Epidemiology and Control of Zoonotic Infections Lecture 6

1. Epidemiology and Control of Zoonotic InfectionsLecture 6 Parasitic Diseases Mycotic Diseases

3. Parasites Organisms which live at the expense of another Ectoparasites � lives on outside of host Endoparasites � lives on inside of host Eukaryotes Single-celled (protozoa) to multicellular (helminthes) to arthropods (fleas)

4. Parasitism Obligate parasites � most parasites are obligate but many have free living stages Facultative parasites � not normally parasitic but won�t pass up the opportunity Accidental parasites � attach or enter wrong host, may or may not survive but can be very pathogenic. Permanent parasites - live adult lives in or on host Temporary parasites - eat and run

5. Notifiable Parasitic Diseases Reportable in CA Amebiasis Anisakiasis Babesiosis Cryptosporidiosis Cysticercosis Echinococcosis Giardiasis Malaria Toxoplasmosis Trichinosis Not reportable in CA Zoonotic ascarids Baylisascaris procyonis Toxocara spp. Cercarial dermatitis

6. Giardia

7. Giardia Protozoan flagellate Global distribution Two-stage life cycle - trophozoite and cyst Reservoirs: domestic and wild animals

8. Giardia � life cycle Simple life cycle. Fecal-oral route of transmissionSimple life cycle. Fecal-oral route of transmission

9. Giardia - cysts In fecal samples. Note 4 nuclei in leftmost image. Image on right stainedIn fecal samples. Note 4 nuclei in leftmost image. Image on right stained

10. Giardia in Animals Symptoms: asymptomatic to diarrhea Transmission, diagnosis and treatment similar to humans Contaminate surface water (e.g. beavers, livestock)

11. Giardia: Transmission to Humans Oral ingestion of cysts Fecal-oral transmission Contamination of water Foodborne transmission Zoonotic transmission from pets and livestock may be important

12. Direct Contact Transmission Person-to-person is 2nd most commonly identified mode of transmission Poor fecal-oral hygiene Children in daycare centers Cyst passage as high as 20-50% Spread the disease within center, homes, and communities Men who have sex with men (MSM) Cyst passage as high as 20% Persons in custodial institutions

13. Giardia: Human Disease Incubation period of 1-25 days (average 7 days) Infectious dose is low (10 cysts) Excreted in the stool intermittently for weeks or months Asymptomatic infections can occur Duration of illness 1 to 3 weeks

14. Giardia: Human Clinical Signs DIARRHEA Other symptoms: flatulence, bloating, weight loss, abdominal cramping, nausea, malabsorption, foul-smelling stools, steatorrhea, fatigue, anorexia, and chills Chronic disease recurrent symptoms malabsorption and debilitation may occur

15. Giardia: Diagnosis Microscopic visualization via wet mount staining (trichrome or iron hematoxylin) Direct fluorescent antibody detection ELISA Alternative - samples of duodenal fluid (e.g., Enterotest) or duodenal biopsy may demonstrate trophozoites

16. Giardia: Treatment Many effective treatment alternatives Metronidazole � first choice for humans and animals Alternatives: Nitazoxanide, Furazolidone, Quinacrine, Tinidazole, Albendazole, and Paromomycin

17. Risk Factors Travel Backpackers/campers To disease-endemic areas Poor sanitation Inadequate drinking water treatment facilities Children in day care with prolonged diarrhea Men who have sex with men Persons drinking water from shallow wells

18. Prevention and Control Proper handling and treatment of water Travelers to developing world or wilderness should boil or treat surface water Good personal hygiene Daycare center foci are a problem Some recommend only symptomatic children be treated However, asymptomatic passers may infect others If strict handwashing and treatment of symptomatic children does not control outbreak, treating all infected should be considered

19. Toxoplasmosis

20. Toxoplasmosis Single-cell organism Global Distribution Reservoir host - Cats Uncommon cause of human disease Except: pregnant women & fetus Immunocompromised persons

21. Toxoplasma gondii Small, banana-shaped cells. Intracellular parasite Can infect any nucleated cellSmall, banana-shaped cells. Intracellular parasite Can infect any nucleated cell

22. Toxoplasma - oocysts Small � 10-13um When mature contain 2 sporocysts, each with 4 sporozoites Sporulation takes 1-5 daysSmall � 10-13um When mature contain 2 sporocysts, each with 4 sporozoites Sporulation takes 1-5 days

