infectious diseases

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ACUTE BACTERIAL INFECTIONS. BACTERIAL INFECTIONS OF THE BLOOD. Acute bacterial infections often lead to a local acute inflammatory reaction at the site of inoculation. Entry of bacterial toxins or bacteria into the blood may lead to: 1. Toxemia 2. Bacteremia 3. Septicemia 4. Pyemia.

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3. BACTERIAL INFECTIONS OF THE BLOOD Acute bacterial infections often lead to a local acute inflammatory reaction at the site of inoculation. Entry of bacterial toxins or bacteria into the blood may lead to: 1. Toxemia 2. Bacteremia 3. Septicemia 4. Pyemia

4. TOXEMIA The circulation of bacterial toxins in the blood with the production of pathologic changes and clinical manifestations. Acute toxemia occurs most commonly in diphtheria, lobar pneumonia and typhoid fever. Chronic toxemia occurs most commonly in tuberculosis.

5. Manifestations of acute toxemia: 1. General manifestations as fever, headache, rigors, pain allover the body and rapid weak pulse. 2. Degenerative changes in parenchymal cells including: a) Toxic myocarditis which may lead to acute heart failure. b) Necrosis of adrenal cortex which may lead to acute adrenal insufficiency. c) Acute tubular necrosis which may lead to acute renal failure. d) Focal necrosis of liver. 3. Septic (endotoxic) shock

6. Manifestations of chronic toxemia: 1. Prolonged low grade fever 2. Loss of weight due to increased catabolism 3. Anemia due to bone marrow depression 4. Secondary amyloidosis

8. BACTEREMIA The presence of bacteria in the blood. Small numbers of bacteria may appear transiently in the blood of normal individuals or those with a minor septic focus. These are usually destroyed by antibodies and complement and by the cells of the reticulo-endothelial system in blood (monocytes), spleen, liver, etc. However, they may rarely settle in various parts of the body causing lesions e.g:

9. 1. Acute hematogenous osteomyelitis due to Staph. aureus derived from a minor septic focus e.g skin boil 2. Subacute bacterial endocarditis due to Strept. viridans derived from a septic tooth 3. Osteomyelitis complicating typhoid fever

10. PYEMIA A condition in which multiple small abscesses (pyemic abscesses) form in various organs as a result of impaction of septic thrombotic emboli

11. Pathogenesis: 1. Injury of venous endothelium or valvular endocardium by bacterial toxins followed by thrombosis. 2. Infection of thrombus by bacteria. 3. Fragmentation of infected thrombus by proteolytic enzymes from neutrophils leading to the formation of septic thrombotic emboli which circulate in the blood stream. 4. Impaction of septic emboli in small blood vessels in various organs leading to pyemic abscesses.

12. Types of pyemia: 1. Systemic pyemia resulting from either: a) Septic thrombosis in sytemic veins or right heart valves leading to pyemic abscesses in the lungs. b) Septic thrombosis in pulmonary veins or left heart valves leading to pyemic abscesses in brain, kidney, spleen and other organs supplied by the systemic arterial circulation. 2. Portal pyemia resulting from septic thrombosis in portal vein tribuitaries leading to pyemic abscesses in the liver.

13. Causes of systemic pyemia: 1. Acute hematogenous osteomyelitis 2. Puerperal sepsis 3. Cavernous sinus thrombosis 4. Acute bacterial endocarditis

14. Causes of portal pyemia: 1. Acute suppurative appendicitis 2. Infected piles 3. Suppuration of gall bladder and large intestine

15. Characteristics of pyemic abscesses: 1. Multiple 2. Usually peripheral 3. Usually small and uniform 4. Surrounded by a zone of congestion

16. SEPTICEMIA The presence and multiplication of highly virulent bacteria in the blood accompanied by severe toxemia. It is a serious condition that occurs most commonly in association with infections by Strept. hemolyticus and the plague bacillus.

