TYPHOID FEVER (ENTERIC FEVER) is an acute intestinal infectious disease. Epidemics are possible but at present the disease is rare, its course is not severe. Etiology and pathogenesis. Typhoid fever is caused by Salmonella typhi. The source of infection is a sick person or a human carrier whose excretions (feces, urine, and sweat) contain the microbes. The infection is parenteral. The incubative period lasts 10—14 days. The bacteria multiply in the lower portion of the small intestine and produce endotoxins. Then they enter Peyer's patches and solitary follicles through the lymphatic vessels, after that they invade regional lymphatic nodes. Then the causative agent enters the blood. Bacteremia develops (1st week of the disease), the bacillus can be isolated from the blood (homo-culture). Bacteremia is associated with gene-ralization of the infection. Beginning with the 2nd week antibodies to the causative agent are determined in the blood with agglutination reaction (Widal's reaction). Bacteremia is also associated with elimi-nation the causative agent that is excreted with the sweat, milk, urine, feces, bile. The patient is especially infective during this period. The most favorable conditions for the life of the bacteria are in the bile where they
intensively multiply (bacteriocholia). They are excreted with the bile to the small intestine and cause hyperergic reaction in the previously sensibilized lymphatic follicles. The condition results in necrosis of the intestine lymphatic system.
Pathology. The changes in typhoid fever can be local and generalized. Local changes occur in the mucous membrane and lymphatic system (group and solitary follicles of the intestine). When they are present mainly in ileum, the disease is called ileoty-phus, colon — colotyphus, both in the ileum and colon — ileocolotyphus. But the most prominent changes develop in the Peyer's patches of the ileum (ileotyphus). These changes develop in 5 stages: medullar swelling, necrosis, ulcer formation, ulcer, healing (recovery). Each stage takes approximately one week. Similar sequence of changes is observed in the lymphatic nodes of the mesentery (especially ileocecal angle).
Common changes. The changes in typhoid fever may be typical only for this disease as well as characteristic for any infection. The former are roseolo-papular rash, typhoid granuloma in different organs, the latter are the processes in the organs of the lymphatic system and degenerative changes in the parenchymal organs.
Atypical forms are pneumotyphus, cholangio-typhus.
Complications: 1) intestinal (intraintestinal hemorrhages, ulcer perforation, peritonitis); extra intestinal (pneumonia, purulent perichondritis of the larynx, Zenker's necrosis of the abdominal muscles, osteomyelitis, intramuscular abscesses).
The death is caused by the complications.
SALMONELLOSIS'^ intestinal infection caused by salmonellas. It is anthropozoonosis and occurs both in human beings and animals. Pathology. There are 3 forms of salmonellosis: interstitial (toxic), septic, typhoid.
Interstitial salmonellosis develops in food poisoning. It is characterized by acute gastroenteritis causing severe dehydration of the organism. The disease resembles cholera that is why it is called home cholera. Septic salmonellosis differs from interstitial one in hematogenic generalization of the causative agent with formation of metastatic abscesses in different organs while the changes in the small intestine are not significantly pronounced.
Typhoid salmonellosis resembles typhoid fever.
Complications. Toxicoinfection shock, purulent complications, dysbacteriosis when the treatment is inadequate.
DYSENTERY (originates from Greek dys — bad, disturbed and enteron-intestine) is an acute intestinal infection characterized by involvement mainly of the large intestine and intoxication phenomena.
Etiology. The disease is caused by Shigella. The route of infection is feco-oral. Incubative period lasts for 3 days.
Pathology. Both local and general changes can be noted in dysentery. Local changes develop in the mucous membrane of the large intestine (mainly in rectum and sigmoid colon). Then colitis develops in 4 stages: catarrhal colitis, fibrinous colitis, ulcer formation (ulcerative colitis), healing of the wound. In case of solitary follicle cell hyperplasia, they enlarge and protrude over the surface of the mucous membrane (follicular colitis and follicular-ulcerative colitis). Lymphadenitis develops in the regional lymphatic nodes. Common changes are spleen hyperplasia, fatty degeneration in the heart and liver, small-focus necroses in the liver, necrosis of renal tubule epithelium.
