1. Zoonotic diseases Meral Sönmezoğlu, Assoc Prof Infectious Diseases Department Yeditepe University Hospital

2. Zoonoses From the Greek: Zoon: Animal Noson: Disease Diseases and infections which are naturally transmitted between vertebrate animals and humans - WHO 1959

3. 1. Know the general terminology and main organisms 2. Know epidemiology and clinical symptoms of main zoonotic diseases 3. Understand the importance of the diseases Learning objects

4. Definition Zoonosis are diseases of vertebrate animals that can be transmitted to man: either directly or indirectly through an insect vector. Zoonosis are a complex group of diseases caused by a remarkable diversity of pathogenic microorganisms that ordinarily reside and cause illness in the nonhuman animal world

5. Defining criteria introduction to the zoonosis include the following: a vertebrate reservoir exclusive of humans; transmission of the agent directly to people or from products derived from the host animal or through an arthropod intermediate; and a recognized infectious disease syndrome in susceptible individuals

6. Zoonosis: Importance –In addition to their natural occurrence many of these microorganisms are prime candidates as biological weapons

7. Human Health Animal Health ZOONOSIS Zoonosis (Zoonotic Diseases) - all diseases naturally transmissible from animals to man

8. Zoonoses Does NOT include –Fish and reptile toxins –Allergies to vertebrates –Diseases in which animal-derived food serves as a vehicle (e.g. hepatitis A contaminated deli meat) –Experimentally transmitted diseases

9. Zoonoses > 250 zoonotic diseases Multiple pets in the home Human-animal bond Exotic species as pets

10. Zoonoses: Common Diseases Frequency – (CDC, 2003) Salmonella39,919 Lyme disease18,991 West Nile (CNS)2,862 Trichinosis4

11. Zoonoses Zoonotic diseases can be severe, life threatening, and contagious and can even warn of an emerging epidemic or a possible bioterror act

12. Zoonoses Spectrum of Disease Severity Death = rabies Severe illness = plague Chronic illness = Q-fever Mild illness = psittacosis

13. Zoonoses: Importance Economics –Zoonotic disease are expensive Rabies post-exposure prophylaxis GI illness due to Salmonella or Campylobacter – lost productivity, medical costs –Import/Export BSE – restriction on cattle Avian Influenza – restriction on chicken Travel/Globalization Decreased transit time - SARS Remote area accessibility

14. Zoonoses: Etiologic Classification Viral Bacterial Parasitic Mycotic

15. Zoonoses: Viral Examples Colorado tick feverJapanese encephalitis EbolaMonkeypox Equine encephalitides (WEE, EEE, VEE) Nipah HantavirusesRabies HendraRift Valley fever Herpesvirus BWest Nile virus InfluenzaYellow fever

16. Zoonoses: Bacterial Examples AnthraxPlague BrucellosisPsittacosis CampylobacteriosisQ fever Cat-scratch diseaseRelapsing fevers LeptospirosisSalmonellosis ListeriosisTularemia Lyme diseaseYersiniosis

17. Zoonoses: Parasitic Examples PROTOZOALHELMINTHIC TrypanosomiasisBaylisascariasis BabesiosisCysticercosis CryptosporidiosisHydatidosis LeishmaniasisSchistosome dermatitis GiardiasisTrichinosis ToxoplasmosisVisceral larva migrans and toxocariasis

18. Zoonoses: Mycotic Examples Aspergillosis Blastomycosis Cryptococcosis Dermatophytosis Histoplasmosis Sporotrichosis

19. Zoonoses: Animal Species Dogs & Cats –Rabies –Roundworm –Ringworm –Lyme Disease (dogs only) –Cat Scratch Disease (cats only) Food Animals –Salmonella –E.coli –Brucellosis

20. Zoonoses: Animal Species Birds: –Psittacosis –West Nile –Cryptococcus Reptiles, Fish, & Amphibians –Salmonella –Mycobacterium Wild Animals –Hantavirus –Plague –Tularemia

21. Routes of Transmission Direct –Droplet or Aerosol –Oral –Contact Indirect –Foodborne –Water-borne –Fomite –Vector-borne –Environmental

22. Routes of Transmission direct contact, ingestion, inhalation, arthropod intermediates, animal bites. Dunne - CIDP January 18, 2005