17. Pathological features: 1. Peticheal hemorrhages in the skin, mucous membranes and serous membranes due to damage of the capillary endothelium by bacterial toxins (toxic capillaritis)

18. 2. The blood is more fluid than normal and postmortem clotting does not occur, due to the effect of hemolysins and fibrinolysins respectively. 3. The spleen is moderately enlarged and extremely soft. The red pulp is congested and easily washed out by running tap water (diffluent). Microscopically, it is heavily infiltrated by neutrophils (acute splenic swelling).

19. 4. Acute bacterial endocarditis may occur due to invasion of heart valves by bacteria. This may be followed by systemic pyemia 5. Manifestations of acute toxemia

20. TYPHOID FEVER A generalized infectious disease caused by Salmonella typhi (the typhoid bacillus), affecting mainly the lymphoid tissue, particularly that of the small intestine. Infection is aquired by ingestion of food or drink contaminated by stools or urine of patients or healthy carriers (through handling or by flies)

21. Pathogenesis: 1. Ingested bacilli enter the lymphoid tissue of the small intestine where they multiply for about 3 weeks which is the incubation period of the disease. 2. By the end of the incubation period, the bacilli enter the circulation through the thoracic duct, where they can be detected by blood culture (bacteremia). They become broken down releasing endotoxins that lead to toxemia with progressive fever. 3. Few days later, immunity begins to develop and the bacilli disappear from the blood. However, they persist in the liver and biliary passages and re-enter the intestine to pass out with the stools where they can be detected by stool culture.

22. Intestinal lesions: Are most prominent in the Peyer’s patches of the ileum but solitary lymphoid follicles elsewhere are also affected. 1.During the first week of the disease, the Peyer’s patches and the solitary lymphoid follicles are swollen due to edema, congestion and infiltration by macrophages, lymphocytes and plasma cells.

23. 2. During the second weak, patchy necrosis develops in the swollen lymphoid structures due to delayed hypersensitivity reaction to bacterial antigens. This is followed by mucosal ulceration producing “typhoid ulcers” with the following features: a) Oval with their long axes parallel to that of the bowel b) Undermined edges c) Raised floor made up of Peyer’s patches or solitary lymphoid follicles showing edema, congestion, infiltration by macrophages, lymphocytes and plasma cells (but NO NEUTROPHILS), and patchy necrosis.

25. 3. Healing begins during the third week and is complete by the fifth week in uncomplicated cases. It occurs by mucosal regeneration with NO SCARRING OR STRICTURE FORMATION

26. Extra-intestinal lesions: 1. The mesenteric lymph nodes are enlarged and show edema, congestion, infiltration by macrophages, lymphocytes and plasma cells and patchy necrosis. 2. The spleen is moderately enlarged and soft. 3. The bone marrow is infiltrated by macrophages, lymphocyte and plasma cells. This results in leucopenia due to depression of granulopoiesis.

27. Complications: A) Local (intestinal) complications: Occur most commonly during the third week and include: 1. Hemorrhage 2. Perforation of bowel leading to generalized suppurative (septic) peritonitis

28. B) Other complications: 1. Endotoxemia which may lead to: toxic myocarditis – degenerative changes in liver and kidney – Zenker’s necrosis of abdominal muscles. 2. Bacteremia which may lead to: osteomyelitis – arthritis – meningitis. 3. Impaired resistance to infection (leucopenia) which may lead to: laryngitis – bronchitis – bronchopneumonia. 4. Typhoid cholecystis with gall stones. Bacilli continue to pass out with the stools after clinical recovery (healthy carrier). 5. Persistent infection of urinary tract (healthy carrier).

29. Diagnosis: 1. Blood culture: positive during first week 2. Widal test: positive from second week onwards 3. Stool culture: positive in second and third weeks 4. Leucopenia with relative lymphocytosis

30. BACILLARY DYSENTERY “Dysentery” is a clinical term meaning a colonic disease characterized by diarrhea, tenesmus and passage of blood, mucus or pus in the stools. There are two main types of dysentery: bacillary dysentery caused by Shigella bacilli (shiga, flenerii and soneii) and amebic dysentery caused by the protozoan parasite Entameba histolytica. The lesion in bacillary dysentery is a membranous (pseudomembranous) inflammation.

