Ch 23 Microbial Diseases of the Cardiovascular and Lymphatic Systems.

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Presentation transcript:

Ch 23 Microbial Diseases of the Cardiovascular and Lymphatic Systems

Student Learning Outcomes List the signs and symptoms of septicemia Differentiate gram-negative sepsis, gram-positive sepsis, and puerperal sepsis. Describe bacterial endocarditis and rheumatic fever. Discuss the epidemiology of tularemia, anthrax, gas gangrene. Describe pathogens that are transmitted by animal bites and scratches. Compare and contrast the causative agents, vectors, reservoirs, symptoms, treatments, and preventive measures for plague, Lyme disease, and Rocky Mountain Spotted Fever. Describe infectious mononucleosis. Compare and contrast the causative agents, vectors, reservoirs, and symptoms for yellow fever, Compare and contrast the causative agents, modes of transmission, reservoirs, and symptoms for Ebola hemorrhagic fever and Hantavirus pulmonary syndrome. Compare and contrast the causative agents, modes of transmission, reservoirs, symptoms, and treatments for Chagas’ disease, toxoplasmosis, malaria, and babesiosis. Describe Swimmer’s Itch

Bacterial Diseases: Sepsis and Septic Shock Septicemia: Pathogens or their toxins persist (and proliferate) in blood. Sepsis = SIRS, caused by focus of infection releasing mediators of inflammation into blood stream. (Signs: Fever, rapid HR and/or RR, WBC) Severe sepsis  BP ? Septic shock  uncontrollable decreased blood pressure Lymphangitis: Inflamed lymph vessels accompanying septicemia and septic shock

Gram-negative sepsis can lead to septic shock or Endotoxic shock BP?? Antibiotics can worsen condition by killing bacteria New possible treatment: Human activated protein C, an anticoagulant Gram-positvive sepsis now most common. Often nosocomial. Staph, Group B streptococci (only one GBS: S. agalactiae), and Enterococcus faecium and E. faecalis Puerperal sepsis (_________________= GAS): due to uterus infection following childbirth or abortion; can progress to peritonitis or septicemia

Subacute Bacterial Endocarditis (SBE) Specific Bacterial Infections of the Cardiovascular and Lymphatic Systems Subacute Bacterial Endocarditis (SBE) Rheumatic Fever Tularemia Anthrax Gas Gangrene Bite Wounds

Subacute Bacterial Endocarditis (SBE): Usually caused by -hemolytic streptococci from mouth (dentist!) Preexisting heart abnormalities are predisposing factors. Signs include fever, anemia, and heart murmur. Acute bacterial endocarditis: usually caused by S. aureus  rapid destruction of heart valves. Pericarditis: Streptococci

Endocarditis Fig 23.4

Fig 23.5 Rheumatic Fever Autoimmune complication of S. pyogenes infections. Expressed as arthritis or heart inflammation. Can result in permanent heart damage. Antibodies against -hemolytic GAS cross-react with heart tissue. Rheumatic fever can follow strep throat. Bacteria might not be present at time of rheumatic fever. Prompt treatment of streptococcal infections can reduce the incidence of rheumatic fever.

Tularemia “Rabbit fever” caused by Francisella tularensis Bacteria reproduce in phagocytes Transmitted by bites and scratches of infected animals, carcass handling, tick bites (~ 200 cases/year) Ulcer at the site of entry and enlargement of the regional lymph nodes  Ulcero-glandular form (most common, plaguelike) Aerosol infection  pneumonic form (bio weapon!)

Reported cases of tularemia -- United States, 2000-2008 CDC MV in MA Ulceroglandular Tularemia Compare to Fig 23.6

Anthrax Bacillus anthracis G+ rod, ES, aerobic, virulence factors: capsule, 3 exotoxins Zoonosis; found in soil Cattle routinely vaccinated Cutaneous anthrax – most common, ES enter through minor cut; 20% mortality, with antibiotics <1% Pulmonary anthrax – (woolsorter’s disease), Inhalation of ES; 100% mortality Gastrointestinal anthrax – Ingestion of undercooked contaminated food; 50% mortality Treated with ciprofloxacin or doxycycline; MABs against toxin

Gas Gangrene Gangrene = Soft tissue death from ischemia  Ischemic tissues susceptible to growth of anaerobic bacteria such as: C. perfringens, G+ rod, ES, anaerobic, release of  toxin (cytotoxic), H2 and CO2 Ubiquitous in soil and dust – “war disease” C. perfringens can also invade wall of uterus during improperly performed abortions Death due to toxemia Treatment: debridement and amputation, hyperbaric chamber. Antibiotics and antitoxin of limited value (why?)