23. Zoonoses - Life Cycle ORTHOZOONOSES –May be perpetuated in nature by a single vertebrate species –E.g. rabies, brucellosis, anthrax

24. Dunne - CIDP January 18, 2005 Zoonosis: Rabies Life Cycle Virus inoculation (bite) Salivary gland excretion

25. Zoonoses - Maintenance Cycle CYCLOZOONOSES –Requires more than one vertebrate species but no invertebrate host –Most are cestodiases (tapeworm diseases) Taenia saginata and T. solium require man to be one of vertebrate hosts Others, such as hydatidosis, man is accidentally involved

26. Life Cycle:

27. Zoonoses - Life Cycle METAZOONOSES –Require both vertebrates and invertebrates to complete transmission –All arboviral infections West Nile virus, Saint Louis encephalitis –Some bacterial diseases Plague, many rickettsia –Some parasitic diseases Leishmaniasis, schistosomiasis

28. Zoonoses: Metazoonoses Invertebrate Host: Mosquitoes Vertebrate Host: Birds Incidental Hosts: –HUMANS, horses, amphibians, other mammals

29. Risk Factors Companion Animal –Dogs & roundworm –Rats & Rat Bite Fever Occupational –Animal control workers & rabies –Wildlife biologists & hantavirus Foodborne –Raw meat & E.coli –Unpasteurized dairy & Listeria

30. Risk Factors Recreational Activities –Camping & Lyme disease Farm Settings –Sheep & Q-fever –Cattle & Cryptosporidium Travel –Malaysia & Nipha –Australia & Hendra

31. Reportable Diseases of Animals By veterinarian or other individual Reported to Health Services –Plague –Rabies Reportable to Dept Food and Agriculture –Anthrax –Brucellosis –Glanders –Listeriosis –Rabies in livestock –Venezuelan equine encephalomyelitis –West Nile –And more…

32. RABIES Dunne - CIDP January 18, 2005

33. Rabies Virus member of the Lyssavirus of the Rhabdoviridae. ssRNA enveloped virus, characteristic bullet-shaped appearance with 6-7 nm spike projections. virion 130-240nm * 80nm -ve stranded RNA codes for 5 proteins; G, M, N, L, S Exceedingly wide range of hosts. There are 5 other members of Lyssavirus : Mokola, Lagosbat, Duvenhage, EBL-1, and EBL-2. Duvenhage and EBL-2 have been associated with human rabies.

34. Rabies Virus Structure of rabies virus (Source: CDC) Rabies virus particles

35. DEFINITION Rabies is an acute, progressive encephalomyelitis The case to fatality rate is the highest of any infectious disease One of the oldest described diseases The leading viral zoonosis as regards global public health significance

36. Epidemiology Rabies is a zoonosis which is prevalent in wildlife. The main animals involved differs from continent to continent. Europe fox, bats Middle Eastwolf, dog Asiadog Africadog, mongoose, antelope N Americafoxes, skunks, raccoons, insectivorous bats S Americadog, vampire bats

37. DISTRIBUTION Rabies is distributed on all continents (with the exception of Antarctica) Several areas are considered ‘free’ of the disease, including many islands in Pacific Oceania Globalization may threaten the disease-free status of many localities, due to the introduction of rabid animals

39. BURDEN More than ~55,000 human rabies deaths per year Most occur in developing countries Millions of human exposures per year The domestic dog is the single most important animal reservoir (>99%) Wildlife important, especially in developed countries

40. RABIES PATHOGENESIS Virus is transmitted via bite Agents are highly neurotropic Enter peripheral nerves Centripetal travel by retrograde flow in axoplasm of nerves to CNS Replicate in brain Centrifugal flow to innervated organs, including the portal of exit, the salivary glands Viral excretion in saliva

41. Pathogenesis The commonest mode of transmission in man is by the bite of a rabid animal, usually a dog. Rabies is an acute infection of the CNS which is almost invariably fatal. Following inoculation, the virus replicates in the striated or connective tissue at the site of inoculation and enters the peripheral nerves through the neuromuscular junction. It then spreads to the CNS in the endoneurium of the Schwann cells. Terminally, there is widespread CNS involvement but few neurons infected with the virus show structural abnormalities. The nature of the profound disorder is still not understood.

42. CLINICAL STAGES Incubation Period (range = ~ 6 years; average is ~4-6 weeks) Prodromal Phase (Non- specific signs) Acute Neurological Phase Coma Death (recovery from rabies?)