32. Complications: 1. Toxemia leading to fever, and rarely peripheral neuritis or myocarditis. 2. Chronic or subacute colitis with relapses and remissions. 3. Prolapse of rectum due to straining at stools. 4. Secondary pyogenic infection of which may be complicated by portal pyemia. 5. Chronic intestinal obstruction due to intestinal stenosis following fibrous scarring


34. TUBERCULOSIS Has been increasing since the mid-1980s because of the following: 1. Mycobacerium tuberculosis frequently infects patients with AIDS who have decreased T-cell mediated immunity. 2. The appearance of multidrug resistant strains of tubercle bacilli.

35. Etiology and pathogenesis: Two species of Mycobacterium cause tuberculosis: 1. M. tuberculosis transimitted by inhalation of droplets coughed or sneezed by a patient with open pulmonary tuberculosis. 2. M. bovis transmitted by ingestion of infected milk (from diseased cows).

36. The pathogenicity of the tubercle bacillus is related to its ability to: 1. Escape killing by lysozomal enzymes of macrophages, attributed to its lipid component. 2. Induce a cell mediated immune response (delayed type hypersensitivity), attributed to its protein component.

37. Susceptibility to infection: The following groups are more susceptible to infection: 1. Immunocompromised and debilitated individuals 2. Malnourished individuals 3. Low socioeconomic classes 4. Children and old individuals 5. African and Asian races

38. Host response to the tubercle bacillus: A) Proliferative reaction: This results in the formation of an epithelioid cell granuloma (tubercle) and occurs as follows: 1. An initial influx of neutrophils occurs, but these are unable to kill the mycobacteria and are, therefore, rapidly replaced by macrophages derived from blood monocytes and tissue histiocytes, which phagocytose the mycobacteria.

39. 2. Phagocytosis of bacilli by macrophages changes them into “epithelioid cells” with vesicular nuclei and abundant pale eosinophilic cytoplasm (so called because they resemble epithelial cells in appearance). Fusion of some of the epithelioid cells results in the formation of multinucleate giant cells, some having peripherally arranged (horse-shoe) nuclei (Langhans’ type), others having their nuclei irregularly dispersed in the cytoplasm (foreign body type).

40. The epithelioid cells and the giant cells usually form well defined aggregates known as “granulomas” which may fuse to form masses visible to the naked eye. 3. Sensitized T-lymphocytes and fibroblasts appear around the granulomas

43. 4. Necrosis, known as caseous necrosis or “caseation” develops in the center of the granuloma after 2 weeks (roughly corresponding to the acquisition of delayed hypersensitivity). It appears grossly as yellowish-white cheesy material and microscopically as structureless, eosinophilic material.

45. B) Exudative reaction: Occurs in serous sacs when large numbers of bacilli reach the serous membranes in highly sensitized individuals. It is characterized by the outpouring of a protein rich exudate containing numerous lymphocytes.

47. Methods of spread of tuberlculous infection: 1. Direct spread: Bacilli are carried by epithelioid cells to the surrounding tissue leading to new tubercles. 2. Lymphatic spread: Bacilli are taken via lymphatics to regional lymph nodes leading to tuberculous lymphadenitis. This occurs more commonly in primary infection.

49. 3. Blood spread following rupture of a tuberculous lesion into a blood vessel and leading to either: a) Miliary tuberculosis if the number of bacilli entering the blood is large. In this, numerous small tubercles develop in many organs eg. Lungs, spleen, liver, kidney. b) Isolated (single) organ tuberculosis if the number of bacilli entering the blood is small. In this, isolated tuberculous lesions develop in one or another distant organ eg. epididymis, kidney, bones, brain, meninges

51. 4. Spread along natural passages eg. bronchi, ureter leading to tuberculous lesions in more distal sites.

52. The immune response to the tubercle bacillus: This is a cell mediated (type IV, delayed) hypersensitivity reaction, which occurs within 2 weeks from the primary infection. It is mediated by T-lymphocytes that have been sensitized and activated by the protein part of the tubercle bacillus on the surface of macrophages.

