Food poisoning and skin abscess: Staphylococcus aureus - Essay Example

Problem Food poisoning and skin abscess: Staphylococcus aureus What was the source of the organism that infected Mr T. Staphylococcus aureusexist everywhere: in air, dust, water, food or on food equipment, humans, and animals. Staphylococcus aureus is a commensal bacteria that resides in the nose and other parts of the body like the groin and gastrointestinal tract. Therefore, autoinfection is possible and occurs when there is a break in the skin tissues, due to wounding or razor nicks, is present. Autoinfection is highly probable, thus the organism’s source was Mr. T himself. 2. What contributed to the development of the abscess in the skin? The abscess in Mr. T’s skin was caused by the localized infection of Staphylococcus aureus. When S. aureus invaded the cells, it released toxins and killed the cells adjacent to the site of invasion. In response, the tissues become inflamed followed by an increase in production of white blood cells and blood flow in the infected area. The abscess is made up of pus, (dead tissue, white blood cells, infecting organisms and toxins released by both organisms and blood cells) and abscess wall of healthy cells that contained the pus to prevent transfer of infection to adjacent healthy cells. However, the infection can still be spread through the bloodstream. 3. How did S. aureus invade Mr T’s bloodstream? S. aureus was able to invade Mr. T’s bloodstream through the open cut in his left forearm. The organism can bind to proteins in the blood therefore avoiding the agents of the immune system (Gordon and Lowy, 2008). S. aureus is then transported to other organs where bacterial colonies produce cellular death and damage. 4. What caused the food poisoning in the patrons of Mr T’s restaurant Cream pies from the restaurant were contaminated by S. aureus that came from Mr. T’s infection. Staphylococcus aureus thrives in foods that are either stored at room or refrigerator temperatures. Sometimes, signs of spoilage are not obvious although the bacterial colonies could already be significantly plenty. S. aureus produces a certain toxin called staphylococcal enterotoxin B (SEB) that is heat stable. 5. What are the properties of S. aureus that allow it to cause such different types of disease S. aureus can cause different types of disease (reviewed in Gordon and Lowy, 2008) for several reasons. It efficiently adheres to and colonizes tissues utilizing surface proteins, called “microbial surface components recognizing adhesive matrix molecules” or MSCRAMMs, initiating endovascular, bone and joint infections. S. aureus persist by forming biofilms (slime) enabling it to evade host immune response and antimicrobials.It also forms small-colony variants (SCVs), which contribute to persistent infection. The organism also produces: (1) antiphagocytic microcapsule which induces abscess formation (2) extracellular adherence protein, which interfere with transport of the immune responses to the site of infection (3) pore formation in cell membranes and destruction of leukocytes. Different strains produce different proteins which lead to blood coagulation, septic shock, toxic shock syndrome and scalded skin syndrome. 6. What molecular techniques could be employed to confirm that the same strain of S. aureus caused Mr T’s infection and the food poisoning experienced by the patrons of the restaurant? Aside from the routine blood culture and stool test that are used to confirm the S. aureus infection, there are many techniques that can be used to determine the microbial strains. Molecular techniques make use of nucleic acid analysis through the polymerase chain reaction (PCR). Used are now are immunoquantitative real-time PCR (Rajkovic et al., 2006) and other PCR-based methods (Alarcon et al., 2006). DNA genotyping utilizing random amplified polymorphism detection is used (Reinoso et al., 2006) that can detect the differences that exist in the DNA sequence of the different S. aureus strains which helps in treatment design. Problem 2: Atypical pneumonia: Mycoplasma pneumoniae 1. How did Michelle acquire the organism? People at highest risk for mycoplasma pneumonia include those living or working in crowded areas such as schools or homeless shelters. The Mycoplasma is spread when the patient came in contact with droplets from the nose and throat of infected people. In schools, the infection spreads slowly because the transmission is thought to occur after prolonged contact with infected persons. The symptoms appear within one to two weeks after contacting the organism. 