Microbiology Final Lecture Exam

This 12-year-old girl was in her normal state of good health when she developed a fever of several days duration. She had no localizing symptoms, except for the development of a large rash on her back (see below). Her history was notable in that she lived in Connecticut near the New York State border and had recently been walking through tall grass where her sister was taking horseback riding lessons. 1. With what organism was she infected? What disease did she have? 2. What in her history is suggestive of this disease? How is this disease transmitted? 3. How, in the absence of a characteristic rash, is the diagnosis of this disease established? 4. She was appropriately treated with antibiotics and did well. What complications can occur in patients with this disease, particularly those in whom there is no treatment or inadequate therapy? 5. What efforts can be taken to prevent this illness?

1. Borrelia Burgdorferi; Lyme disease 2. She rides horses in Connecticut and walks through tall grass 3. Flu-like symptoms, fever for several days 4. Without treatment, symptoms can lead to meningitis, erythema 5. Cover up, insect repellent, remove tick ASAP

The patient was a 36-year-old female who worked in a fast-food restaurant. At 4 p.m. on the day prior to admission, the patient told a coworker that she felt "dizzy" and thought she had been "drugged." She awoke at 3:00 a.m. on the day of admission and reported that her tongue was "thick" and she was having difficulty swallowing. On physical examination, she was weak and somnolent but her tongue and epiglottis appeared normal. She did not have a fever, rash, or any ticks on her skin. She gave no history of recent flu-like illness, tick bites, exposure to toxic chemicals, or ingestion of shellfish. Her condition worsened and she developed descending quadraparesis, requiring intubation. Cultures of stool, gastric contents, and food samples from her home were negative. A serum test revealed the etiology of her illness and an electromyogram (EMG) supported the diagnosis. She received approximately 6 weeks of supportive care, including 5 weeks of ventilatory assistance, and eventually returned to her baseline state of health. 1. What was wrong with this patient? Did she have an infection? Explain. 2. What serum test was done to diagnose her disease? Explain how it is done. 3. Explain the purpose behind culturing the different patient and environmental specimens. 4. Describe the three different forms of this disease and the epidemiology of each. Which form did this patient have? 5. Explain the pathogenesis of her disease. 6. What is appropriate therapy in this patient?

1. Clostridium Botulinum; Botulism. Dizzy, difficulty swallowing, quadraparesis 2. Clostridium botulinum toxin assay; blood, stool, and vomit may be collected the tested for the bacteria. 3. 4. Foodborne botulism: caused by eating contaminated foods (mostly canned) Infant botulism: the baby consumes spores of the bacteria which then grow in the baby's intestine and release the neurotoxin Wound botulism: due to Clostridium bacteria infecting a would and releasing neurotoxins 5. Botulin toxin is absorbed from the gut and carried via the blood to peripheral nerve synapses, where it blocks release of acetylcholine. 6. Drugs called antitoxin

The patient was an 80-year-old female who 10 days previously had had a cystocele repair performed. At the time of that hospital admission, a urine culture was obtained that revealed> 100,000 CFU/ml of an Escherichia coli strain that was susceptible to all antimicrobial agents against which it was tested. Postoperatively, she began a 7 day course of oral cephalexin. She was discharged after an uneventful postoperative course of 3 days. Ten days postoperatively, she presented with a 3-day history of diarrhea. The patient noted multiple, watery loose stools without blood, crampy abdominal pain, and vomiting. She presented with a temperature of 38.2°C, pulse rate of 90/min, respiratory rate of 20/min, and blood pressure of 116/53 mm Hg. Her white blood cell count was normal, but a large number (53%) of immature polymorphonuclear cells were seen. Physical examination, electrolytes, liver enzymes, and lipase were all within normal limits. A methylene blue stain for fecal leukocytes indicated presence of bacteria (arrow in figure below). Cultures for Salmonella, Shigella, Yersinia, and Campylobacter spp. were all negative. An enzyme immunoassay (EIA) test which was positive for the presence of a bacterial toxin in the stool established the patient's diagnosis. 1. What organism was causing this woman's diarrhea? How would you confirm this diagnosis? Why was toxin detection rather than culture used to establish the diagnosis of this patient's illness? 2. What in her history was a predisposing factor for her development of this infection? How did it predispose her? 3. What virulence factors does this organism produce, and what roles do these factors play in the pathogenesis of disease? 4. Why is this organism particularly problematic as a nosocomial pathogen? 5. Why are treatment failures and disease relapses thought to occur frequently with this organism?