Complications of dysentery are perforation (microperforation) of the ulcer with development of paraproctitis or peritonitis, intestinal phlegmon. Intraintestinal hemorrhage, scar stenosis of the intestine are less common. Extraintestinal complications are bronchopneumonia, pyelonephritis, serous (toxic) arthritis, pylephlebitic abscesses of the liver, amyloidosis, intoxication, cachexia.
The death is caused by intestinal or extraintestinal complications.
AMEBIASIS is an infectious disease caused by the protozoan parasite Entamoeba histolytica. The disease is common in India, Mexico, and Colombia, where
approximately 40 million cases of dysentery are observed.
Etiology. E. histolytica cysts, which have a chitin wall and four nuclei, are the infectious form of the parasite because they are resistant to gastric acid. In the colonic lumen, cysts release trophozoites, the ameboid form, that reproduce under anaerobic conditions without harming the host.
When amebae attach to the colonic epithelium, lyse colonic epithelial cells, and invade the bowel wall they cause clinical features of dysentery — bloody diarrhea, intestinal pain, fever.
Morphology. Amebiasis most frequently involves the cecum and ascending colon, followed in order by the sigmoid, rectum, and appendix. In severe, fullblown cases, however, the entire colon is involved. Amebae can mimic the appearance of macrophages because of their comparable size and large number of vacuoles; the parasites, however, have a smaller nucleus, which contains a large karyosome. Amebae invade the crypts of the colonic glands, burrow through the tunica propria, and are halted by the muscular mucosa. There the amebae fan out laterally to create a flask-shaped ulcer with a narrow neck and broad base. As the lesion progresses, the overlying surface mucosa is deprived of its blood supply and sloughs. The earliest amebic lesions show neutrophilic infiltrates in the mucosa, which later develop into ulcers that contain few host inflammatory cells and areas of extensive liquefactive necrosis.
In amebic dysentery, parasites can penetrate portal vessels and embolize to the liver to produce solitary, or less often multiple, discrete abscesses. Amebic liver abscess has a scant inflammatory reaction at its margins and a shaggy fibrin lining. Because of hemorrhage into the cavities, the abscess is sometimes filled with a chocolate-colored, odorless, pasty material resembling to anchovy paste. Secondary bacterial infection may make this abscess purulent. Sometimes, amebic abscesses reach the lung and the heart by direct extension or spread through the blood into the kidneys and brain.
CHOLERA (originates from Hebrew choul ran — bad disease) is acute infection disease with primary lesion of the stomach and small intestine. Cholera is quarantine (convection) infection, it is extremely contagious. This disease belongs to the group of anthroponoses.
Etiology. The disease is caused by the vibrio isolated by R. Koch in 1884. The most significant are Koch vibrio and El Tor vibrio (El Tor is a quarantine site in Egypt where it was isolated in 1906, earlier it was regarded as conditionally pathogenic).
Epidemiology and pathogenesis. The disease propagates in the form of epidemics or pandemics. There have been 7 pandemics of cholera during the recent 150 years. The 7th one began in 1961 in Indonesia (Sulavesi), then it spread over the countries of Asia, Europe, Africa. It was caused by El Tor vibrio
which is more resistant when compared with the vibrio of Asia cholera and exists both in fresh and salt water. It also lives longer in the environment. The source of infection is a sick person or vibrio carrier. The reservoir of the causative agent is water. The infection is enteral and develops when drinking infected water. Incubative period lasts for 3—5 days.
Pathology. Cholera develops in 3 stages: choleric enteritis, choleric gastroenteritis, algid period. The manifestations of exsicosis are noted both at external and internal examination of the corpse. Rigor mortis develops quickly and persists for several days. The outlines of the muscles are well pronounced («gladiator posture»). The skin, as a rule, is dry, creasy (especially on the fingers, «beef-steak hands»). Due to rapid development of rigor mortis, it resembles goose's skin. The mucous membranes, subcutaneous fat and muscles are dry, the muscles become dark red. The blood in the veins is thick, dark. The serous membranes are also dry, covered with sticky transparent mucus which is stretched out in the form of threads.
