Undulant Fever Brucellosis Bangs Disease

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Only about 150 cases of human brucellosis are reported each year in the United States. Between 10 and 20 times that number of cases, however, go unreported annually. Brucellosis is often called

Table 28.2 "

Rabbit Fever" (Tularemia)

Symptoms

Ulcer at site of entry, enlarged lymph nodes in area, fever, chills, achiness

Incubation period

1 to 10 days; usually 2 to 5 days

Causative agent

Francisella tularensis, an aerobic Gram-negative rod

Pathogenesis

Organisms are ingested by phagocytic cells, grow within these cells, spread throughout body

Epidemiology

Present among wildlife in most states of the United States. Risk mainly to hunters, trappers, game wardens, and others who handle wildlife. Mucous membrane or broken skin penetration of the organism, as with skinning rabbits, for example; bite of infected insect or tick. Occasionally, inhalation

Prevention and treatment

Vaccination for high-risk individuals; avoiding bites of insects and ticks; wearing rubber gloves, goggles, when skinning rabbits; taking safety precautions when working with organisms in laboratory.Treatment: gentamicin or tetracycline

"undulant fever" or "Bang's disease," after Frederik Bang (1848-1932), a Danish veterinary professor who discovered the cause of cattle brucellosis.

Symptoms

The onset of brucellosis is usually gradual, and the symptoms are vague. Typically, patients complain of mild fever, sweating, weakness, aches and pains, enlarged lymph nodes, and weight loss. The recurrence in some cases of fevers over weeks or months gave rise to the alternative name "undulant fever." Even without treatment, most cases recover within 2 months, and only 15% will be symptomatic for more than 3 months.

Causative Agent

Four varieties of the genus Brucella cause brucellosis in humans. DNA studies show that all members of the genus fall into a single species, Brucella meliten-sis, but traditionally, the different varieties were assigned species names depending largely on their preferred host: B. abortus invades cattle; B. canis, dogs; B. melitensis, goats; and B. suis, pigs. Brucella sp. are small, aerobic, nonmotile, Gram-negative rods with complex nutritional requirements. The distinctions between the various strains are mainly useful epidemiologically and generally have little pathogenic significance.

Pathogenesis

As with tularemia, the organisms responsible for brucellosis penetrate mucous membranes or breaks in the skin and are disseminated via the lymphatic and blood vessels to the heart, kidneys, and other parts of the body. The spleen enlarges in response to the infection. Like Francisella tularensis, Brucella sp. are not only resistant to phagocytic killing but also can grow intracel-lularly in phagocytes, where they are inaccessible to antibody and some antibiotics. Mortality, generally due to endocarditis, is about 2%. Bone infection, osteomyelitis, is the most frequent serious complication.

Epidemiology

Brucellosis is typically a chronic infection of domestic animals involving the mammary glands and the uterus, thereby contaminating milk and causing abortions in the affected animals. Abortion is not a feature of human disease. Sixty percent of the cases of brucellosis occur in workers in the meat-packing industry; less than 10% arise from ingesting raw milk or other unpas-teurized dairy products. Worldwide, brucellosis is a major problem in animals used for food, causing yearly losses of many millions of dollars. In the United States, infections have been acquired by hunters from elk, moose, bison, caribou, and reindeer. About 20% of the Yellowstone Park bison herd are infected, and more than 1,000 have been killed when they wander outside the park because of fear that they will transmit the disease to cattle.

Prevention and Treatment

The most important control measures against brucellosis are pasteurization of dairy products and inspection of domestic ani-

Nester-Anderson-Roberts: I IV. Infectious Diseases I 28. Blood and Lymphatic I I © The McGraw-Hill

Microbiology, A Human Infections Companies, 2003

Perspective, Fourth Edition

28.3 Bacterial Diseases of the Lymph Nodes and Spleen 723

Table 28.3 "Undulant Fever" (Brucellosis, "Bang's Disease")

© Causative organism Brucella melitensis enters the body through mucous membranes, skin abrasions or ingestion of unpasteurized milk

@ The bacteria are taken up by phagocytes but resist digestion and grow within cells

© The bacteria enter the lymphatics and bloodstream and are carried throughout the body

@ Infection is established in other body tissues, such as the heart valves, kidneys and bones

© Osteomyelitis is the most common serious complication. Most deaths are due to endocarditis

Symptoms Fever, body aches, weight loss, enlargement of lymph nodes; symptoms may subside without treatment but then recur Incubation period Usually 5 to 21 days Causative agent Brucella melitensis, a small, aerobic

Gram-negative rod Pathogenesis Organisms penetrate mucous membranes and are carried to heart, kidneys, and other parts of the body via the blood and lymphatic system; they are resistant to phagocytic killing and grow within these cells Epidemiology Main sources of human infections:

domestic animals. Disease also occurs in wild animals such as moose, caribou, bison; butchers, farmers, veterinarians, those who drink unpasteurized milk at risk

Prevention and Vaccination of domestic animals; treatment pasteurization of milk and milk products;

gloves and face protection.Treatment: tetracycline with rifampin mals for evidence of the disease. The use of goggles or face shield and rubber gloves helps protect veterinarians, butchers, and slaughterhouse workers; remember, the bacterium can penetrate mucous membranes. An attenuated vaccine effectively controls the disease in domestic animals. Treatment using tetracycline with rifampin for 6 weeks is usually effective. ■ pasteurization, p. 114 Table 28.3 gives the main features of brucellosis.