Generally occurs at wound or surgical site  painful swelling and tissue destruction. Rapidly progressive, often fatal.

Animal Bites and Scratches Anaerobic bacteria infect deep animal bites Pasteurella multocida – normal flora of oral and nasopharyngeal cavity of dogs and cats; may cause septicemia Bartonella henselae – (rickettsia) Cat scratch disease. Relatively common (~22,000 cases in US) – mostly in young – occasionally serious Human bites – (not in book) normal mouth flora (incl. S. aureus,  hemolytic viridans group Streptococci, H. influenza and various anaerobes) What is most common human bite wound?

Typical bite wound inflicted by a human: This gentleman presented with a draining sinus on the dorsal aspect of his proximal phalanx, about one month after sustaining a clenched fist bite injury.  He could not clearly recall details of his initial treatment.

. . .leading to Osteomyelitis Evidence of osteomyelitis with bone erosion and subperiosteal bone formation (arrows).

Vector-Transmitted Diseases Plague Lyme Disease Ehrlichiosis Typhus Epidemic Typhus Spotted Fevers Caused by rickettsias or rickettsia-like bacteria

Plague Bubonic plague: Bacterial growth in blood and lymph “Black death”: Yersinia pestis, G- rod, bipolar staining Endemic in Southwest  sylvatic plague Reservoir: Rats, ground squirrels, and prairie dogs Vector: infected fleas Bubonic plague: Bacterial growth in blood and lymph Septicemia plague: Septic shock Pneumonic plague: Bacteria in the lungs 15th Century Physician’s Plague suit

The Black Death Fig 23.12 History of Bioterrorism: Plague (CDC Podcast)

Biological Weapons Review Applications of Microbiology p. 654 (11th ed Biological Weapons Review Applications of Microbiology p. 654 (11th ed.) / 577 (10th ed.) 1346: Plague-ridden bodies used by Tartar army against Kaffa 1937: Plague-carrying flea bombs used in the Sino-Japanese War 1979: Explosion of B. anthracis weapons plant in the Soviet Union 1984: S. enterica used against the people of The Dalles 1996: S. dysenteriae used to contaminate food 2001: B. anthracis distributed in the United States

Potential Biological Weapons 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 burnetii Monkeypox Francisella tularensis Nipah virus Rickettsia prowazekii Smallpox Shigella spp. Yellow fever Vibrio cholerae Yersinia pestis

Lyme Disease 3 stages with various symptoms Zoonosis caused by Borrelia burgdorferi Reservoir: mice, deer; Vector: Ixodes ticks 3 stages with various symptoms Early localized stage: Bull’s eye rash = erythema (chronicum) migrans ECM; flu-like symptoms Early disseminated stage: Heart and Nervous system symptoms; also skin and joints affected Late stage: Chronic arthritis

Ixodes scapularis & Ixodes pacificus

Diagnosis Symptoms alone often lead to misdiagnosis In most cases not possible to isolate and culture B. burgdorferi  indirect serological tests (ELISA and Western blot) PCR Prevention Treatment in early stages!

Fig 23.14

Viral Diseases of the Cardiovascular and Lymphatic Systems Infectious Mononucleosis Cytomegalovirus Viral Hemorrhagic Fevers Yellow Fever Dengue Fever Marburg, Ebola, Lassa Hantavirus pulmonary syndrome

Infectious Mononucleosis “Kissing disease” – caused by Epstein-Barr virus (EBV) of Herpesviridae, also known as HHV-4 Well-established relationship between HHV-4 and oncogenesis (Burkitt’s Lymphoma etc.) Virus multiplies in parotid glands and is present in saliva. It causes the proliferation of atypical lymphocytes (life-long infection) – Transmission via saliva Most people (~95%) infected. Childhood infection usually asymptomatic. Adolescent infection  Mononucleosis. Characteristic triad: fever, pharyngitis, and lymphadenopathy (also spleno- and hepatomegaly) lasting for 1 to 4 weeks.

