus– Reservoir is the cave-dwelling fruit bat

near the Ebola River in Africa– Spread by contact with infected body

fluids– Damages blood vessel walls and interferes

with blood coagulation• Blood leaks into surrounding tissue

– Mortality rate of 90%

Emerging Viral Hemorrhagic Fevers• Hantavirus pulmonary syndrome

– Caused by the Sin Nombre virus– Fatal pulmonary infection; lungs

fill with fluids– Found in the western United

States– Transmitted via inhalation of virus

in dried urine and feces of small rodents– Hemorrhagic fever with renal syndrome

• Found in Asia and Europe• Affects kidney function

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Protozoan Diseases of the Cardiovascular and Lymphatic Systems

Learning Objectives

Compare and contrast the causative agents, modes of transmission, reservoirs, symptoms, and treatments for Chagas' disease, toxoplasmosis,

l i l ish i sis d b b si sismalaria, leishmaniasis, and babesiosis.Discuss the worldwide effects of these

diseases on human health.

Chagas' Disease (American Trypanosomiasis)• Caused by Trypanosoma cruzi

–Flagellated protozoan–Reservoir in rodents, opossums, and armadillos;

grows in the gut of the kissing buggrows in the gut of the kissing bug–Cardiovascular disease

• Vector is the reduviid bug (kissing bug)–Defecates trypanosomes into the bite wound of

humans–In Arizona, 40% of this bug carried T. cruzi

Ch i f f th di • Chronic form of the disease causes megaesophagus and megacolon–Death due to heart damage

• Therapy is difficult due to trypanosome multiplying intracellularly

S th A i South America Infects 18 millionKills 50,000 annually

Toxoplasmosis• Disease of blood and lymphatic vessels• Caused by Toxoplasma gondii

– Spore forming protozoanUndergoes its sexual phase in cat – Undergoes its sexual phase in cat

intestines• Oocysts shed in cat feces

• Contact with cat feces or undercooked meat introduces oocysts to the intestines– Oocysts form trophozoites that invade cells; may become a chronic

infection

• Primary danger is congenital infection if infection is acquired Primary danger is congenital infection if infection is acquired during pregnancy– Stillbirth– Neurological damage

• In US, 4000 cases annually; most are asymptomatic• Infected sea otters acquire a fatal encephalitis

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Life cycle of Toxoplasma gondii, the cause of toxoplasmosis

Cat ingests bradyzoites in tissue cysts of animals, usually mice.

Immature oocyst isshed in cat feces.

I

Sporogony

Sporocysts

Mature oocysts develop by sporogony and contain two sporocysts, each withfour infective sporozoites.

Mature oocyst(10–13 µm x 9–11 µm)

Definitive hostImmature cyst

Sporozoite

Bradyzoitesin tissue cyst

Tachyzoites

Oocysts can infect many hosts, including mice, domestic animals, and humans, via ingestion. Intermediate hosts

Sporozoites from ingested oocysts invade animal tissue and develop into bradyzoiteswithin tissue cysts or into tissue-invading tachyzoites.

If humans eat undercooked meat containing tissue cysts, they may become infected.

If a pregnant woman accidentallyingests oocysts (contacted whenchanging a cat litter box), prenatalinfection of the fetus may occur.

Malaria• Caused by Plasmodium parasites• Transmitted by Anopheles mosquitoes

Aff t 300 t 500 illi l b ll • Affects 300 to 500 million globally • 2 - 4 million deaths annually• Four major forms:

– Plasmodium vivax: mildest and most prevalent form; dormant in the liver

– Plasmodium ovale and Plasmodium malariae: benign; restricted geographically

– Plasmodium falciparum: most deadly; severe anemia; blocks capillaries; affects the kidneys, liver, and brain

Malaria in the United States

Estimated to kill one African child every 30 secs

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Malaria• Mosquito bite transmits sporozoite

into the bloodstream– Enters the liver cells (which undergo

schizogony asexual reproduction) schizogony, asexual reproduction), resulting in the release of merozoites into the bloodstream

• Merozoites infect RBCs and again undergo schizogony– Ruptures the infected RBCs, releasing

toxic compounds An erythrocyte being invaded by a merozoite– Causes sudden occurrences of chills

and fever

• Some merozoites develop into gametocytes and are taken up by a mosquito, repeating the cycle

invaded by a merozoite

Male and female gametocyes

Figure 23.25 Malaria.

M it

RBCs

Merozoites

Ri fRBCs Ring forms

Merozoites being released from lysed RBCs

Malarial blood smear; note the ring forms.

Life cycle of Plasmodium vivaxMalaria

• Difficult to develop a vaccine– Plasmodium rapidly mutates and evades an immune

response

Difficult to diagnose without sophisticated • Difficult to diagnose without sophisticated equipment; examine a blood smear

• Prophylaxis– Chloroquine; Malarone for chloroquine-resistant areas

• TreatmentA t misi i– Artemisinin

• Prevention– Insecticide-treated bed nets– Anopheles mosquito is a

night feeder

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Leishmaniasis• Transmitted via female sandflies

– Promastigote transmitted in saliva from bites

– Amastigote proliferates in phagocytic cells– Smaller than mosquitoes

• Leishmania donovani (visceral leishmaniasis)– Invades the internal organs– Often fatal

• Leishmania tropica (cutaneous m p (leishmaniasis)– Forms a papule that ulcerates and leaves a

scar

• Leishmania braziliensis (mucocutaneous leishmaniasis)– Affects the mucous membranes

Helminthic Disease of the Cardiovascular and Lymphatic Systems

Learning Objective

Diagram the life cycle of Schistosoma,and show where the cycle can be interrupted to prevent human disease.

Schistosomiasis• Caused by small blood flukes called Schistosoma

– Parasitize blood capillaries– Feces carrying eggs get into the water supply

• Snails serve as the intermediate host• Snails serve as the intermediate host– Cercariae released from the snail penetrate the skin of humans– Eggs shed by adult schistosomes in the host lodge in tissues, forming

granulomas

• Second to malaria in the number of people killed or disabled

• Schistosoma haematobium: urinary schistosomiasisy• Schistosoma japonicum: intestinal inflammation; found in Asia• Schistosoma mansoni: intestinal inflammation; found in South

America

• Sanitation and elimination of the snail host are useful control measures

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Adult female flukes lay eggs.

Female (size:15–20 mm)

EggsMale

Adultflukes

Definitive host

Cercariae travel through circulatory system to intestinal blood vessels,

Male

MouthSuckerFemaleMouth

Schistosomiasis

Male and female

Cercaria(0.13 mm)

Eggs reach body of water afterbeing excreted in human feces or urine.

Cercaria(0.33 mm)

Egg (0.15 mm)

Free-swimmingcercariae penetratehuman skin,losing tail.

where they mature into adults.

schistosomes. The female lives in a groove on the ventral (lower) surface of the male schistosome("split-body"), is continuously fertilized, and continuously lays eggs. The sucker is used by the male to attach to the host.

( mm) (0.15 mm)

Eggs hatch into free-swimming larvae (miracidia).

Miracidium(0.2 mm)

Miracidiumpenetrates snail.

Life cycle of Schistosoma, cause of schistosomiasis

Miracidium reproducesin snail, formingseveral cercariae.

Cercariae arereleased fromthe snail.

Intermediate host

Schistosomiasis affects almost 210 million people worldwide, and an estimated 12,000 to 200,000 people die from it annually.

BIO 3372 Chapter 23-1 - gsau

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