23. Toxoplasma gondii � life cycle Presence of cats in environment is necessary Oocyst excretion in 1% of cats in various areas No T. gondii infection in areas without cats Complex life cycle Infects any warm-blooded animal (mammals and birds) � one highly successful pathogen! 2 cycles: Sexual cycle in cat Asexual cycle in all hosts (including cat) � predator-prey transmissionComplex life cycle Infects any warm-blooded animal (mammals and birds) � one highly successful pathogen! 2 cycles: Sexual cycle in cat Asexual cycle in all hosts (including cat) � predator-prey transmission

24. Toxoplasma: Animal Disease Infects all animals, including birds Cats infected by ingestion of cyst (feces or raw meat) Asymptomatic Shed for 1-2 weeks No treatment necessary Diagnostic tests Serology Do NOT routinely perform serologic test of cats Cannot determine whether excreting oocysts Microscopic evaluation of feces

26. Toxoplasma: Human Transmission Infection in humans typically through ingestion Raw/undercooked meat Estimated to occur in � of T. gondii infections in U.S. Parasite isolated from 32% pork chops, 4% lamb chops (1960s) Ingestions of oocyst from cat feces or soil Water or food contaminated with oocysts Also transplacental transmission Mother acquires infection during gestation

27. Toxoplasma: At Risk for Severe Disease Congenitally infected fetuses and newborns Estimated 400-4000 cases each year in the U.S. Immunologically impaired individuals, most commonly with defects in T-cell-mediated immunity Hematologic malignancies Bone marrow and solid organ transplants AIDS, e.g. leading to toxoplasmic encephalitis

28. Toxoplasmosis: Clinical Signs Usually asymptomatic (80-90%) Flu-like illness Lymphadenopathy Self-limiting Toxoplasmic encephalitis (AIDS) Congenital toxoplasmosis Retinochoroiditis

29. Toxoplasmosis � ocular lesions Examples of retinal lesions caused by ToxoplasmaExamples of retinal lesions caused by Toxoplasma

30. Congenital toxoplasmosis Infant with hydrocephalusInfant with hydrocephalus

31. Toxoplasma: Diagnosis Serologic testing Observation of parasites in patient specimens Isolation of parasites from blood or other body fluids, by intraperitoneal inoculation into mice or tissue culture PCR (for congenital infections in utero)

32. Toxoplasmosis: Treatment Consideration should NOT depend on cat exposure Treatment may or may not be indicated based on presence of active disease, immune status, site of infection Prevention most important in seronegative pregnant women and immunodeficient patients

33. Prevention and Control Education Avoid ingestion of and contact with cysts or sporulated oocysts Cook meat to well done with no visible pink in center Wash hands thoroughly after handling raw meat or vegetables Avoid areas with cat feces Change litter every day (before sporulation) Wear disposable gloves when disposing of cat litter, working in garden, cleaning child�s sandbox Serologic screening for pregnant women

34. The Zoonotic Ascarids: Toxocara canis/cati Baylisascaris procyonis Jason Stull, VMD, MPVM CDHS, Veterinary Public Health Section jstull@dhs.ca.gov 916-552-9782

35. Outline Background Toxocara sp. Lifecycle Infection in dogs/cats Infection in humans Baylisascaris procyonis Lifecycle Infection in raccoons Infection in humans

36. Ascarids � Background (1) Biology adult size: <1 mm to >1 m complete digestive system with anterior mouth and posterior anus Reproduction separate male and female eggs shed in environment T. Canis � 4-18 cm long, B. procyonis � 12-23 cmT. Canis � 4-18 cm long, B. procyonis � 12-23 cm

37. Ascarids � Background (2) Humans � definitive host Ascaris lumbricoides Humans � aberrant host Toxocara canis/cati Baylisascaris procyonis Ascaris suum

38. Toxocara canis / cati Definitive host: Dogs and cats Transmission Transplacental Transmammary Environmental Prevalence: Neonate: ~ 100% (puppies) Adult: ~ 20-40%

39. Toxocara � Life cycle Toxocara canis similar to Baylisascaris Utilizes dogsToxocara canis similar to Baylisascaris Utilizes dogs

40. Toxocara - Life cycle Key concepts Adult worms live in small intestines of dogs/cats, with eggs shed in feces Eggs shed into the environment require 2-5 weeks to become infectious Animals/humans are infected when ingesting infectious eggs Eggs are very resistant and may survive in environment for months - years Infected dogs contaminate the environment with ~ 1.4 million eggs / day 10,000 eggs/ gr of feces, average dog -> 136 gr of feces/day10,000 eggs/ gr of feces, average dog -> 136 gr of feces/day

41. Toxocara � Dogs and Cats Clinical signs None Diarrhea Weight loss Cough Diagnosis � fecal examination Outcome Most asymptomatic with occasional death in the young

42. Toxocara - Humans Larva Migrans Migration / presence of nematode larvae of animals within the tissues of a human Named by location: Visceral larval migrans (VLM) Ocular larval migrans (OLM) Neural larval migrans (NLM)

43. Toxocara - Humans Infected after ingestion of an infectious egg Visceral, ocular, or neurological larval migrans Tissue trauma, inflammation, necrosis Granulomatous immune response (eosinophils) Abscesses (?)