53. The mycobacterium-activated T-lymphocytes release chemical mediators called cytokines or lymphokines including: 1. Macrophage chemotactic factor which attracts new macrophages to the infected area. 2. Macrophage migration-inhibition factor which prevents the migration of macrophages from the infected area. 3. Interferon gamma which increases the ability of macrophages to kill intracellular mycobacteria. 4. Interleukin 2 (IL 2) which causes accumulation of T-lymphocytes in the infected area. 5. Cytotoxic factors which lyse macrophages resulting in caseous necrosis.

54. Primary tuberculosis: Occurs when the body is exposed to the tubercle bacillus for the first time i.e in individuals who have not been previously infected or immunized and, therefore, have not yet developed immunity to the tubercle bacillus. It is commoner in children (childhood tuberculosis) and is characterized by:

55. 1. A mild local reaction that may not be visible to the naked eye. 2. Marked enlargement of the draining lymph nodes The local tuberculous lesion at the site of infection along with tuberculous lymphangitis and tuberculous lymphadenitis of the draining lymph nodes constitute what is known as the “primary complex” of which there are three types:

56. 1. Primary cervical complex involving tonsil, cervical lymphatics and cervical lymph nodes

57. 2. Primary pulmonary complex involving the lung (Ghon’s focus), pulmonary lymphatics and tracheobronchial and mediastinal lymph nodes

58. 3. Primary intestinal complex involving intestine, mesenteric lymphatics and mesenteric lymph nodes (tabes mesenterica).

59. Fate of primary tuberculosis: 1. Good fate in individuals with good resistance. It occurs in most cases and involves healing of the granulomas by resolution or fibrosis and dystrophic calcification of caseous foci. 2. Bad fate in individuals with poor resistance eg. immunocompromised, debilitated or malnourished. The lesion increases in size, causes local tissue destruction and may spread by blood.

60. Secondary (reinfection, reactivation) tuberculosis: Occurs when the body has been previously exposed to the tubercle bacillus i.e in individuals who have been previously infected or immunized. In contrast to primary tuberculosis, the patient has already acquired immunity to the tubercle bacillus. It is characterized by:

61. 1. Marked local tissue destruction with extensive caseation and cavity formation or ulceration. 2. Minimal affection of the draining lymph nodes

63. LEPROSY A slowly progressive chronic granulomatous inflammatory disease caused by Mycobacterium leprae, affecting mainly the skin and peripheral nerves and leading to disfigurement and disability

64. Infection is acquired through inhalation of droplets from lesions in the upper respiratory tract. Intimate contact with a patient is necessary and the incubation period is prolonged. Inhaled bacilli are disseminated through the blood (bacteremia) and preferentially localize in cooler tissues e.g skin and peripheral nerves.

65. Two main forms of the disease occur depending on whether the patient has developed an adequate cell mediated immune response to the protein fraction of the lepra bacillus or not, namely: 1. Tuberculoid (maculoanesthetic) leprosy in patients who developed an adequate immune response, and 2. Lepromatous (anergic, nodular) leprosy which occurs in anergic patients.

66. Tuberculoid leprosy Is characterised by: 1. Skin lesions consisting of one or at most few hypopigmented, hyposthetic or anesthetic macules. 2. Involvement of cutaneous and peripheral nerves leading to muscle atrophy and loss of sensation, followed by trophic changes in the form of chronic ulcers, contractures and autoamputation of fingers and toes

67. 3. A tuberculoid reaction in the involved tissues consisting of epithelioid cell granulomas with variable numbers of Langhans’ giant cells, lymphocytes and plasma cells. Bacilli are almost never detected in these lesions.

68. Lepromatous leprosy: Differs from tuberculoid leprosy in the following: 1. It also affects upper respiratory tract, anterior eye, testis, lymph nodes and other organs. 2. Skin lesions are more widespread and consist of papules and nodules in addition to macules. Extensive lesions in the face give a characteristic “leonine facies”.

70. 3. Nerve lesions lead to nodular or diffuse thickening of the affected nerves and occur mainly in the ulnar, peroneal and facial nerves. 4. Lesions consist microscopically of sheets of foamy macrophages containing numerous lepra bacilli that often form masses (globi). There are no granulomas.