43. RABIES RECOVERY? Five historical human case recoveries, after vaccination, but before illness onset Only one documented unvaccinated human survivor after clinical presentation

45. RABIES DIAGNOSIS Based upon history of animal exposure and typical neurological clinical signs Postmortem demonstration of viral antigen in CNS is gold standard In humans, antemortem detection of virus or viral amplicons, antibodies, or antigens (sera, csf, saliva, nuchal biopsy)

46. Laboratory Diagnosis Histopathology - Negri bodies are pathognomonic of rabies. However, Negri bodies are only present in 71% of cases. Rapid virus antigen detection - in recent years, virus antigen detection by IF had become widely used. Corneal impressions or neck skin biopsy are taken. The Direct Fluorescent Antibody test (DFA) is commonly used. Virus cultivation - The most definitive means of diagnosis is by virus cultivation from saliva and infected tissue. Cell cultures may be used or more commonly, the specimen is inoculated intracerebrally into infant mice. Because of the difficulties involved, this is rarely offered by diagnostic laboratories. Serology - circulating antibodies appear slowly in the course of infection but they are usually present by the time of onset of clinical symptoms.

47. Negri Body in neuron cell (source: CDC) Positive DFA test (Source: CDC Diagnosis of Rabies

48. PROPHYLAXIS Pre-exposure Vaccination Postexposure Prophylaxis (PEP)

49. Management and Prevention Pre-exposure prophylaxis - Inactivated rabies vaccine may be administered to persons at increased risk of being exposed to rabies e.g. vets, animal handlers, laboratory workers etc. Post-exposure prophylaxis - In cases of animal bites, dogs and cats in a rabies endemic area should be held for 10 days for observation. If signs develop, they should be killed and their tissue. Wild animals are not observed but if captured, the animal should be killed and examined. The essential components of postexposure prophylaxis are the local treatment of wounds and active and passive immunization. Once rabies is established, there is nothing much that could be done except intensive supportive care. To date, only 2 persons with proven rabies have survived.

50. Postexposure Prophylaxis Wound treatment - surgical debridement should be carried out. Experimentally, the incidence of rabies in animals can be reduced by local treatment alone. Passive immunization - human rabies immunoglobulin around the area of the wound; to be supplemented with an i.m. dose to confer short term protection. Active immunization - the human diploid cell vaccine is the best preparation available. The vaccine is usually administered into the deltoid region, and 5 doses are usually given. There is convincing evidence that combined treatment with rabies immunoglobulin and active immunization is much more effective than active immunization alone. Equine rabies immunoglobulin (ERIG) is available in many countries and is considerably cheaper than HRIG.

51. RABIES BIOLOGICALS Rabies Vaccines (for pre- and PEP) Rabies immune globulin (only in PEP)

52. PRE-EXPOSURE VACCINATION Vaccine given on days 0, 7, and 21 or 28 Serology occurs every 6 months to 2 years (if remaining at risk) If antibody titer not adequate, administer a single booster dose If ever exposed, give a vaccine dose on days 0 and 3, regardless of titer

53. POSTEXPOSURE PROPHYLAXIS Wash lesions well with soap and water (tetanus booster ad hoc) Infiltrate rabies immune globulin (20 IU/kg) into and around the margin of the bites Administer vaccine on days 0,3,7,14, and 28

54. Control of Rabies Urban - canine rabies accounts for more than 99% of all human rabies. Control measures against canine rabies include; –stray dog control. –Vaccination of dogs –quarantine of imported animals Wildlife - this is much more difficult to control than canine rabies. However, there are on-going trials in Europe where bait containing rabies vaccine is given to foxes. Success had been reported in Switzerland.