44. Toxocara - Visceral Larval Migrans Larvae lodged in liver, lungs, heart, muscle Clinical manifestations depend on number of larvae and location Most cases mild or asymptomatic Symptoms are variable including: Fever, GI / respiratory signs, lymphadenopathy, persistent eosinophilia Majority of patients < 3 yrs of age asthma, pneumonia, hepatosplenomegalyasthma, pneumonia, hepatosplenomegaly

45. Toxocara - Ocular Larval Migrans Larvae lodged in eye Inflammation and retinal scarring Vision loss (progressive or sudden blindness) - unilateral without systemic signs May be misdiagnosed as retinoblastoma Majority of patients older children Granulamatous lesion near optic discGranulamatous lesion near optic disc

46. Toxocara - Neurological Larval Migrans Larvae lodged in CNS Meningitis, encephalitis, convulsions, motor deficiencies MRI of child with Baylisascaris infection Note high signal in white matter (white arrows) MRI of child with Baylisascaris infection Note high signal in white matter (white arrows)

47. Toxocara � Human Diagnosis: Fecal not useful Larvae do not develop into adults in humans Antibody detection (blood, aqueous/vitreous humor) EIA; indicates previous exposure Clinical signs, fecal exposure, laboratory results, Toxocara antibodies Treatment � antiparasitics, antiinflammatories Enzyme imunoassayEnzyme imunoassay

48. Toxocara � Public Health (1) Estimate 10,000 human cases/yr in U.S. 700 cases of OLM/yr Risk factors: Children Pica (dirt consumption) Dog/cat ownership

49. Toxocara � Public Health (2) Prevention: Regularly treat dogs/cats for worms (especially young) Hygiene Limit contact with feces Clean pet�s area regularly Dissuade pica Education

51. Baylisascaris procyonis

52. B. procyonis � Background (1) Definitive host: raccoons Transmission: Environmental (consumption of eggs or infected animals) Prevalence: common in raccoons Geographic distribution Widespread throughout the U.S.

53. B. procyonis � Background (2) Can infect numerous animals (including humans) Similar epidemiology to Toxocara Eggs only passed by definitive host Eggs require 2-4 weeks to become infectious Eggs resistant to environmental conditions Humans: ingestion of infective eggs ? larval migrans

54. Baylisascaris � Life cycle

55. B. procyonis � Background (3) Raccoon behavior influences epidemiology Habitually defecate in latrines Latrines associated with natural and human-made structures Rooftops, attics, decks, stumps, woodpiles, lawns (especially near trees) Where raccoon densities are high, substantial amounts of feces and B. procyonis eggs accumulate

56. B. procyonis � Raccoons Diagnosis fecal examination Outcome most asymptomatic with occasional death in the young

57. B. procyonis - Humans Clinical features May be asymptomatic Often severe disease (VLM, OLM, NLM) Larvae: larger than Toxocara extensive migration neurotropic Clinical signs consistent with larval burden and location of migration � similar to Toxocara Usually 2-4 wks after infectionClinical signs consistent with larval burden and location of migration � similar to Toxocara Usually 2-4 wks after infection

58. B. procyonis - Humans Diagnosis Clinical findings Limited diagnostic tests No commercially available serologic test Diagnosis requires biopsy specimen with adequate cross-section MRI of child with Baylisascaris infection Note high signal in white matter (white arrows) MRI of child with Baylisascaris infection Note high signal in white matter (white arrows)

59. B. procyonis - Humans Treatment No drugs have been demonstrated to be completely effective Antiparasitics If suspect ingestion of eggs, consult a physician immediately Brain biopsy showing larval worm Brain biopsy showing larval worm

60. B. procyonis � Public Health < 25 cases diagnosed in US (5 in CA) 5 deaths Many cases undiagnosed, misdiagnosed Risk factors: Children Pica (dirt consumption) Raccoon contact CA � 4 NLM and 1 OLM CA � 4 NLM and 1 OLM

61. Latrines and B. procyonis in CA* 3 communities Pacific Grove Carmel San Jose Latrines found on 73% of Pacific Grove, 72% of Carmel, and 46% of San Jose properties 244 latrines identified on 164 properties