1. Clostridium Difficile. Stool test. The presence of toxins is a sensitive test for C. difficile. 2. Cystocele repair caused an imbalance in the intestines. 3. Spores. enterotoxin A, and cytotoxin B. Ingestion of c. diff spores, germination and vegetative form, alter lower intestine flora allows proliferation, toxin A and B released. 4. They create heat resistant spores which makes it hard for them to be killed with medical equipment. 5. It produces spores when attacked by antibiotics.

Be able to describe the 3 categories of autoimmune diseases and give examples of each.

1. Cytotoxic Example: Grave's disease 2. immune complex reactions Example: Lupus 3. Cell mediated reactions Example:Hashimoto's thyroiditis

A 57-year-old woman with type II diabetes mellitus, Mrs. S. came to the emergency department slightly feverish after 2 days of pain in her right forefoot. When the pain started, she had noted tenderness and serous (watery) discharge between her third and fourth toes. She had been bothered before by an ulcer on the sole of her foot, apparently caused by constant scraping against her shoe. On physical examination she appeared ill and had a temperature of 39.8°C. Her right foot was swollen with patchy erythema, cyanosis, and signs of necrosis. Crusting and oozing was evident around her third and fourth toes. Cultures of the exudate and blood were obtained, and Mrs. S. was treated with antibiotics. After 24 hours she showed no clinical improvement, and the infection continued to ascend proximally. She was taken to the operating room, and multiple incisions revealed necrotic fasciitis extending to the upper thigh. As much of the necrotic tissue was removed as possible. Cultures from the wound grew the organism cultured below. Her blood cultures were negative. Mrs. S. slowly recovered and underwent a second operation for closure of her wound. 1. How does diabetes mellitus predispose to the development of skin infections? 2. What is the name of the pathogen that caused the necrotizing fasciitis? 3. What characteristics of the pathogen enabled it to invade tissues and cause massive damage? 4. Would antibiotics alone have been sufficient in eradicating this infection?

1. Diabetes causes high blood sugar which weakens immune symptoms; some diabetes causes nerve damage, reduces blood for that increases infection vulnerability 2. Group A Streptococci 3.

This 39-year-old intravenous drug user (actively using cocaine on the date of admission) was admitted with cellulitis of the right arm after experiencing fevers for several weeks. He had been treated with outpatient antibiotics without relief of either associated chills or dizziness. Two sets of blood cultures were obtained on admission. A trans-thoracic echocardiogram demonstrated a 1cm vegetation on the ventral surface of the aortic valve. The patient left the hospital against medical advice, but was readmitted 2 days later for antimicrobial therapy. Past medical history was notable for multiple hospital admissions for both cellulitis and abscesses primarily involving the patient's arm. He had had multiple drug rehabilitation treatment attempts without success. Physical examination demonstrated a thin, unkempt man in no acute distress with multiple "needle track" marks on both his upper and lower extremities. No splinter hemorrhages or signs of embolic phenomena were noted on the extremities. Cardiac exam was notable for a grade II/VI systolic murmur best heard at the left sternal border. The spleen tip was palpable. The right arm had a 10-by-6-cm excoriated area with surrounding induration. Gram stain of an organism detected in both sets of the blood cultures obtained at admission. The organism grew in broth containing 6.5% NaCl, hydrolyzed esculin in the presence of bile (i.e., was bile esculin positive), and was catalase negative. 1. What type of infection does this patient have? 2. What organisms frequently cause this type of infection in intravenous drug users (lVDUs)? What organism is causing his infection? 3. How does intravenous drug use predispose the patient to this type of infections? Briefly describe the pathogenesis of this infection. Describe what other organs may be secondarily infected and the mechanism by which secondary infections occur. 4. When considering antimicrobial therapy for this infection, what general strategy should be employed? 5. What antimicrobial resistance problems have recently emerged involving this organism? What strategies have been employed to reduce the spread of these organisms?

1. Enterococcus Spp

The patient was a 55-year-old male with a 2-month history of fevers, night sweats, increased cough with sputum production, and a 25-lb weight loss. The patient denied intravenous drug use or homosexual activity. He had had multiple sexual encounters, "sipped" a pint of gin a day, was jailed 2 years ago in New York City, and had a history of gunshot and stab wounds. His physical examination was significant for bilateral anterior cervical and axillary adenopathy and a temperature of 39.4°C. His chest radiograph showed paratracheal adenopathy and bilateral interstitial infiltrates. His laboratory findings were significant for a positive HIV serology and a low absolute CD4+ lymphocyte count. The results both an acid-fast stain and colony isolation is seen below. The same organism was detected in bronchoalveolar lavage fluid from the right middle lobe. 1. What is bronchoalveolar lavage fluid? How is it obtained? What is its value as a diagnostic specimen? 2. Which organisms can be positive for an acid-fast stain? 3. Given the medical history, which organism is likely to be causing his infection? How does the finding that the patient is HIV positive affect this conclusion? 4. What is a PPD test? What is its value in this patient? What additional tests would you order with a PPD test? 5. What infection control measures must be taken during this patient's hospitalization? What other issues are important in the management of this patient?