72. Diagnosis: 1. Demonstration of lepra bacilli in nasal discharge or scrapings (modified ZN or “Wade-Fite” stain) 2. Skin or nerve biopsy 3. Lepramin test

73. SYPHILIS A highly infectious, venerial, systemic chronic granulomatous inflammatory disease caused by the spirochete Treponema pallidum. Mode of transmission: 1. Sexual contact with an infected person which is the usual mode of transmission. 2. Transplacental transmission from an infected mother

74. The spirochetes penetrate intact mucous membrane or enter through an abrasion in the skin. They then rapidly invade lymphatics, then appear in the blood within 24 hours (bacteremia) before any local lesion appears.

75. Syphilitic reaction: The histologic hallmarks of syphilis are: 1. A mononuclear inflammatory cell infiltrate rich in plasma cells, reflecting an immunological response, more importantly a delayed hypersensitivity reaction. 2. An obliterative endarteritis, secodary to binding of spirochetes to the vascular endothelium (mediated by fibronectin molecules).

77. Classification: 1. Acquired syphilis which appears in three stages: primary, secondary and tertiary, depending on the development of hypersensitivity to syphilitic antigens in different tissues at different times. 2. Congenital syphilis

78. Primary Syphilis: The characteristic lesion of primary syphilis is known as “chancre” (hard sore). It appears at the site of infection which may be genital or rarely extragenital after an incubation period of 2 – 6 weeks. Genital sites include penis, scrotum, vulva, vagina and cervix. Extragenital sites include mainly the lips, tongue, mouth, fingers and nipple.

79. The chancre appears as a painless, slightly elevated, indurated red papule that soon ulcerates to give a clean-based, shallow ulcer that contains a large number of spirochetes. It persists for some weeks after which it heals with little or no scarring

80. The second lesion in primary syphilis is seen in the regional lymph nodes which are enlarged, indurated and show nonspecific acute or chronic lymphadentis, plasma cell rich infiltrates or focal epithelioid granulomas.

81. Secondary Syphilis: Lesions of secondary syphilis appear few months after disappearance of the chancre and are highly infective. They include: 1. Skin lesions: a) Syphilitic rash which may be macular, papular or pustular. b) Leucoderma (white patches). c) Alopecia (loss of hair due to damage of hair follicles in the scalp).

83. 2. Mucous patches, mainly in the mouth and vagina. These may ulcerate giving “snail track” ulcers. 3. Condylomata lata at the mucocutaneous junctions, particularly around the vulva and anus. These are polypoid soft masses made up of syphilitic granulation tissue covered by epidermis.

84. 4. Generalized enlargement of lymph nodes (lymphadenopathy), particularly the epitrochlear and suboccipital lymph nodes. The lesions of secondary syphilis disappear within few months.

85. Tertiary syphilis: Occurs years after the initial infection and most frequently involves the aorta (80 -85%) and the CNS (5 – 10%). The reaction in tertiary syphilis may take one of two forms: 1. Diffuse syphilitic reaction, seen most commonly in syphilitic aortitis. 2. Localised syphilitic reaction (gumma).

86. Gumma: Appears grossly as a “rubbery” white-grey mass that varies in size from a microscopic focus to a large tumor-like mass. It may be single or multiple. Gummas lead to destruction of the affected tissues. Thus when they occur in the skin or mucous membranes, they often ulcerate giving a gummatous ulcer with the following features: -Shape: irregular (serpigenous) -Edges: sharp -Base: indurated -Floor: yellowish, necrotic

87. Microscopically a gumma is formed of an area of necrosis resembling caseation, surrounded by a cellular infiltrate made up of many plasma cells, lymphocytes, macrophages, fibroblasts and variable foreign body giant cells. Blood vessels show obliterative endarteritis.

88. Sites and effects of gumma: Gummas may occur in most organs but are commonest in: 1. Skin and subcutaneous tissue, where they usually ulcerate. 2. Tongue (midline on dorsum), where they usually ulcerate and are precancerous. 3. Hard palate leading to its perforation. 4. Nose resulting in saddle shaped nose due to destruction of the nasal bridge.

