Clinical Topics Conference: Chapter 9b, Infectious and Parasitic Diseases I

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  1. Pelvic inflammatory disease (PID)
  2. Rocky Mountain Spotted Fever
  3. Tularemia
  4. Mycobacterium avium intracellulare pneumonitis
  5. Tuberculosis
Case 1: Pelvic inflammatory disease (PID)

Clinical vignette 1

The patient was a 19 year old female who was admitted because of vaginal bleeding of one week duration and lower abdominal pain of 3 weeks duration. Pelvic examination revealed a 5 cm, soft, non-cystic mass occupying the left adnexa. This mass appeared separate from the uterus. The right adnexae were non-palpable. The mass was noted to project into the cul-de-sac. At surgery, the left adnexal mass was found to consist of an enlarged, inflamed Fallopian tube. A peri-tubal abscess was localized and drained. The inflammatory mass did not appear to involve the left ovary. The distended portion of the tube was excised and a tuboplasty was performed. A Gram-stain of the pus aspirated from the abscess revealed intracellular Gram-negative diplococci. The culture grew Neisseria gonorrheae.

Discussion topics

  1. What micro-organisms are most commonly associated with this condition? Is drug resistance a problem?

  2. What media must be used to culture N. gonorrheae? Why must the media be immediately inoculated by the attending physician, rather than waiting for the laboratory to do it?

  3. What is the etiologic relationship of salpingitis to tubal pregnancy? to sterility?

References

  1. CDC prevention guidelines.Guide for the diagnosis of gonorrhea using culture and Gram-stained smear.

  2. CDC prevention guidelines. Policy guidelines for prevention and management of pelvic inflammatory disease (PID).


  3. MMWR 42 (RR-14), 1993. 1993 Sexually Transmitted Diseases Treatment Guidelines.

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    Case 2: Rocky Mountain Spotted Fever

    Clinical vignette 2

    The patient was a 49-year-old male Kansas University (Lawrence Campus) professor who was in apparent good health until one week prior to admission when he became febrile (104 oF), anorexic, and developed a sore throat and myalgia. He was hospitalized at Lawrence Memorial Hospital, where it was thought that he had a viral syndrome with hepatitis, because of elevated liver enzymes. During his 2 day hospitalization in Lawrence, he had severe headaches, nausea, vomiting, and he became progressively obtunded and finally developed focal seizures. He was then transferred to KUMC when he became oliguric and azotemic. His spinal fluid protein was elevated to 84 mg/dl. He developed status epilepticus and died on the evening of his admission.

    At autopsy, a generalized petechial and purpuric rash was present, which included the palms of hands. There were petechiae of the laryngeal and tracheal mucosa. The surface of the kidneys had a "flea-bitten" appearance, due to cortical hemorrhages. The spleen was friable. The brain was edematous and showed hyperemia.

    After the autopsy, it was discovered that the patient owned several hunting dogs, which his wife confirmed were infested with ticks. Although no history of tick bites was elicited in the patient or his wife, it was known that both routinely removed ticks from the dogs. It may be that removal of ticks from the dogs resulted in an infectious aerosol, although about half of patients with Rocky Mountain Spotted Fever don't remember being bitten by a tick, and they may have just been unaware of a bite. The patient's wife, upon questioning, was found to have suffered from a similar illness, although in a much milder form. Serologic examination of the wife's serum confirmed recent Rocky Mountain Spotted Fever.

    Discussion topics

    1. What other diseases are transmitted by ticks?

    2. What time of the year does RMSF occur?

    3. What is the most common geographic location for RMSF?

    4. What causes the rash of RMSF?

    References

    1. Fact Sheet on Ticks, US Army, Entomology Division

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    Case 3: Tularemia

    Clinical vignette 4

    The patient was a 44 year old male from a small town in Southeast Kansas. He was in excellent health until 7 days prior to admission, when he developed fever, arthralgias, and swelling of his right axillary lymph nodes. An ER physician prescribed a cephalosporin of unknown type, and he was sent home. He returned to the ER 2 days later with hemoptysis and jaundice. A chest x ray showed pneumonia, and liver enzymes were markedly elevated. His creatinine was 3. The family thought the patient was confused, and was perhaps experiencing hallucinations. The patient was transferred to KUMC.

    Physical exam on admission revealed a pulse of 126, respirations of 36/min, BP of 80/0, and a temperature of 102 oF. The patient was near comatose, with obvious respiratory distress. The liver was 10 cm below the right costal margin, and the spleen was palpable.

    Laboratory examination revealed a sodium of 122 meq/L, potassium 4.4 meq/L, chloride 89 meq/L, CO2 15, BUN 52, and creatinine 4.5. The hemoglobin was 13.1 g/dl. The WBC count was 5.7/ul, with 7% segs, 80% bands, and 5% lymphs. Platelets were decreased at 87,000 / ul. The AST was 2070 IU/ml and the CPK was 2820 IU/ml. A chest x ray showed a RUL pneumonia, cardiomegaly, and pulmonary congestion.

    Despite triple antibiotic treatment, the patient expired a few hours after admission. The infectious disease physician suspected tularemia, which was confirmed by the clinical microbiology lab from blood collected pre-mortem and lymph node tissue obtained at autopsy.

    After the patient's death, it was discovered that he had recently hunted rabbits. Indeed, the family had about a dozen rabbits frozen in their freezer. They were instructed to dispose of them.