1. Fluid squirted into a small part of the lung and then collected for examination; used to diagnose lung disease. 2. Mycobacterium 3. Mycobacterium Tuberculosis. Since he has HIV, it will be harder to get redo the infection because he has a weaker immune system. 4. Purified Proven Derivative test is a skin test that determines if you have tuberculosis. An Xray is also needed to determine whether a person has TB disease. Mantoux test 5. Isolate infected person, use surgical masks.

A nonprofit day care center in Juneau, Alaska cared for about 30 children, both infants and toddlers. In late August 1982, five cases of diarrhea were identified when a nursery employee submitted stool samples from children with chronic diarrhea to the Southeastern Regional Lab, Division of Public Health. As part of the epidemiological investigation, the Juneau Health Center, in cooperation with the nursery, discovered an additional eight cases of diarrhea caused by the same pathogen from the nursery population. Nine of 10 infants less than 16 months old were affected, and 4 of 24 toddlers (aged 16 months through 3 years) were affected. Two cases of diarrhea caused by the pathogen were identified among siblings of positive children. Both had attended the nursery during July and were enrolled in the day care center. Clinical signs and symptoms of the infected children showed that 52% had suffered from foamy diarrhea for more than 1 week during the summer, with bloating and loss of appetite in half of them. 48% of the infected children were asymptomatic. The pathogen was identified by microscopically examining fecal smears. Oval cysts were observed. 1. What is the pathogen causing the infection? List 4 additional pathogens that could cause the diarrhea. 2. How would you have treated those infected by the pathogen? 3. Describe an appropriate way to have managed the outbreak.

1. Guardia Lambia - Yersinia enterocolitica - Shigella spp. - Salmonella spp. - Clostridium difficile 2. Antibiotics: Trinidazole 3. Wah your hands, caution when traveling, don't drink dirty water, etc. ;

A 26-year old white female presents in her physician's office with genital itching and sharp, severe pain on the labia. She complains of three previous episodes of pain over the past 6 months, each of which were followed by the appearance of red sores which crusted and healed without a scar. On examination the physician observes a cluster of small red blisters localized in the area of the worst pain. No significant discharge was observed from the vagina. The patient's urine was clear and yellow. Urinalysis revealed normal specific gravity, no sugar, no protein, no white blood cells or red blood cells and no bacteria. The patient's temperature was 36.5C. The patient history reveals that she is unmarried. She is moderately sexually active and currently using an oral contraceptive which she has been taking for about 4 years. The woman stated that she has had 5 sexual partners over the past year. She reported that her episodes have become progressively more severe. 1. What is the cause of this woman's complaint? 2. As her physician, would you recommend that this woman modify her sexual activity? 3. Is there an effective treatment for this condition? 4. What serious long-term risk does this woman have?

1. Herpes Simplex Virus 2. I would recommend using condoms 3. There is not a cure but there are drugs that help with the symptoms (Acyclovir, Famciclovir, Valacyclovir). 4. Reoccurring painful genital blisters and it may play a role of the spread of HIV.

Sixty-year-old Mr. R. was brought to the hospital with confusion, right-sided weakness, and fever. His daughter, who was visiting him, reported that when she arrived he thought "there were devils in the room." On the way to the hospital he hallucinated intermittently, telling her that he smelled roses. Three days previously he had complained of mild nausea and vomited once. When he arrived at the emergency department, Mr. R. had a generalized seizure. A CT scan of the head was normal, but a magnetic resonance imaging (MRI) scan documented T1-hypointense and T2-hyperintense signal in the cortex and gray-white matter junction in the left temporal lobe. CSF obtained by lumbar puncture contained 50 WBCs/mm3 (90% mononuclear cells) and 300 RBCs/mm3, glucose in the normal range (70 mg/dL), and elevated protein (100 mg/dL). CSF was sent for bacterial and viral culture. An electroencephalogram (EEG) revealed periodic high-voltage spike wave activity from the left temporal region. Intravenous acyclovir was started immediately. Mr. R. was continued on intravenous acyclovir for 3 weeks, which halted the progression of his neurological symptoms. However, he had many residual signs of neurological impairment and required extensive rehabilitation therapy. 1. What microbe is most likely causing this patient's symptoms? 2. What is the best single diagnostic method to establish this diagnosis 3. What is the prognosis for patients who survive this disease?