62. B. procyonis - Prevention & Control (1) Prevent human exposure to eggs Dissuade pica Periodic inspection of home for latrines Weekly removal of latrines and feces Personal protective equipment Removal of underlying soil 5-7.5 cm deep Burn, bury, landfill Boiling water Cover sand boxes xylene:ethanol (1:1 mixture), sodium hypochlorite (nonadherent, but still viable), removal soil top layer propane flame torchingxylene:ethanol (1:1 mixture), sodium hypochlorite (nonadherent, but still viable), removal soil top layer propane flame torching

63. B. procyonis - Prevention & Control (2) Avoid or limit contact with raccoons When handling raccoons/potentially contaminated items: Wear coveralls, rubber boots, gloves, facemask Vigorously wash hands Wash clothing in hot (~200 F) water with bleach Reduce enticements for raccoon activity Do not keep, feed, or adopt raccoons as pets

64. Take Home Points

65. Ectoparasites Mange � Sarcoptes Ringworm - Dermatophytes

66. Scabies An arthropod � skin mite Sarcoptes sp. Obligate parasite Species specific (different for humans and animals) AKA Mange, Sarcoptes, Norwegian mites

68. Human scabies Mites burrows and breeds on man Norwegian Scabies � more severe clinical manifestation Does not �infect� animals

69. Animal Scabies Dogs � Sarcoptic Mange Hair loss and pruritis Distribution to ears, face, and feet Demodex vs. Sarcoptes Sarcoptes scabiei canis infestation is a highly contagious disease of dogs found worldwide Dog scabies can produce an unpleasant papulovesicular eruption in humans

70. Animal Mites rat mite Ornithonyssus bacotifowl mite Ornithonyssus sylviarumdog mite Cheyletiella yasguricat mite Cheyletiella blakeirabbit mite Cheyletiella parasitovoraxsparrow mite Pellonyssus passeribat mite Chiroptonyssus robustipes

71. Mycotic Disease Ringworm - Dermatophytosis

72. Ringworm Fungus not a �worm� Global Distribution Skin infection Infections are self-limiting

73. Ringworm: the Fungus Several different species of fungi Epidermophyton Microsporum Trichophyton Grow only in keratinized tissue Stops at living tissue Infects the hair shaft Can live in humans, animals, and soil Not always a zoonotic disease

74. Ringworm in Animals All animals can be infected: cats, dogs, cows, goats, pigs, and horses Transmitted from direct contact from an infected animal's skin or hair to susceptible animal Hair loss, rash/red skin, +/- pruritis Infections are self-limiting Rare chronic or generalized diseases

75. Ringworm: Transmission Direct skin-to-skin contact with an infected person or pet Indirect/Fomite contact Contaminated from infected person or animal hats, combs, brushes, bed linens, stuffed animals, telephones, gym mats, and shower stalls Rarely, by contact with soil

76. Ringworm: Human Clinical Signs A skin and scalp disease Incubation 4 to 10 days after contact Dry and scaly or wet and crusty Duration weeks, months Chronic infections

77. Ringworm: Clinical Signs RASH a flat, round patch anywhere on the skin Ringworm of the scalp usually begins as a small pimple that becomes larger, leaving scaly patches of temporary baldness. Infected hairs become brittle and break off easily As the rash gradually expands, its center clears to produce a ring More than one patch might appear, and the patches can overlap. Sometimes itchy Ringworm of the foot (athlete's foot), groin (Jock itch), and the nails not typically from animals

78. Ringworm: Diagnosis Wood's lamp Direct microscopical examination of hair or skin scale Fungal culture (gold standard)

79. Ringworm: Treatment Ringworm usually responds well to self-care within 4 weeks without having to see a doctor Keep your skin clean and dry Over-the-counter antifungal or drying powders, lotions, or creams Wash sheets and nightclothes every day while infected. Antifungals Prescription and OTC Miconazole, clotrimazole, etc.

80. Ringworm: Prevention Difficult Very common Contagious before symptoms appear Steps to prevent infection include the following: Educate the public, especially parents, about the risk of Ringworm from infected persons and pets. Clean common-use areas (including disinfect sleeping mats and gym mats) Do not share personal items

81. Ringworm Prevention Infected persons and animals should follow these steps to keep the infection from spreading: Complete treatment as instructed, even after symptoms disappear Do not share towels, hats, clothing, or other personal items with others Minimize close contact with others until treated Make sure the person or animal that was the source of infection gets treated

82. Webcast Students Paper due next week � March 1 Email to gdunne@dhs.ca.gov

83. Questions?