55. Arenaviruses Enveloped ssRNA viruses virions 80-150nm in diameter genome consists of 2 pieces of ambisense ssRNA. 7-8 nm spikes protrude from the envelope. host cell ribosomes are usually seen inside the outer membrane but play no part in replication. Members of arenaviruses include Lassa fever, Junin and Macupo viruses. Lassa fever virus particles budding from the surface of an infected cell. (Source: CDC)

56. Lassa Fever Found predominantly in West Africa, in particular Nigeria, Sierra Leone and Liberia. The natural reservoir is multimammate rat (Mastomys) Man may get infected through contact with infected urine and faeces. Man to man transmission can occur through infected bodily fluids and Lassa fever had caused well-documented nosocomial outbreaks. Mastomys

57. Clinical Manifestations Incubation period of 3-5 days. Insidious onset of non-specific symptoms such as fever, malaise, myalgia and a sore throat. Typical patchy or ulcerative pharyngeal lesions may be seen. Severe cases may develop the following: –Myocarditis –Pneumonia –Encephalopathy –Haemorrhagic manifestations –Shock The reported mortality rate for hospitalized cases of Lassa fever is 25%. It carries a higher mortality in pregnant women.

58. Laboratory Diagnosis Lassa fever virus is a Group 4 Pathogen. Laboratory diagnosis should only be carried out in specialized centers. –Detection of Virus Antigen - the presence of viral antigen in sera can be detected by EIA. The presence of viral antigen precedes that of IgM. –Serology - IgM is detected by EIA. Using a combination of antigen and IgM antibody tests, it was shown that virtually all Lassa virus infections can be diagnosed early. –Virus Isolation - virus may be cultured from blood, urine and throat washings. Rarely carried out because of safety concerns. –RT-PCR - being used experimentally.

59. Management and Prevention Good supportive care is essential. Ribavirin - had been shown to be effective against Lassa fever with a 2 to 3 fold decrease in mortality in high risk Lassa fever patients. Must be given early in the illness. Hyperimmune serum - the effects of hyperimmune serum is still uncertain although dramatic results have been reported in anecdotal case reports. Postexposure Prophylaxis - There is no established safe prophylaxis. Various combinations of hyperimmune immunoglobulin and/or oral ribavirin may be used. There is no vaccine available, prevention of the disease depends on rodent control.

60. Hantaviruses Forms a separate genus in the Bunyavirus family. Unlike under bunyaviridae, its transmission does not involve an arthropod vector. Enveloped ssRNA virus. Virions 98nm in diameter with a characteristic square grid-like structure. Genome consists of three RNA segments: L, M, and S.

61. History Haemorrhagic Fever with Renal Syndrome (HFRS: later renamed hantavirus disease) first came to the attention of the West during the Korean war when over 3000 UN troops were afflicted. It transpired that the disease was not new and had been described by the Chinese 1000 years earlier. In 1974, the causative was isolated from the Korean Stripped field mice and was called Hantaan virus. In 1995, a new disease entity called hantavirus pulmonary syndrome was described in the “four corners” region of the U.S.

62. Some Subtypes of hantaviruses associated with human disease Hantaan, Porrogia and related viruses - This group is found in China, Eastern USSR, and some parts of S. Europe. It is responsible for the severe classical type of hantavirus disease. It is carried by stripped field mice. (Apodemus agrarius) Seoul type - associated with moderate hantavirus disease. It is carried by rats and have a worldwide distribution. It has been identified in China, Japan, Western USSR, USA and S.America. Puumala type - mainly found in Scandinavian countries, France, UK and the Western USSR. It is carried by bank voles (Clethrionomys glareolus) and causes mild hantavirus disease (nephropathia epidemica). Sin Nombre - found in many parts of the US, Canada and Mexico. Carried by the Deer Mouse (Peromyscus maniculatus) and causes hantavirus pulmonary syndrome.

63. Rodent Carriers of Hantaviruses Stripped field mouse (Apodemus agrarius) Bank vole (Clethrionomys glareolus) Deer Mouse (Peromyscus maniculatus) Rat (Rattus)

64. Clinical Features of Hantavirus Disease The multisystem pathology of HVD is characterized by damage to capillaries and small vessel walls, resulting in vasodilation and congestion with hemorrhages. Classically, hantavirus disease consists of 5 distinct phases. These phases may be blurred in moderate or mild cases. –Febrile phase - abrupt onset of a severe flu-like illness with a erythematous rash after an incubation period of 2-3 days. –Hypotensive phase - begins at day 5 of illness –Oliguric phase - begins at day 9 of illness. The patient may develop acute renal failure and shock. Haemorrhages are usually confined to petechiae. The majority of deaths occur during the hypotensive and oliguric phases –Diuretic phase - this occurs between days 12-14. –Convalescent phase - this may require up to 4 months.