1. Herpes simplex virus 2. HSV testing, MRI 3. Outbreaks may vary

An 18-year-old coed came to the infirmary at the University of Florida complaining of nausea and left flank pain. She has been having fevers and chills off and on for about five days. The chills and fever started at about the time that she noted increased urinary frequency with some burning and pain when she urinated. She took some amoxicillin that had been given to her four months ago for cystitis. That infection had been successfully treated by the amoxicillin, but it didn't seem to be having an effect on this infection. Today she is somewhat worried because she has noted some blood in her urine. You examine the patient and ask her for a urine sample. You note a temperature of 39° C, and your physical examination shows left costovertebral angle tenderness. You note that the urine sample of your patient is cloudy and frankly foul smelling. The Gram stain of the sediment showed more than 50 white blood cells per high-power field and the microbe shown below (Figure 1). Several red blood cells were also seen. The organism was also plated on MacConkey's agar shown below (Figure 2). 1. What is the most likely site of the problem? What is an infection of this organ called? 2. What organism is most likely causing the disease? 3. What tests would you order to confirm the diagnosis? 4. Why are woman more commonly affected by this condition than men?

1. Kidneys; Pyelonephritis 2. E. coli 3. Urine test 4. Urethra is shorter

A white male, 17 years of age presented at the emergency room with a severe headache, vomiting, and a stiff neck with pain running up his back. On admission, his temperature was 101F. The young man appeared to have trouble hearing during the nurse's interview and also seemed to have trouble concentrating. The history revealed that the young man is a wrestler for the local high school team. He had felt as though he were getting a cold the past few days, since his last meet in Hicksville. He did not smoke or drink, but he had attended a party two days earlier thrown by his girlfriend and the other cheerleaders to celebrate his victory in the sectionals. He had been holding his weight at 162 for the season, so he ate little and did not drink on the day of meets (today is a day of the meet). On physical exam, the physician noticed several areas of small purplish spots on the skin of the back, thigh and arm. The boy thought those were from wrestling. 1. What is the disease and what is the most likely etiological agent? 2. Which were the critical factors in your choice of diagnosis? 3. What will most likely happen if the disease is not treated? 4. What would you prescribe to treat this disease and why?

1. Nisseria Meningitidis; Meningitis 2. Vomiting, stiff neck, fever, purplish spots 3. Coma and lasting disabilities such as deafness, speech impairment, brain damage, blindness, and paralysis. 4. Penicillin to stop growth and kills bacteria and steroids to reduce inflammation and for tissue growth.

Ms. C., a 14-year-old female, came to the emergency room with an acutely painful abdomen. Her temperature was 38.5°C, and laboratory tests indicated an elevated white blood cell count and sedimentation rate. Before results of the urinalysis and a pregnancy test were returned, a pelvic examination revealed a purulent cervical discharge. A culture was sent, and a Gram stain of the discharge was prepared and examined (see below). Abdominal tenderness was apparent during the bimanual examination. Ms. C. reported that her last menses was 4 days ago. When asked about her sexual behavior, she told the resident physician that she had intercourse for the first time 2 years ago. That relationship ended a few months ago, and she recently began "going steady" with a new friend. She and her partners have never used condoms or any other form of birth control. 1. What test should be ordered for the cervical specimen and what organism do you suspect is causing the disease? 2. Assuming that Ms. C. has PID, how did she acquire the infection? 3. What feature of this disease-causing organism prevents her from developing immunity and being immune to catching this STD in the future?