Dehydration causes changes in different organs (spleen, liver, gallbladder, kidneys, myocardium, brain). The spleen diminishes, its capsule becomes creasy, the follicles are atrophic, pulp hemosiderosis is observed. Hepatocyte degeneration and focal parenchyma necroses develop in the liver. Bile formation is disturbed. The gallbladder is not distended, filled with clear light bile («white bile»).
Tubular epithelium necrosis of the main portions of nephron (the changes observed in oliguria and acute renal failure) is noted in the kidneys. There are degenerative and necrobiotic changes in the brain and myocardium.
Complications. There are specific and unspecific complications of cholera. Cholera typhoid and post-cholera uremia are specific complications. Unspecific complications are pneumonia, abscesses, phlegmon, erysipelas, sepsis. The death occurs in algid period and is caused by dehydration, coma, uremia, intoxication. At present owing to early adequate treatment (administration of water and salts, antibiotics) the death rate has been considerably decreased. The death may be caused by complications, uremia being the most frequent.
ANTHRAX known since antiquity, it was described in Homer's Iliad. It is of great historical interest for it was the first human disease of proved bacterial origin. Although numerous, large, rod-shaped organisms had been observed in the blood of animals dying of anthrax in 1850, it remained for Robert Koch to prove that these organisms were actually the cause of anthrax. This he did in 1876, at the same time formulating what we now accept as Koch's postulates. In 1881 Pasteur succeeded in attenuating the organism and produced an effective vaccine, the first successful practical application of active immunization in the control of disease.
Etiology and pathogenesis. Bacillus anthracis is a long (4.5 to 10 μm), square-ended, gram-positive rod that often grows in short chains. It is capable of forming very resistant spores, but spore forms do not occur in animals or humans with the disease. Many species of animals are susceptible to infection, but grazing animals are most commonly affected, especially sheep and cattle. The disease in animals almost invariably results in septicemia and death. In the so-called apoplectic form, death may occur within an hour or two after symptoms are first noticed. Animals, in contrast to humans, usually become infected by ingesting the spores. These pass unharmed through the stomach and invade the intestinal mucosa. The spore forms are so resistant that pastures once seeded with B. anthracis remain a source of infection indefinitely.
Human gastrointestinal anthrax occurs when unenlightened or impoverished people eat the carcasses of animals dead of anthrax. Farmers, butchers, and veterinarians are occasionally infected, and a small number of cases have been reported in which the disease followed the use of a shaving brush or hairbrush with contaminated bristles. Infection also occurs from the biting of flies (family Tabanidae).
Pathology. Most commonly the disease occurs in the form of the malignant pustule, as a result of entry of B. anthracis into an abrasion or scratch of the skin. In the majority of instances, the primary infection is
of the head or neck. The lesion first appears as a papule, soon surrounded by a zone of edema and hyperemia. Vesiculation occurs, and on rupture of the small blister an eschar forms. Soon there is central necrosis, and a small ragged black ulcer develops. This may be surrounded by minute vesicles or pustules. Sometimes the local lesion involves a large area. The lesion is not particularly painful, though characteristically there is intense itching. Regional lymph nodes are somewhat swollen and tender, but involvement is not comparable to that seen in tularemia or plague. In the majority of instances the disease remains localized, and in a week or two the small ulcer heals. The eschar may separate from the underlying tissue, leaving a suppurating slough. Especially if lymphadenopathy is a prominent feature, forces of localization may be overcome and septicemia may result. This is accompanied by profound systemic manifestations, and death is the usual consequence. Generalization of the infection (septicemia) is more likely to occur here than in the case of the malignant pustule. Next in frequency is the pneumonic form (wool-sorter's disease), which occurs from inhalation of the spores. In this case the malignant pustule forms in a bronchus, and this soon leads to an extensive hemorrhagic consolidation of the involved lobe or lobes. There are striking systemic manifestations, progressive dyspnea, and cough productive of bloody sputum.