65. Comparative Clinical Features of Recognized Hantavirus Disease (HVD)

66. Hantavirus Pulmonary Syndrome (HPS) More than 250 cases of HPS have been reported throughout North and South America with a mortality rate of 50% In common with classical HVD, HPS has a similar febrile phase. However, the damage to the capillaries occur predominantly in the lungs rather than the kidney. Shock and cardiac complications may lead to death. The majority of HPS cases are caused by the Sin Nombre virus. The other cases are associated with a variety of other hantaviruses e.g. New York and Black Creek Canal viruses.

67. Diagnosis Serological diagnosis - a variety of tests including IF, HAI, SRH, ELISAs have been developed for the diagnosis of HVD and HPS. Direct detection of antigen - this appears to be more sensitive than serology tests in the early diagnosis of the disease. The virus antigen can be demonstrated in the blood or urine. RT-PCR - found to of great use in diagnosing hantavirus pulmonary syndrome. Virus isolation - isolation of the virus from urine is successful early in hantavirus disease. Isolation of the virus from the blood is less consistent. Sin Nombre virus has never been isolated from patients with HPS. Immunohistochemistry - useful in diagnosing HPS.

68. 68 National Statutory Notifiable Communicable Diseases Group A: Plague, Cholera Group B: SARS, AIDS, Viral hepatitis, Poliomyelitis, HPAI, Measles, HFRS, Rabies, Japanese encephalitis, Dengue fever, Anthrax, Bacillary & amebic dysentery, TB, Typhoid fever/Paratyphoid fever, Meningococcal Meningitis, Pertussis, Diphtheria, Neonatal Tetanus, Scarlet fever, Brucellosis, Gonorrhea, Syphilis, Leptospirosis, Schistosomiasis, Malaria Group C: Influenza, Mumps, Rubella, Acute hemorrhagic Conjunctivitis, Leprosy, Epidemic typhus/Endemic typhus, kala- azar, Echinococcosis, Filariasis, Infectious diarrhea

69. 69 Animal Health - Human Health Collaboration - “Effective control of zoonotic disease relies on active involvement of both veterinary and human health services.” “This dual involvement needs to take place at every stage, from research, organizing funding, planning, surveillance, creating public awareness, to implementing the actual control activities.”

70. TULAREMIA Dunne - CIDP January 18, 2005

71. Tularemi Francisella tularensis is the causative agent of tularemia (a reportable disease) F. tularensis is a small, Gram-negative, nonmotile, encapsulated, pleomorphic coccobacillus (short rod). It is a facultative intracellular parasite that grows poorly or not at all on most lab media and requires a special blood agar Dunne - CIDP January 18, 2005

72. Human commonly acquires tularemia via the insect bites (ticks primarily, but also deer flies, mites, blackflies, or mosquitoes) or by handling infected animal tissues. Human disease (rabbit or deer fly fever) is characterized by a focal ulcer at the site of entry of the organisms and enlargement of the regional lymph nodes. Dunne - CIDP January 18, 2005

73. As few as10-50 bacilli will cause disease in humans if inhaled or introduced intradermally, whereas a very large inoculum (~10 8 organisms) is required for the oral route of infection. Dunne - CIDP January 18, 2005

74. Incubation period is 3-10 days. A small skin papule usually develops at the site of entry. Ulceration occurs together with fever, chills, malaise, fatigue, and usually lymphadenopathy. Dunne - CIDP January 18, 2005

75. Bacteremia usually occurs and the bacilli then grow intracellularly in the reticuloendothelial system. Dissemination of the organisms through the bloodstream permits focal lesions to develop in numerous organs Dunne - CIDP January 18, 2005

76. Epidemiology Summer peak related to ticks –90% pediatric cases Winter peak related to trapping and hunting of rabbits Photo courtesy of National Archives

77. Tularemia

78. Geographic distribution

79. Clinical Manifestations Six classic froms; –Ulceroglandular –Glandular –Oculoglandular –Pharyngeal –Typhoidal –Pneumonie

80. Diagnosis of tularemia Clinical suspicion Organism rarely seen on Gram stained smears Direct fluorescent antibody staining of smears,tissues Antigen detection in urine PCR Most common way of diagnosis serology (tube agg, microagg, hemagg, ELISA)

81. Treatment First choice is streptomycin Gentamycin alternative

82. YERSINIA Dunne - CIDP January 18, 2005

83. Yersinia pestis Plague, disease of antiquity Three catastrophic pandemics Latest pandemic began in China in the 1860s. Recently resurged in sub-Saharan Africa. Aerosol weapon during the Cold War (catagory A biologic agent).