    Discussion topics

    1. What precautions should be taken by rabbit hunters to avoid tularemia?

    2. What precautions should be taken by laboratorians if tularemia is suspected clinically?

    3. Is this a typical case of tularemia? Describe the various clinical presentations of tularemia.

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    Case 4: Mycobacterium avium intracellulare pneumonitis

    Clinical vignette 5

    The patient was a 2 year old, previously healthy African-American female from Raleigh, NC, who presented to Duke University Medical Center with a history of low-grade fevers x 1 month, coughing and wheezing, occasional night sweats, and cervical lymphadenopathy. Chest X-ray demonstrated mediastinal widening, with an upper lobe infiltrate noted on the right. The patient had no known exposure to tuberculosis, and was tuberculin negative. The working diagnosis was lymphoma, and she proceeded to thoracotomy to biopsy a mediastinal lymph node and the infiltrate in the RUL of the lung. The lymph node showed reactive lymphoid hyperplasia, but the lung biopsy showed confluent, well-formed granulomas, with focal caseation. AFB stains were negative; however, fluorescent staining of the biopsy with auromine-rhodamine (AR) showed rare bacilli. AR staining in the mycobacteriology lab was negative from the tissue. The Bactec (liquid mycobacterium media) vial went positive after 7 days, was DNA probe positive for MAI and negative for M. tb.

    After the lab grew the organism, followup by the pediatrician revealed that the family had several cockatiels that they had obtained from the NCS Vet School at Raliegh, NC. Prior to the patient's illness, the birds had all become ill and died. One of the birds lived in a cage in the girl's room. The birds had been originally been obtained from the Avian Respiratory Diseases Laboratory. Unfortunately, no necropsies were performed on the birds.

    Discussion Topics

    1. What is the typical clinical presentation of MAI in an immunocompetent host? in an immunosuppressed host? What histopathologic reaction would you expect to see in each case?

    2. What other diseases could your future patients get from a pet?
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    Case 5: Tuberculosis

    Clinical vignette 3

    The patient was a 67 year old Caucasian female who first presented for medical attention to a rural physician in 1989, with a chief complaint of hoarseness. She was evaluated, and a vocal cord biopsy was performed. A diagnosis of "granulomatous inflammation" was made by the examining pathologist, who also performed acid fast stains. No organisms were seen. A clinical diagnosis of sarcoidosis was made. The patient was begun on corticosteroids and concomitant anti-tuberculosis therapy. However, the anti-tuberculosis therapy was soon discontinued because of "patient intolerance".

    In January of 1990, he patient began to complain of pulmonary symptoms, including fever, chills, cough and shortness of breath. Nodular lesions were seen on chest x-ray, and a trans-bronchial biopsy was performed. The examining pathologist made a diagnosis of "non-caseating granulomas", and again special stains were reported as negative. The small size of the biopsy precluded a culture. A tuberculin skin test was reported as negative; however, a control reaction was not reported.

    The patient developed heme positive stools, which prompted colonoscopy and biopsy of her colon in February, 1991. The examining pathologist reported "granulomatous inflammation, consistent with Crohn disease". All AFB stains were reportedly negative. Since by this time the patient was continuing to experience chills, plus the new appearence of arthralgias, mental status changes, and diarrhea, the family requested transfer to a Medical Center. The transfer note gave a diagnosis of "steroid-resistant sarcoidosis".

    On admission, the WBC count was 20,000, with 60 segs and 37 bands. A chest x-ray showed patchy infiltrates in all lobes. The surgical pathology slides from the outside colon biopsy were reviewed at the the Medical Center, and acid-fast organisms were identified on AFB stains. Anti-tuberculosis therapy was begun with 4 drugs. A sputum AFB stain and culture were obtained. Numerous AFB were seen on auromine-rhodamine fluorescent staining. The culture grew Mycobacterium tuberculosis within 1 week. Urine cultures were also positive for M. tuberculosis

    However, by this time the patient was experiencing refractory ileus. She had also developed Pneumocystis carinii pneumonia. This was treated with trimethoprim/sulfa. The patient then developed refractory thrombocytopenia. All life support measures were eventually withdrawn at the request of the family, and the patient expired on 4/5/91. An autopsy was performed, which showed extensive miliary tuberculosis.

    Discussion topics

    1. Contrast and compare tuberculosis and sarcoidosis. Was it reasonable to have made a diagnosis of sarcoidosis in this case?

    2. Why do you think the patient's Tb skin test was negative? What kind of skin test control should be administered?

    3. List factors that may contribute to drug resistance. Do you think it is likely that this woman had a drug-resistant organism?

    4. What is the prognosis for individuals that develop resistance to multiple drugs (MDR Tb)? Are physicians in danger from such patients? What preventive measures should be taken?

    5. What public health methods are available to prevent the emergence of drug resistance?

    References


    1. MMWR 42(RR-7), 1993. Initial therapy for tuberculosis in the era of multi-drug resistance.


    2. MMWR 42(RR-15), 1993. Tuberculosis control laws, United States, 1993.


    3. MMWR 43(RR-13), 1994. Guidelines for preventing the transmission of Mycobacterium tuberculosis in health care facilities, 1994.


    4. MMWR 45: (RR-4), 1996The role of BCG vaccine in the control and prevention of tuberculosis in the United States

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