Morphologic changes are characterized principally by a bloody mucinous edema that affects many tissues and is found in most serous cavities. Meningitis may be a prominent feature. The damage wrought by B. anthracis in the septicemic form of anthrax is so overwhelming that there is relatively little cellular reaction, principally necrosis with massive bloody edema. In the acute septicemic forms death occurs in over 90% of the patients unless they are treated promptly with specific antiserum or sulfonamides.
PLAGUE (bubonic plague, black death, pest). History. Epidemiology. This most dreaded of medieval diseases has ravaged Europe and Asia in numerous pandemics. One of the most serious of these began in China in 1374, killing 13 million people there and spreading to involve all of Europe. An estimated 25 million lives were lost to the disease within a 3-year period, approximately one fourth of the total population of Europe at that time. There have been recent pandemics, the most serious of which raged intermittently for 30 years, affecting principally India and costing 12 million lives there.
Etiology. The causative organism is Yersinia pestis, a pleomorphic, gram-negative coccobacillus that presents bipolar bodies; it is often encapsulated. Depending on the animal reservoir, two forms of the disease are recognized. In murine plague, rats (most commonly the gray sewer rat) serve as the primary source of infection. As the rodent succumbs to the
disease, it often enters some human dwelling to die. Infected fleas leave its body, and an acceptable host is found in the common black house rat. In sylvatic plague, rodents of non-domestic habits are the source of infection. The disease is endemic in India, China, East Africa, and South America. The disease is transmitted to humans in two principal ways. More commonly, infection results from the bite of an infected flea (especially Xenopsylla cheopsis and Pulex irritans). The body louse and bedbug also may serve as vectors of infection. Less common is the pneumonic form of the disease, spread directly from person to person by droplets. Occasionally, especially in children who may handle dead rodents, there is direct infection of wounds or other lesions.
Pathology. The incubation period averages 2 to 4 days. Although there may be prodromal symptoms such as malaise and headache, more often the individual first responds with a sudden chill, fever, and other symptoms of severe toxemia or septicemia, including nausea and vomiting. As in the case of tularemia, it may be a day or two before onset of the obvious lymphadenitis. This occurs most commonly in the inguinal lymph nodes, less often in the axillary nodes, and only occasionally in the cervical nodes. The buboes (bubonic plague) are very painful and may attain great size, up to 4 or 5 cm in diameter. Within a day or two, organisms find their way into the bloodstream by entering blood vessels directly or in
infected thoracic duct lymph, and the septicaemic stage of the disease develops. Profound systemic manifestations progress, and the patient, at first very nervous and apprehensive, may sink into coma and die within a few days. There are three clinical forms of the disease. That just described represents the bubonic type, which is the most common. Death occurs in 60% to 90% of the patients. In the primary septicaemic type there may or may not be buboes. This form of the disease is almost always quickly fatal, as is the highly infectious pneumonic type, in which death may occur within a few hours after first symptoms.
Morphologic changes in those dying of plague represent the effects of overwhelming infection by bacteria that produce potent necrotizing toxins coupled with disseminated intravascular coagulation. The picture is much the same everywhere. Large areas of necrotic tissue are seen, and these tissues are teeming with organisms. In the fulminant forms of the disease, lesions include relatively little inflammatory exudate but much hemorrhage. When the infection is not so overwhelming, exudation of inflammatory cells may be prominent, even to the point of suppuration. For instance, in the pneumonic form of the disease, only severe hyperemia and sanguineous edema may be found in the lungs of persons dying quickly. If the process continues longer, lobular pneumonia develops and may progress to confluence, giving the picture of lobar pneumonia.
In involved lymph nodes (buboes), the gland is almost replaced by hemorrhagic necrotic tissue. This reaction spreads beyond the confines of the capsule, and in the surrounding tissues, necrosis, hemorrhage, and cellulitis are also evident.
Causes of death are septicemia, cachexia, intoxication and pulmonary complications.
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