84. Yersinia pestis Gram negative, bipolar-staining bacillus Grows aerobically on most culture media, more slowly and optimally at 28°C Non-motile and non-spore forming Not ferment lactose Citrate, urease and indole negative

87. Transmission of plague Plague is primarily an infection of animals Transmitted by flea bites Domestic rats are the most dangerous reservoirs Most efficient vector to humans is oriental rat flea

88. Clinical manifestations Bubonic Septicemic Pneumonic Pharingeal Meningitis Fever, painful lymphadenopathy (bubo) Fever, hypotension comp. of inflammatory response syndrome Cough, hemoptysis with /without bubo Painful, inflamed pharinx, local lymphadenopathy Fever, nuchal rigidity with bubo

90. Diagnosis WBC elevated (10.000-20.000) predominance of neutrophils Clinical specimens (blood, bubo aspirate) Chest x-rays Serologic test (passive hemagg test, ELISA,), PCR

91. Treatment Streptomycin drug of choice Gentamicin Tetracycline Chloramphenicol

92. BRUCELLOSIS Dunne - CIDP January 18, 2005

93. Brucella are Gram-negative, nonmotile, coccobacilli. They are strict aerobes that grow very slowly (fastidious) on blood agar. In the host, they live as facultative intracellular pathogens. Dunne - CIDP January 18, 2005

94. Brucellosis is primarily a disease of animals and it affects organs rich in the sugar erythritol (breast, uterus, epididymis, etc.). The organism localizes in these animal organs and causes infertility, sterility, mastitis, abortion, or resides as carriage. Humans in close contact with infected animals (slaughterhouse workers, veterinarians, farmers, dairy workers) are at risk of developing undulant fever. Dunne - CIDP January 18, 2005

95. PATHOGENS Four different species of Brucella are known to infect humans: B. abortus (cattle), B. suis (swine), B. melitensis (goats/sheep) and B. canis (dogs). Dunne - CIDP January 18, 2005

96. B. abortus and B. canis cause a mild suppurative febrile infection whereas B. suis causes a more severe suppurative infection which can lead to destruction of the lymphoreticular organs and kidney. B. melitensis is the cause of most severe and prolonged recurring disease. Dunne - CIDP January 18, 2005

97. PATHOGENESIS The bacteria enter the human host through the mucous membranes of the oropharynx (ingestion/inhalation routes), through abraded skin, or through the conjunctiva. Usually infection occurs by direct contact with infected material, although it may also occur by ingestion of milk or milk products. Dunne - CIDP January 18, 2005

98. TREATMENT Prolonged treatment with Tetracyclin combined with Rifampin that penetrates cells, is effective. Control measures include animal vaccination and avoidance of infected material (e.g., unpasteurized dairy products). Dunne - CIDP January 18, 2005

99. The symptoms in brucellosis are due to the presence of the organism and appear 2-4 weeks (sometimes up to 2 months) after exposure. Dunne - CIDP January 18, 2005

100. Diagnosis is based on prolonged (at least a week) presence of undulant fever, myalgia, arthralgia and the history of exposure (contact with animals or consumption of unprocessed material from infected animals). Definitive diagnosis can be made by culturing blood samples on blood-enriched media. The (fastidious) organisms grow very slowly (4-6 weeks in blood culture). B. abortus but not other Brucella grow better in 5% CO 2 atmosphere (microaerophilic). On blood agar, they produce white glistening colonies. Specific antibodies can be used to further confirm the diagnosis Dunne - CIDP January 18, 2005

101. TTUS 2013 Aşağıdaki etkenlerden hangisi, insana artropod ısırığı ile bulaşır? A) Listeria monocytogenes B) Nocardia brasiliensis C) Francisella tularensis D) Chlamydia psittaci E) Campylobacter jejuni Dunne - CIDP January 18, 2005

102. TTUS 2013 Aşağıdaki etkenlerden hangisi, insana artropod ısırığı ile bulaşır? A) Listeria monocytogenes B) Nocardia brasiliensis C) Francisella tularensis D) Chlamydia psittaci E) Campylobacter jejuni Dunne - CIDP January 18, 2005

103. QUESTION