1. Nucleic Acid Test; Neisseria Gonorrhoeae 2. It moved from cervix to the reproductive organs. 3.

The patient was a 41-year-old man who had returned from Central Africa 12 days prior to his admission. He had been in Africa for approximately 7 months, working as a civil engineer on road building projects in Rwanda, Zaire, and Uganda. Seven days before admission, the patient noted the acute onset of fevers with chills as well as cough and myalgias. For the next 3 days he had episodes of fevers and chills approximately three times a day. After 3 days of fever, he sought care at a local urgent care center. He told the physician that he had just returned from Africa and had not taken malaria prophylaxis. He had a white blood cell count of 2,200/I and a platelet count of 102,OOO/I. No hematocrit was reported. A PPD test was placed. The patient was diagnosed as having bronchitis, treated with azithromycin, and instructed to return in 48 h to have his PPD read. On his return to have his PPD read, the patient was found to be hypotensive and had mental status changes. He was noted to be icteric. He was referred to the emergency room of the local hospital to "rule out hepatitis." A diagnosis was made in the hematology laboratory (blood stain below). At the time of his diagnosis, he was noted to have a hematocrit of 25%. After 24 h of antimicrobial and aggressive fluid therapy, he had a cardiopulmonary arrest. He was resuscitated. In the next 24 h, he developed acute respiratory distress syndrome and became progressively hypotensive. He was transferred to our hospital. On arrival, he was intubated and comatose. On physical examination, he was grossly icteric and tachycardic and was noted to be oozing bright red blood from his mouth and catheter sites. His laboratory tests were significant for a hematocrit of 23%, platelets of 39,OOO/I, prolonged bleeding times, and 3+ hemoglobin and 25 to 50 red blood cells in his urine. He was given fresh frozen plasma, platelets, and cryoprecipitate for his disseminated intravascular coagulation. Exchange transfusion was begun, with the patient receiving seven units of packed red blood cells. His condition continued to deteriorate, and he had a cardiac arrest from which he could not be resuscitated. 1. With what organism was this patient infected? (You should be able to identify this organism to the species level.) 2. Describe two complications associated with this organism, including the pertinent clinical findings seen in this case. What unique characteristic of this organism is important in producing these complications, and how did it contribute to producing these complications? 3. Why do you think exchange transfusion was used as a therapeutic strategy in this patient? 4. Discuss the problems associated with chemotherapy for infection with this organism.

1. Plasmodium Falciparum

Cape Verde, 2000: Between 16 August and 17 October 2000, 33 cases of acute flaccid paralysis, including 7 (21%) deaths, were reported in Cape Verde, an archipelago of 10 islands west of Senegal and Mauritania. The first patient was a child aged 2 years from the capital city of Praia; the onset of paralysis occurred on 16 August. Twenty-two cases were reported from the island of Sao Tiago, seven from Sal, three from Sao Vicente, and one from Maio. The ages of the acute flaccid paralysis patients ranged from 3 months to 38 years. The estimated population of Cape Verde in 2000 was 437,500 (World Health Organization, unpublished data, 2000). The reported routine vaccination coverage had been <80% every year since 1995. In addition to paralysis, those who were affected had experienced stiffness in the neck, flu-like symptoms, and diarrhea. The viral pathogen, identified by enzyme-linked immunosorbent assay, was a positive-sense, single-stranded ribonucleic acid (RNA) virus with a polyhedral capsid belonging to the picornavirus family (TEM is shown below). 1. What disease was involved in this outbreak? 2. Identify the pathogen and describe how it is typically transmitted. 3. How does the virus cause paralysis? 4. Would you have expected more than 33 people to have been infected by this virus during the outbreak? 5. In order to minimize the number of deaths and cases of the disease, how would you have managed the outbreak?

1. Polio 2. Poliovirus; through contaminated food or water. 3. Invades a person's brain and spinal cord 4. 5. Vaccination

An extensive ongoing outbreak of typhus occurred in refugee camps in Rwanda, Burundi, and Zaire. For people in the camps, daily living was an immense hardship. Following the outbreak of civil war in 1993, over 760,000 refugees lived in camps under appalling conditions. Sanitation and clean water were hard to find, and disease was rampant. Besides typhus, outbreaks of typhoid fever, dysentery, and malaria also affected the refugee communities. The United Nations World Food Program distributed emergency rations to curb malnutrition. In some refugee camps, the people were required to work like a chain gang, collectively, on a single tract of land at a time. Those that left the camps were assumed to be rebel forces and could be shot by government soldiers. The civil war between the two main tribes for control of the government degraded into a tit-for-tat massacre of civilians. Against this background, a typhus epidemic emerged among the displaced population of Burundi. The outbreak may have begun among prisoners in a jail in N'Gozi in 1995. Clinical aspects of the disease included headache, chills, fever, prostration, confusion, photophobia, vomiting, and rash (seen below, generally starting on the trunk). There was a fatality rate of 15% among jail inmates. At the time, the disease was not recognized and was referred to as sutama. Reports of sutama among the civilian population date back to late 1995, and in association with body louse infestation, the disease subsequently swept across the higher and colder regions of the country. During a field study in February 1997, 102 refugees with sutama underwent clinical examinations and interviews. Serum samples were collected, and infesting body lice (pictured below) were removed. Analysis of blood sera by immunofluorescence microscopy found antibodies present against the causative agent, a small obligately intracellular pathogen (TEM below). Most of the 102 patients with sutama during initial assessment presented with typical manifestations of the disease. Up to September 1997, 45,558 cases were clinically diagnosed, most of which occurred in regions at an altitude of over 1,500 meters. 1. What pathogen caused the typhus outbreak? 2. How is the pathogen typically transmitted? 3. How does the pathogen cause the bleeding under the skin that leads to the rash? 4. What recommendations would you have made to treat this pathogen? Explain why. 5. Why would the disease be most common in higher altitudes of eastern Africa? 6. Why did the outbreak first appear among prisoners?

