23 Microbial 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.
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
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) erythemamarginatum 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
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.
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
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
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 Trypanosomabrucei Trypanosomacruzi Toxoplasmagondii Leishmania
PROTOZOA FROM OTHER BODY SITES Free-living Amebae Naegleria Acanthamoeba Trichomonasvaginalis
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 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).
Gametocytes of P. falciparumin thin blood smears. Note the presence of a “Laveran’s bib”, which is not always visible.
P. falciparumrings 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.
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. malariaeschizonts: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. malariaetrophozoites: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 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).
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. vivaxtrophozoites:show amoeboid cytoplasm, large chromatin dots, and have fine, yellowish-brown pigment.
Positive IFA result with P. malariaeschizont 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
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: 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. gondiioocysts 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.
L. tropica complex: Old Word Cutaneousleishmaniasis (oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil)
L. mexicana complex: New Word Cutaneousleishmaniasis (chiclero ulcer, bay sore)
L. braziliensis complex: Mucocutaneusleishmaniasis (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. tropicaamastigotes:ovoid in shape; large & eccentric nucleus; small, rodlikekinetoplast positioned opposite the nucleus; rodlikeaxoneme perpendicular to the kinetoplast
Babesiamicroti 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
Schistosomiasis Tissue damage (granulomas) in response to eggs lodging in tissues
Schistosomamansoni 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
Intermediate host: snail (Bulinus, Physopsis, and Biomphalaria sp)
Infective stage: cercariae
Lab Dx: eggs in stool; cystoscopy
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.