Welcome
Parasitic Zoonoses
2 Protozoan zoonoses
Parasitic Helminthiases zoonoses
Arthropod Zoonoses 3 Trematode Zoonoses
Cestode Zoonoses Helminthiases
Nematode Zoonoses 4 Nematode Zoonoses (Nematodiases)
5 1. Trichinellosis 5- Anisakiasis
2- Cutaneous Larva Migrans 6- Capillariasis
3- Visceral Larva Migrans 7- Gnathostomiasis
4- Ascariasis 8- Zoonotic Filariasis
6 1) Trichinellosis (Trichinosis)
8 Trichinella – Adult worms
Male
Female
9 Trichinella spp.:
The smallest parasite nematode of humans.
The world’s largest intracellular parasite.
Female is viviparous.
Public health threat is referred to the parasite larvae.
It is a parasitic infection of carrion-feeding carnivores with cannibalistic and scavenger habits.
Most Trichinella infections in domestic and wild animals are asymptomatic affected animals normally display no clinical signs of infection.
But, it is a serious disease in humans. -Occurrence.
- Priority.
12 - Encysted (encapsulated) larvae can survive & remain infectious for years (may be greater than 30 years).
13 14 Reservoir
15 Trichinosis – The polar bear connection
16 Transmission:
- Consuming raw or undercooked pork or pork products containing viable larvae of Trichinella spiralis; Domestic swine & Wild Boar.
- Wild game, predominantly bear, ……
17 Transmission:
N. B:
- Not thoroughly cleaning a meat grinder…………
- Home-made pork sausage.
18 Question
“Avoidance of a stage in the external environment” is a strategy for maintenance of Trichinella spiralis, explain.
19
A strategy of maintenance
Life Cycle is spent entirely in the mammalian host body
20 Trichinella spiralis larvae in muscle section.
21 22 Clinical forms
23 - The severity of the disease is related to: the number of viable larvae ingested, fatalities can occur with high doses.
- The symptoms depend of the stage of infection.
• Intestinal trichinosis: • Muscle trichinosis:
• Complications:
CNS involvement - myocardial failure 24 25 Trichinellosis
26 27 Diagnosis
28
Control Treatment
29
Man-made trichinosis
30
2) Cutaneous Larva Migrans /CLM (Creeping eruption) (Creeping verminous dermatitis)
32 Dog & Cat Hookworms
33
35 36 Migrating larva cause serpiginous pruritic tracts in subcutaneous tissue.
37 Cutaneous Larva Migrans
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38
Prevention: - Wearing shoes on ground that could be contaminated with dog or cat feces.
- The exclusion of dogs from recreation areas frequented by children.
- Regularly de-worming….
40
3) Visceral Larva Migrans / VLM
42 VLM / TOXOCARIASIS
• Agent: • Toxocara canis. • Toxocara cati. . Toxocara vitulorum.
43 TOXOCARIASIS
• Life cycle:
44 45
Transmission:
- Ingestion of embryonated eggs in food contaminated with …….
- Ingestion of insufficiently-cooked meat and organs of infected paratenic host.
- Consumption of raw milk containing L3 from …
47 Clinical forms
• VLM.
• OLM.
48
Ocular Larva Migrans (OLM)
49
Prevention:
- P. Hyg. after playing with pets & outdoor activities.
- Children should be taught not to eat soil or sand.
- Regular de-worming…………
51
4) Ascariasis
53 Ascaris suum Large Roundworm of Swine
54 Life Cycle: Tracheal Migration
55
- Ingestion of vegetables or salad containing viable embronated eggs.
56
5) ANISAKIASIS (Herring worm disease)
• Agent: • Anisakis simplex (herring worm)
• Anisakis pegreffii
58 D. H.: Marine mammals (whales, Dolphins, Sea Lion & Porpoises).
59 Sea lion
60
6) Capillariasis
62 6.1. Intestinal capillariasis
6.2. Hepatic capillariasis
6.3. Pulmonary capillariasis
63 6.1. Intestinal capillariasis
64 Capillaria philippinenesis
65
The eggs are ovoid or peanut-shaped , operculated with flattened bipolar plugs, broad shoulders and a striated shell
67
7. Gnathostomiasis
69 70
8) Zoonotic Filariasis
72 8.1. Pulmonary Dirofilariasis
8.2. Subcutaneous Dirofilariasis
8.3. Brugian filariasis
73 8.1. PULMONARY DIROFILARIASIS (Dog Heartworm)
74 Dirofliaria immitis A parasitic nematode that can kill your dog
75 dog mature larvae immature larvae
76 77 8.2. SUBCUTANEOUS DIROFILARIASIS
Dirofliaria repens
78 8.3. Brugian filariasis (Elephantiasis)
Brugia malayi
79 Microfilaria of B. malayi
80 Lymphatic filariasis: elephantiasis is the last consequence of the swelling of limbs and scrotum.
81 Elephantiasis of leg due to filariasis
82 Elephantiasis due to Brugia malayi.
83 • Elephantiasis due to Brugia malayi, complicated by severe dermatitis and secondary bacterial infection.