90. 5. Liver: Scarring of multiple gummata may lead to lobulation of the liver (hepar lobatum). 6.Testes: May lead to sterilty if bilateral 7. Skull bones leading to a “worm eaten appearance” due to irregular bone destruction

91. Congenital syphilis: Because spirochetes do not invade the placental tissue or the fetus until the fifth month of gestation, transplacental syphilitic infection may lead to one of the following possibilities: 1. Late abortion 2. Still birth or death soon after delivery 3. Live borne neonate with syphilitic manifestations 4. Live borne apparently healthy neonate that develops syphilitic manifestations later on

92. In case of still birth: 1. The skin is macerated 2. The spleen is enlarged 3. The liver shows congenital syphilitic (monocellular) cirrhosis i.e diffuse fibrosis surrounding small nests o hepatic cells 4. The lung shows pneumonia alba i.e pale and airless

94. A living neonate with syphilitic manifestations shows a combination of secondary and tertiary syphilitic lesions including skin rash, mucous patches, saddle shaped nose and perforated palate, in addition to: congenital syphilitic cirrhosis, syphilitic periostitis (sabre blade tibia), syphilitic epiphysitis, syphilitic rhagades (radiating scars at the angles of the mouth) and craniotabes (thinned out skull bones)

95. Late syphilitic manifestations: 1. Interstitial keratitis leading to blindness 2. Syphilitic neuritis of the 8th nerve leading to deafness 3. Syphilitic orchitis leading to sterilty 4. Hutchinson’s teeth: The incisors are small, widely separated and notched (peg shaped) 5. Late nervous manifestations: Juvenile tabes dorsalis, juvenile GPI

97. ACTINOMYCOSIS A suppurative chronic granulomatous inflammatory disease caused by Actinomyces israeli, a Gram positive branching bacillus. The organism is found as a normal commensal in the mouth (particularly with bad teeth) and intestines. Infection is endogenous

98. The resulting lesions are in the form of multiple abscesses, each containing one or more colonies of the organism, separated by fibrous septa infiltrated by macrophages, lymphocytes, plasma cells and occasional foreign body giant cells. The bacterial colonies can sometimes be seen in the pus discharged from the lesions as small, yellow, brown or grey gritty granules called “sulphur granules”.

100. There are 3 types of actinomycosis: cervicofacial (65%), intestinal (20%) and pulmonary (15%). Cervicofacial actinomycosis: Infection results from invasion of the oral mucosa, usually following a tooth extraction. Lesions develop about the jaw and often discharge pus containing sulphur granules through multiple skin sinuses. Infection may spread by blood to the lungs.

101. Intestinal (ileocecal, abdominal) actinomycosis: Infection usually follows abdominal surgery or perforation of a viscus. Lesions occur in the ileocecal region or appendix producing a firm mass in the right iliac fossa. This may become adherent to the anterior abdominal wall, then opens through the skin by multiple sinuses discharging pus containing sulphur granules. Infection may spread by portal blood the liver leading to multiple abscesses (honey comb liver).

102. Pulmonary actinomycosis: Infection results from inhalation of microorganisms from the mouth or direct spread of infection from the liver through the diaphragm. Lesions take the form of multiple abscesses, usually in the base of the lung, which may be followed by empyema and involvement of the chest wall due to direct spread of infection from the lung. Infection may rarely spread by blood leading to lesions in the kidneys, brain and bones. N.B: Actinomyces do not usually spread by lymphatics owing to their large size.

103. MYCETOMA (MADURA FOOT, MADURAMYCOSIS) A suppurative chronic granulomatous inflammatory disease caused by either: 1. Fungi, most importantly Madurella mycetomatis, or 2. Actinomyces bacteria, most importantly Nocardia and Streptomyces species. The etiologic distinction is important since drugs are effective in bacterial but not in fungal mycetomas.

104. The organisms enter through an abrasion in the skin and lead to lesions similar to those of actinomycosis in soft tissues and bones, usually in the foot and leg, rarely in the hand. The foot becomes swollen, deformed, firm and shows multiple abscesses which open into the skin by sinuses discharging pus containing sulphur granules. Infection does not spread by blood or lymphatics.

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