"Black Death" (Plague)

Plague, once known as the "black death," was responsible for the death of approximately one-fourth of the population of Europe between 1346 and 1350. Crowded conditions in the cities and a large rat population undoubtedly played major roles in the spread of the disease. Plague is a potential bioter-rorism disease.

Symptoms

The symptoms of plague develop abruptly 1 to 6 days after an individual is bitten by an infected flea. The person characteristically develops markedly enlarged and tender lymph nodes called buboes—hence the name bubonic plague—in the region that receives lymph drainage from the area of the flea bite. High fever, shock, delirium, and patchy bleeding under the skin quickly develop, and in many cases, there may also be cough and bloody sputum if the lungs become involved, which is called pneumonic plague.

Yersinia Pestis Person

5 mm

Figure 28.6 Yersinia pestis Each pole of the organism is stained intensely by certain dyes, producing a safety pin appearance.

5 mm

Figure 28.6 Yersinia pestis Each pole of the organism is stained intensely by certain dyes, producing a safety pin appearance.

Causative Agent

Plague is caused by Yersinia pestis, a facultatively intracellular enter-obacterium that grows best at 28°C. The organism resembles a safety pin in stained preparations of material taken from infected lymph nodes because the ends of the bacterium stain more intensely than does the middle (figure 28.6). Extensive study has revealed some of the complex mechanisms by which Y. pestis achieves its impressive virulence. The bacterium has three kinds of plasmids distinguishable by their size. The smallest has 9.5 kilobase pairs (9,500 base pairs) and codes for an important protease called Pla that causes blood clots to dissolve by activating a substance in the body called plasminogen activator. Another activity of the Pla protease is that it destroys the C3b and C5a components of complement. ■ plasmids, pp. 66,209 ■ complement, p. 381

The middle-sized plasmid has 72 kilobase pairs, and almost its entire genome codes for (1) a group of proteins that interfere with phagocytosis and (2) regulators of the proteins' expression. These proteins are referred to as Yops, for Yersinia outermembrane proteins. The bacterium loses its virulence if this plasmid is lost. Yops are injected into host cells by a type III secretion system and are responsible for several kinds of actions. For example, Yop E destroys actin filaments of host cells, Yop H interferes with the ability of phagocytes to receive environmental signals, Yop J blocks cytokine synthesis and promotes apoptosis, and Yop M prevents the release of cytokines, which would normally call forth an inflammatory response to infection. The sum of the effects of Yops is to interfere with phagocytes that normally would kill Y. pestis and initiate an immune response to the bacterium. ■ secretion systems, p. 467 ■ actin filaments, p. 73

The size of the largest plasmid is 110 kilobase pairs, and one of its genes codes for an important antigen, F1. This protein becomes part of an antiphagocytic capsule and is an important component of plague vaccine. The stimulus for capsule production is the relatively increased temperature of a mammalian host (37°C for humans) compared with that of a flea (about 26°C). The genes for some other Y. pestis virulence factors reside on the bacterial chromosome. Included in these properties are resistance to the lytic action of activated complement, mechanisms for storing hemin and using it as an iron source, and production of a pilus adhesin. These genes are probably activated as a result of intra-cellular growth. ■ iron requirement, p. 90 ■ adhesins, p. 466

A summary of these potential virulence factors is presented in table 28.4.

Pathogenesis

Masses of Y. pestis partially obstruct the digestive tract of infected rat fleas (figure 28.7). Consequently, not only is the flea ravenously hungry, causing it to bite repeatedly, it also regurgitates infected material into the bite wounds. Chronically infected fleas do not have their digestive tract obstructed but discharge Y. pestis in their feces; the organisms can then be introduced into human tissue when a person scratches the flea bite.

The Y. pestis protease Pla is essential for the spread of the organisms from the site of entry of the bacteria by clearing the lymphatics and capillaries of clots. The organisms are carried to the regional lymph nodes, where they are taken up by macrophages. The bacteria are not killed by the macrophages and instead multiply and elaborate F1 capsular material and other virulence factors in response to the intracellular growth conditions.

Table 28.4 Virulence Factors of Yersinia pestis

Factor

Coded by

Action

Pla (protease)

9.5-kbp plasmid

Activates plasminogen activator; destroys C3b, C5a

Yops (proteins)

72-kbp plasmid

Interferes with phagocytosis and the immune response by differing mechanisms

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Responses

  • aida aman
    What is the causative agent for bangs disease?
    7 years ago
  • agostina
    Why bangs disease called?
    7 years ago
  • matthew
    What is the causative agent of undulant fever?
    5 years ago
  • michael
    What is the causal agent of bangs disease?
    5 years ago
  • Narciso
    What are the causative organisms of undulant fever?
    5 years ago
  • kati
    Can you get undulant fever from flea bite?
    3 years ago
  • Garland
    Why is brucellosis called bangs?
    3 years ago
  • Albino
    What Is The Causative Organism Of Undulant Fever?
    2 years ago
  • Christian
    What is causative agent of brucellosis?
    1 year ago

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