84 How Do Animal Parasites gain access to the Human Body?
85 1-Passive introduction of the parasite into the body by ingestion of: • cysts, eggs or larvae • raw or undercooked food containing larvae of the parasite. • larval stage in its appropriate host accidentally.
2- Active penetration of the infective stage into the skin.
3- Biting by biological vectors.
4-Skin contamination by the infective stage of the parasite. 86
87
Prion Diseases
88 Prion diseases (Transmissible Spongiform Encephalopathies) (TSEs)
اعتالل الدماغ اإلسفنجي
89 Prion diseases (Transmissible Spongiform Encephalopathies) (TSEs)
(Variant Creutzfeldt-Jakop Disease) (vCJD)
90
The word “Prion” is an abbreviation for
“ proteinacious infectious particle ”
91 (TSEs)
- Group of diseases causing the same pathology in respective hosts. - Microscopic sponge like holes in brain. - Clinical signs are all neurological in nature.
92 TSEs
• Neurodegenerative diseases • Rapidly progressive, always fatal • Affect humans and animals • Long incubation periods • Brain, spinal cord, and adjacent tissues are considered infectious • Prion theory widely accepted
93 Human TSEs
• Kuru • Creutzfeldt-Jakob disease (CJD) • Fatal familial insomnia (FFI) • Variant Creutzfeldt-Jakob disease (vCJD)
94 Kuru
95 Animal TSEs • Bovine Spongiform Encephalopathy (BSE, “mad cow disease”) • Scrapie (sheep) • Chronic wasting disease (CWD) (Mule, elk and deer) • Mink Spongiform Encephalopathy (TME) • Feline Spongiform Encephalopathy (FSE)
96 In April, 27, 2012 , the United States announced a case of BSE
It was the first case of BSE in the United States since 2006
97 On 8 December 2012, the Japanese government issued a ban on imports of raw beef from Brazil, based on reports that a cow which died in southern Brazil carried disease-carrying proteins.
The Brazilian Ministry of Agriculture informed that the animal in question didn't manifest the disease and didn't die of this cause.
98 Symptoms of Bovine Spongiform Encephalopathy restlessness aggressiveness loss of motor function loss of appetite convulsions blindness self mutilation
99 • In most animals, 3-7 years dormant incubation where the animal is asymptomatic.
• Therefore, the animal may be infected but still asymptomatic at time of slaughter.
100 A cow with BSE. A feature of such disease is the inability of the infected animal to stand
101 102 103 Prion theory
• Identified by Dr. Stanley Prusiner, who in 1997 won the Nobel Prize for his research on prions.
104
The word “Prion” is an abbreviation for
“ proteinacious infectious particle ”
105 Normal prion (PrPc)
• Easily soluble • Easily digested by proteases
106 Abnormal prion (PrPSc)
• The same amino acid sequence and primary structure as normal prion
107 Abnormal prion
• Insoluble • Highly proteases-resistant • Survives in tissues post-mortem • Extremely resistant • No detectable immune response
108 prions
• Does not contain RNA or DNA (therefore not technically alive like other infectious agents like viruses or bacteria) • Does not evoke any detectable immune response or inflammatory reaction in host animals.
109 In 1986, 4.5 million cows were incinerated in the U.K. after the discovery of BSE.
110 112 Transmission
• Humans consuming cattle products infected with BSE can develop vCJD
113 CJD Transmission:
• Humans can acquire the prion by exposure to meat that has come in contact with the brain or spinal In common slaughtering practices, the animal is often sliced at least cord of the animal. once through the torso, severing the spinal column and exposing all the the surrounding flesh to the infectious agent.
114 Transmission
• Maternal spread • Blood transfusion
115 Transmission
• Via surgical instruments • Growth hormone injections
116
The most likely scenario for the emergence of vCJD and BSE117 CJD Symptoms:
• restlessness. • aggressiveness (biting and hitting). • loss of motor function. • loss of appetite. • convulsions. • blindness. • self mutilation. • inability to swallow.
118 vCJD is different from CJD
• Variant CJD patients tend to be much younger,
• have a delayed onset of neurologic signs,
• tend to have a longer duration of illness
119 vCJD CJD Average age 28 Years 65 years at Onset 29 (18-41) (50-70) Duration of 24 months 4.5 months Illness (Max. 12 mon.) Transmission Eating BSE ……….. contaminated products
120 Diagnosis: vCJD • MRI, CT, EEG • Biopsy
121 Florid plaques.
122 Treatment: vCJD
• Symptomatic treatment • Supportive care
123 Prevention and Control
124 125 Thank you for your attention!
126