1. Rickettsia Prowazekii

A 20-year-old college athlete, Ms. G., had arthroscopic knee surgery. Over the next week she noticed mild swelling, increasing pain, and a small amount of redness at the incision site. Within three weeks the incision site had nearly completely healed, but the patient's knee remained swollen and painful. In addition, she was febrile (41.3°C) and had developed vomiting and diarrhea. She came to the emergency department for treatment. Examination revealed a "toxic-appearing" young woman who had a sunburn-like rash on her face, mild skin peeling above the eyes, and red eyes and lips (Figure A). Her blood pressure was 70/50 mm Hg, indicating she was hypotensive, and she had elevated white cells in the blood and a significantly reduced number of platelets. Ms. G. was admitted to the intensive care unit for management of her fever and hypotension. Throat, anterior nares, and vaginal cultures were negative for S. aureus and Streptococcus pyogenes, but because the surgical incision site had healed, it was not cultured originally. Over the next day her condition worsened, despite being treated with oxacillin and supportive care (fluid and electrolytes and vasopressors to maintain blood pressure), and she developed gangrenous toes (Figure B). A needle was inserted into the site of the previous knee surgery, and 300 ml of serous fluid was removed that cultured positive (see Gram stain and Blood Agar plate (colony at end of arrow) below). The bacterium also was methicillin resistant. The treatment therapy was changed to include vancomycin, rifampin, and intravenous immunoglobulin. Two weeks after recovery the patient's hand showed extensive peeling (Figure C). 1. What is the most likely organism causing the infection? 2. Why is the incision site not highly inflamed? 3. What toxin was the target of the immunoglobulin and how does it result in the patient's symptoms? 4. What are the properties of the organism that prevented it from being cleared by oxacillin? 5. This species of bacterium was found to have infected five other patients in this same hospital unit. All had undergone surgery over a recent 3-week period. What could be done to determine if these patients were infected with the same or different strains of this bacterium?

1. S. aureus 2. the incision is not highly inflamed because the wound was opened up and drained 3. Neutralizing 4. S. aureus is resistant to penicillin allowing it to survive in the presence of penicillin 5. To determine if it is the same bacteria, you can test the antibiotics and observe the resistance.

A 24-year old, female graduate student in biology presented with exhaustion, weakness and a low grade fever. She was pale and showed poor ability to concentrate. Her history revealed that she had gradually become increasingly tired and weakened over the past two months. She had experienced low-grade fevers over the past month and felt she would need to drop out of her graduate program if she did not get this under control. She had had a severe strep throat about a year earlier and showed some signs of rheumatic fever at the time. She had had minor dental surgery about two months earlier. On examination, she had a temperature of 100°F. She had slightly enlarged cervical lymph nodes. She had a heart murmur, with abnormal valve sounds. Her ears, eyes and throat were clear. She had clear lungs and there were no significant findings in other systems. Organisms were isolated from her blood and plated on blood agar.. 1. What would be your primary diagnosis of this patient? 2. What agent do you think is causing this problem? 3. How would you make a definite diagnosis? 4. What are the possible outcomes when this disease is left untreated?

1. Subacute endocarditis 2. Streptococcus Pyogenes

Mr. D., a 33-year-old fully immunized, rather nervous accountant who is blood group O positive and taking H2 blockers for ulcer disease; his 29-year-old healthy wife; and their 10-month-old baby boy returned from a 2-week trip to South America. The next morning Mr. D. passed a semisolid stool, which was quickly followed by a large watery bowel movement. Within an hour he passed another large watery stool, now opaque gray-white in color. He vomited several times and became slightly sweaty. After passing another large watery stool, Mr. D. called his physician, who advised him to go to the emergency department. When he arrived there Mr. D. was afebrile but had a rapid heart rate with a feeble pulse and low blood pressure. He complained of muscle cramps and dizziness. All these signs and symptoms were consistent with a significant loss of extracellular fluids. Laboratory studies showed a normal leukocyte count, a slightly elevated level of serum sodium, a normal serum potassium level, and an elevated blood urea nitrogen level, also consistent with dehydration. Mr. D. was immediately given 2 liters of fluid intravenously and then started on oral rehydration solution. His stool volumes progressively diminished over 48 hours, and he was discharged. Because of the suspected diagnosis, special media were used to isolate organisms other than E. coli and they came back positive. Mrs. D., a native Peruvian, had two loose bowel movements on the second day of her husband's illness. Her stool culture grew only Escherichia coli. 1. What is the most likely organism causing Mr. D's disease? 2. Are all enteric bacteria capable of causing disease, or are some more frequently pathogenic than others? 3. What are the clinical manifestations caused by the diagnosed pathogen? 4. Why did Mrs. D. not show the same symptoms? 5. What factors are involved in colonization? What factors are involved in causing symptoms? 6. What is the proper therapy for this disease?