Triad Swollen lymph nodes, sore throat, fatigue and headache are some of the symptoms of mononucleosis. It is generally self-limiting and most patients can recover in 4 to 6 weeks without medications.

Proliferation of infected B cells results in massive activation and proliferation of CD8 cells  characteristic lymphoid hyperplasia. Transformation of B cells to immortal plasmacytoid cells  secrete a wide variety of IgMs = heterophile antibodies (Monospot test) Commercially-available test kits are 70-92% sensitive and 96-100% specific Compare to Fig 23.21 "Downy cell“: lymphocytes infected by EBV or CMV in infectious mononucleosis. Cytoplasmic rim is intensely blue and has tendency to "stream" around adjacent red cells.

Cytomegalovirus Infections Cytomegalovirus: HHV-5. (Similar to EBV) Infected cells swell (cyto-, mega-) ~80% of Americans infected Latent May be asymptomatic or mild Transmitted across the placenta; may cause damage to fetus (e.g.: mental retardation) Transmitted via bodily fluids (sexually, day care centers, transplanted tissue etc.)

Viral Hemorrhagic Fevers Classic hemorrhagic fevers, caused by arboviruses: Yellow Fever: attenuated vaccine Dengue Fever (Caribbean) Emerging Viral hemorrhagic fevers, e.g.: Marburg VHF: 1967 outbreak in Marburg (D) – imported from Africa; Mortality rate 25% Ebola HF: 1995 major outbreaks in Zaire and Sudan; Mortality rate 50 – 90% For some viruses human to human transmission Human cases or outbreaks sporadic and irregular. Not easily predictable

Hantavirus Pulmonary Syndrome (HPS) Korean hemorrhagic fever caused by Hantaan virus of Bunyaviridae HPS first reported in US in spring of 1993. Transmission through urine, droppings, or saliva of infected rodents  humans inhale aerosolized virus. No person to person transmission in US Sudden respiratory failure Mortality rate > 35%

Hanta Virus Cases

Viral Hemorrhagic Fevers Pathogen Portal of Entry Reservoir Method of Transmission Yellow fever Arbovirus Skin Monkeys Aedes aegypti Dengue Humans Marburg, Ebola, Lassa etc. Filovirus, arenavirus Mucus membrane Fruit bats, other mammals Contact with blood Hantavirus pulmonary syndrome Bunyavirus Respiratory tract Field mice Inhalation

Protozoan Diseases of the Cardiovascular and Lymphatic Systems American Trypanosomiasis (Chagas’ Disease) Toxoplasmosis Malaria Babesiosis

Toxoplasmosis Toxoplasma gondii > 60 mio people infected in US (mostly asymptomatic) Zoonosis – Transmission via undercooked meat, cat feces, drinking water. Flu-like symptoms Can cross placenta  Congenital risk (TORCH)  brain damage or vision problems Risk of new infection or reactivation in the immunosuppressed T. gondii undergoes sexual reproduction in the intestinal tract of domestic cats, and oocysts are eliminated in cat feces. Toxoplasmosis can be identified by serological tests or PCR (more accurate)

Compare to Fig.23.24

Malaria Four species of Plasmodium: P. falciparum (malignant), P. vivax (begnin), P. ovale, P. malariae Vector: Anopheles mosquito Worldwide 300-500 million cases; ~ 1.5 – 3 million people die; ~ 1,200 cases in US Plasmodium infects red blood cells  microscopic diagnosis Symptoms: chills, fever, vomiting, headache; at intervals of 2 to 3 days New drugs are being developed as the protozoa develop resistance to drugs such as chloroquine.

Microscopic Diagnosis Fig 23.26 Diagnostic!

Compare to Fig 12.20

Sickle cell trait provides protection!

….Other Schistosomes: Swimmer’s Itch or Cercarial Dermatitis Small fluke  Schistosome cercaria accidentally enters human skin (bird is definitive host for adult parasite) Almost every state in US & > 30 other countries. Most predominant in north. Disappears without treatment ( 7 days) – no internal organs involved

Parasites die after entering  dermatitis in previously sensitized individuals. Sensitivity rarely disappears; usually gets worse in subsequent exposures. the end Widely scattered from Michigan lakes to Alaska.