2. What are the distinguishing features of the mycoplasma? Mycoplasma pneumoniae belongs to the class Mollicutes (soft skin). Mycoplasmas have no bacterial cell wall, are smaller than bacteria and have small genome; its DNA codes for only ¼ of what bacteria can. The bacterium is not free-living and it can survive without a cell wall because it is always found in a host cell that has a stable environment. The presence of a triple-layered membrane which is composed mostly of sterols and fatty acids, and its protein network provide support. Mycoplasma therefore resemble mammalian cells rather than other bacteria. 3. What is known about the pathogenic properties of these organisms? Mycoplasma are extremely fastidious and therefore are highly host-specific. They reside in and infect the genitourinary and mucosa of hosts. They are also sensitive to antibodies in the host system; thus they can be found only near tissue surfaces and not deep in the cells. First phase of infection involves the mycoplasma tip organelle, made up of proteins called adhesins, which colonizes the respiratory tract. This organelle is composed of a network of interactive proteins. There are also proteins that bind fibronectins in the cytoplasms and perinucleus of the host cells (reviewed by Kannan and Baseman, 2006). However, no toxins have so far been isolated from mycoplasma. The course of infection is due to immune and inflammatory response of the host cells. Newer studies have used host surface proteins to identify virulence factors, but more needs to be done in this aspect. 4. What are “cold agglutinins”? Cold agglutinins are auto antibodies that are responsible for hemaglutination or agglutination of erythrocytes. Normally, the cold agglutinins bind to the surface antigens of erythrocytes at low temperatures but those which cause disease have a high temperature optimum near 37 ºC (reviewed in (Berentsen et al., 2007). Prevalence of cold agglutinins is in response to M. pneumonia infection and could lead to anemia. 5. What class of antibiotic is contra-indicated for mycoplasma infections and why? The beta (Β)-lactam group of antibiotics are contra-indicated for the treatment of M. pnuemoniae pneumonia. Penicillin, amoxicillin and cephalosporins are members of this group. The B-lactam antibiotics interfere with the peptide linkages that are part of the peptidoglycan molecules that are structural components of bacterial cell walls of bacteria. Since M. pneumonia do not have cell walls, then B-lactams cannot be utilized to control the organism. 6. How could a definitive diagnosis be made? Normally, the diagnosis requires blood tests for antibodies to mycoplasma. Sputum culture may also be performed; chest x-rays are routinely taken. For a definitive diagnosis, serological testing and DNA amplification are conducted. Serological tests using IgM and immune-blotting are done but M. pneumonia grows fastidiously in culture which adds difficulty to the techniques based on serology. However, the bacteria is easily detected by molecular or DNA amplification techniques based on the polymerase chain reaction (PCR) (Bebear, 2008, Cimolai, 2008). Problem 3. Tuberculosis: Mycoplasma tuberculosis 1. Could Mrs C have contracted tuberculosis from her aunt. Yes, it is possible that Mrs C could have contracted the tuberculosis from her aunt. Tubercle bacilli are easily passed on from one person to the next and in Mrs. C’s case, it was very probable that she got the bacilli from her aunt. However, upon entry to the body, natural defences are able to expel or kill the bacteria. Sometimes the bacteria will lodge in the lungs where the immune system build a defensive wall, called a tubercle, around the colonies. But inside the tubercles, the bacteria continue to multiply and when the body’s defences are down due to overwork, stress, sickness and other factors, the bacilli will multiply very rapidly leading to tuberculosis. This is the reason why symptoms of tuberculosis take years before they are manifested. 