1. Vibrio Spp. 2. Yes, yes 3. Diarrhea, dehydration, nausea 4. She only had E. coli. 5. It colonizes in the intestine 6. Rehydration, IV fluids, antibiotics

Differentiate between the 4 types of hypersensitivities and give examples. How does the role of the immune system differ in each?

1. anaphylactic reactions 2. cytotoxic reactions ABO blood group system 2. cytotoxic reactions hemolytic disease of newborn 3. immune complex reactions 4.cell mediated reactions

Compare and contrast congenital and acquired immunodeficiency. Give one examples of each.

CONGENITAL IMMUNODEFICIENCY: Inability due to individual's genotype to produce specific antibodies or T-cells; genetic, present from birth Examples: IgA immunodeficiency & SCID (severe combined immunodeficiency disorder): affects B, T & stem cells; allows severe infection, treated w/ bone marrow & fetal thymus transplants ACQUIRED IMMUNODEFICIENCY: Inability obtained during life of individual to produce specific antibodies or T-cells due to drugs or disease. Ex: HIV: Virus destroys CD4+ & T-cells; allows cancer and bacterial, viral, fungal and protozoan diseases; retrovirus RNA > DNA (reverse transcription)

The patient is a 10 year old female, active in dance classes. She is referred to rheumatology at UPMC following a week-long bout of malaise accompanied in the last several days by a pruritic lacy rash on her trunks and limbs (Figure 1). An anti-nuclear antibody (ANA) assay obtained by the outside physician at an outside laboratory was positive to a titer of 1:1,280. On presentation at the rheumatology clinic, the pruritic lacy rash is again evident on the trunks and limbs. No photosensitivity or any appearance of a malar-type rash is appreciated. The patient is afebrile and reports no significant constitutional symptoms. On physical examination, the oropharynx is normal and no splenomegaly is appreciated. She provides additional history of exposure to parvovirus and Epstein Barr virus in dance class prior to the onset of her recent illness. There is no family history of rheumatologic disease. Believing this condition to represent infectious disease versus early rheumatologic disorder (given the high-titer positive ANA), additional laboratory studies were obtained. C-reactive protein, complement protein C3, and immunoglobulin subtype quantities were within normal limits. Complement protein C4 was below detectable limits. Specific antibody testing for anti-double stranded DNA, anti-centromere, rheumatoid factor, Epstein Barr virus nuclear antigen IgG, Epstein Barr virus capsid antigen IgG and IgM were all negative. Anti-parvovirus IgG is negative; however, anti-parvovirus IgM is positive at 6.6 mg/dL. 1. What specific genus and species is causing the symptoms? 2. What is the most likely disease? 3. What were the critical factors for your diagnosis? 3. How would you treat this disease and what is the prognosis?

Erythrovirus B19

HIV is one of the most recognized immunodeficiencies of our generation. Describe how HIV create this condition and use this to explain how HIV does not kill people. What does?

HIV virus weakens your immune cells by infecting the T helper cells which results in the immune system fighting against the T helper cells.

Differentiate between hypersensitivity, autoimmunity, and immunodeficiency.

Hypersensitivity: Immunological over-response to antigen; leads to pathological changes and/or tissue damage Autoimmunity: Loss of self-tolerance; immunity against self tissue. Immunodeficiency: Decreased or loss of function of immune system; can be congenital or acquired.

Describe the role antibodies play in the hemolytic disease of the newborn called "erythroblastosis fetalis"

If you're Rh-negative and your baby is Rh-positive, your body will react to the baby's blood as a foreign substance. It will create antibodies against the baby's blood.. Does;t usually cause problems in first pregnancy. May cause problems in later pregnancies, if the baby is Rh-positive. This is because the antibodies stay in your body once they have formed. The antibodies can cross the placenta and attack the baby's red blood cells leading to Rh disease.

Hypersensitivity

Immunological over-response to antigen; leads to pathological changes and/or tissue damage

Explain the antigenicity and cross reactions involved with the human ABO blood types.

Persons ABO blood type depends on presence or absence of antigens on cell membranes of RBCs (ie; blood type O lacks A & B antigens). -Incompatible transfusion of type A (for example) with type B causes antigens on type B blood cells to react with anti-B antibodies; activating complement which causes lysis of type B RBCs. Rh factor also plays a role in antigenicity. roughly 85% of people possess Rh antigen (Rh+), 15% don't (Rh-)If Rh factors come into contact with each other they will develop Rh(+) or (-) antibodies and upon secondary exposure responds to them by lysis.

Define the term stem cell. Differentiate between pluripotent, multi-potent, and unipotent.

Stem cell: Undifferentiated cell that gives rise to a variety of specialized cells. Pluripotent stem cells: cells derived from totipotent cells; capable of generating multiple tissue types from the three germ layers Multipotent stem cells: cells capable of generating cells of related type (e.g. Hematopoietic stem cells can form blood and lymphatic tissue) Unipotent stem cells: cells can only form one cell type, but can regenerate

A 23 year old male, a known asthmatic, developed a 'cold' a week before a referral letter was written in March. He complained of malaise, generalized dull headache, a mild sore throat and non-productive cough. After four days he suffered a severe shaking chill lasting 15 minutes, his cough worsened and the patient produced rusty colored sputum. The patient was pyrexial when examined and was admitted to hospital. Your notes are below: Presenting complaint Cold - one week Cough - one week Headache - one week Shaking chill three days ago. History of presenting complaint Known asthmatic, cold week ago, tired, headache, sore throat, general aches, chestiness. Just before tea-break three days ago suffered a chill. Cough worsened. Started coughing up sputum, wheezing got worse, pain on breathing in. Past history Known asthmatic, tonsillectomy aged 7, LGI. Current Medication Sodium chromoglycate 20 mg qds (for asthma) No recent antibiotics Social History Non-smoker, Social drinker Physical Examination 23 year old male, respiratory distress and an obvious herpetic lesion on his top lip. No signs of anaemia. Temperature: 40 C Blood pressure: 112/ 70 Rapid, shallow breathing, rate 36/min. Reduced expansion on right side. Dullness to percussion over right middle lobe. Fine crepitations over right middle lobe. Laboratory reports Blood chemistry: normal Hematology: normal, except total wbc 15,000/cu mm 1. What is your diagnosis of the patient? 2. What is the most likely etiological agent of this disease? 3. What is your proposed treatment regimen and how do his predisposing factors affect this, if at all?

Streptococcus Pneumoniae

Describe the different types of hypersensitivities and give examples of each.

TYPE I: ANAPHYLACTIC REACTIONS commonly referred to as "allergies" can be localized or systemic Reactions occur in 2 steps: Sensitization: B cell make IgE to Ag; IgE binds to mast & basophil cells Secondary exposure: Immediate reaction due to cross-linking of antigen binding to 2 IgE, causing degranulation (major release of histamines & leukotrienes) Examples: Anaphylactic shock from drug injections & insect venom; common allergies hay fever & asthma TYPE II: CYTOTOXIC REACTIONS IgG & IgM bind to target cell; triggers/activates complement system & macrophages; causes cell death Examples: Rh factor incompatibility; can lead to hemolytic disease of newborn; and ABO blood group systems TYPE III: IMMUNE COMPLEX REACTIONS Immune reaction against soluble antigens Slight excess of antigen to antibody ratio causes binding to occur; the antigen/antibody complexes stick to basement membrane of cells, triggering inflammation via neutrophils. Examples: Lupus and Rheumatoid arthritis; immune complexes of IgG, IgM & complement are deposited in the joints TYPE IV: CELL-MEDIATED REACTIONS Does not involve antibodies; mediated by cellular immune system Mostly involves allergies of skin Reactions occur in 2 steps: Sensitization: Ag combines w/ skin protein, macrophage engulfs it, presents Ag/MHC II, which activates T-cells Secondary Exposure: Memory T-cells migrate; activates T-cells & macrophages; causes dermatitis Examples: Rejection of transplanted tissues; contact dermatitis (poison ivy), and TB

Allergy

a damaging immune response by the body to a substance to which it has become hypersensitive.

Allergen

a substance that causes an allergic reaction

Anaphylaxis

an acute allergic reaction to an antigen (e.g., a bee sting) to which the body has become hypersensitive. symptoms are caused by the sudden release of chemical substances, including histamine, from cells in the blood and tissues where they are stored. The release is triggered by the interaction between IgE and the substance (allergen) causing

Explain what is meant by the term "self-recognition"

the process by which the immune system of an organism distinguishes between the body's own chemicals, cells, and tissues and those of foreign organisms and agents.