2. Did she later develop clinical signs and symptoms from this possible early contact with tubercle bacilli, despite receiving BCG vaccination as an infant. Yes, it is possible to develop tuberculosis despite having BCG vaccination as an infant. The BCG serves as a vaccine; it has a dilute concentration of killed bacilli. However, after a period of time, the body will also develop a tubercle around the bacilli from BCG and will test positive to the tuberculin test. So in people where BCG has been given, a positive tuberculin test is not an indicator of tuberculosis. 3. What pathobiological events account for her current signs and symptoms i.e. why did she have fevers, weight loss, cough, bloody sputum, a “positive” skin reaction, and an abnormal chest X-ray. The tubercle bacillus’ surface has a waxy coating that defends it from the actions of the body’s immune system. The bacillus contains tuberculin, a special protein, which stimulates special sensitivity in the tissues. Thus if the bacillus migrates to other parts of the body, they produce an allergic reaction in the tissues which leads to tissue damage. This is the reason for the positive reaction to the tuberculin test. If the tuberculosis bacilli has been in the different parts of the body like the lungs and lymph nodes, there is a tendency for the tubercles to calcify and produce sensitivity. Once the germs escape, the surrounding tissues, already sensitized, are easily damaged. The abnormal chest x-ray, where the film shows white areas in the lungs, is also due to the formation of tubercles in the lungs. Cough and bloody sputum are present due to the irritation and wound that are due to the calcified tubercles. Fevers develop when the body’s immune system is activated, recognizes the infection and busily fights off the infection. 4. What is the chance that Mrs C may pass the disease to her husband, or students and what precautions should be considered? There is a large chance that Mrs. C will pass the disease to her husband’s and other persons whom she has contact with. The tuberculosis bacilli are passed on easily when infected people spit and talk because the germs are forced into the air and can be breathed in by unsuspecting persons. Children who play with soil and eat without cleaning their hands are also in danger of getting tuberculosis. Direct contact is also sure to pass on the causative organisms; thus Mrs. C, unless she takes precautions, is in danger of passing on the bacilli to her immediate family. Fortunately, the bacilli are easily killed by boiling; thus the things, especially those that touch the mouth, should be boiled after every use. Spitting should be avoided and cleanliness should always be practiced. Moreover, the immune system must be boosted by proper exercise, nutrition and enough amount of sleep. Emotional stress should also be managed. Children should be vaccinated with BCG to provide them with protection during their childhood. This has been done in European countries leading to lowered rates of tuberculosis (Winje et al., 2008) Problem 4: Echinococcosis : Echinococcus granulosus 1. What two parasitic (i.e. helminthic or protozoan) diseases are most commonly associated with large fluid-filled masses in the liver? Based on the literature, there are two parasitic diseases that are most commonly associated with large fluid-filled masses in the liver. These are amoebic dysentery or amoebiasis and hydatid disease or echinococcosis. In amoebiasis, abscess in the liver (usually there is only one) occasionally develops. In the hydatid disease, which is due to tapeworm, surviving worms lodge in the liver resulting in cyst formation. 2. Based on epidemiological and clinical findings, which is the most likely parasitic diagnosis in this case, and why? The most likely parasitic diagnosis would be hydatid disease or echinococcosis. The patient is a sheep farmer and has lived only in temperate countries. He does not show any symptoms other than the jaundice. His liver has a large cyst. Echinococcosis is a tapeworm disease that can be found in sheep and can infect farm animals like dogs. The disease does not cause any symptoms until the infection is already well ahead. In comparison, amoebiasis is more common in tropical countries and before a liver abscess is formed, there are other symptoms like diarrhea and stomach cramps with stools having mucus and blood. , These symptoms are absent in the case of the patient. 3. Describe in detail how this disease is acquired. The disease is acquired by handling sheep and dogs contaminated with the tapeworm and ingesting the eggs through the mouth. Once the eggs hatch, the larva resides in the intestines for only a short period and then transfer to the liver where they cause cysts formation. Other sources of contamination are sheep and dog feces. 4. Give a full account of the diagnostic methods that are available to confirm this diagnosis, and suggest specific test(s) that should be undertaken in this patient. The definitive diagnosis of liver echinococcosis requires using radiologic methods like CT scans, X-ray and ultrasound. However, there are newer, less expensive and non-invasive antibody tests which can utlilize blood, urine and saliva (Sunita et al., 2007). 5. Describe the life cycle of the infecting organism as fully as possible, using appropriate terminology. Compare and contrast this life cycle with that of Taenia saginata, the beef tapeworm. The beef tapeworm, Taenia saginata can grow to nearly thirty feet. It has a segmented body and each segment can also produce eggs. Thus, they multiply to big numbers in the intestines. Due to this, the victim of infestation develops a big appetite. As an adult Echinococcus granulos produces eggs in feces of host organisms, dogs, and this can be ingested by humans. In humans, the worm goes to the intestines where the eggs hatch. The worms then move to the liver and in other organs like the lungs forming the hydatid cysts. Cysts could release the worms which reach adult size outside the cysts. 6. Give a full account of the treatment options that are available for this disease, and the possible complications of the disease and and/or its treatment? Anti-worm agents have been developed against liver hydatid disease, but the best treatment is still surgery to remove the cyst and prevent further contamination. There are currently new operative techniques that are less invasive and therefore do not result in recurrence of the condition (Filippou et al., 2007). Complications of the disease can occur when cysts are formed in other organs of the body resulting in organ failure and life threatening conditions. Since the disease is asymptomatic, cystic rupture could occur before the disease is even detected. References ALARCON, B., VICEDO, B. & AZNAR, R. (2006) PCR-based procedures for detection and quantification of Staphylococcus aureus and their application in food. J Appl Microbiol, 100, 352-64. BEBEAR, C. M. (2008) [Pathogenesis and laboratory diagnosis of Mycoplasma pneumoniae infections]. Arch Pediatr, 15, 1253-6. BERENTSEN, S., BEISKE, K. & TJONNFJORD, G. E. (2007) Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy. Hematology, 12, 361-70. CIMOLAI, N. (2008) Comparison of commercial and in-house immunoblot assays for the rapid diagnosis of Mycoplasma pneumoniae infection. J Infect Chemother, 14, 75-6. FILIPPOU, D., TSELEPIS, D., FILIPPOU, G. & PAPADOPOULOS, V. (2007) Advances in liver echinococcosis: diagnosis and treatment. Clin Gastroenterol Hepatol, 5, 152-9. GORDON, R. J. & LOWY, F. D. (2008) Pathogenesis of methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis, 46 Suppl 5, S350-9. KANNAN, T.R.& BASEMAN, J.B.(2006) ADP-ribosylating and vacuolating cytotoxin of Mycoplasma pneumoniae represents unique virulence determinant among bacterial pathogens. Proc Natl Acad Sci U S A., 103, 6724–6729. RAJKOVIC, A., EL-MOUALIJ, B., UYTTENDAELE, M., BROLET, P., ZORZI, W., HEINEN, E., FOUBERT, E. & DEBEVERE, J. (2006). Immunoquantitative real-time PCR for detection and quantification of Staphylococcus aureus enterotoxin B in foods. Appl Environ Microbiol, 72, 6593-9. REINOSO, E. B., IBANEZ, F., RASPANTI, C., BOGNI, L. O. & BOGNI, C. I. (2006) Characterization of Staphylococcus aureus strains isolated from humans in Argentina. J Basic Microbiol, 46, 286-93. SUNITA, T., DUBEY, M. L., KHURANA, S. & MALLA, N. (2007) Specific antibody detection in serum, urine and saliva samples for the diagnosis of cystic echinococcosis. Acta Trop, 101, 187-91. WINJE, B. A., OFTUNG, F., KORSVOLD, G. E., MANNSAKER, T., LY, I. N., HARSTAD, I., DYRHOL-RIISE, A. M. & HELDAL, E. (2008) School based screening for tuberculosis infection in Norway: comparison of positive tuberculin skin test with interferon-gamma release assay. BMC Infect Dis, 8, 140. Read More