Marine Mammal Parasitology Flashcards
1
Q
What is the species of whale lice infesting callosities of right whales?
A
Cyamus ovalus, Cyamus gracilis (N and S); C. erraticus (S) (F8)
2
Q
What Barnacle spp on gray whales can be used for ID?
A
Cryptolepas rhachianecti (F8)
3
Q
Parasite within pterygoid sinuses of odontocetes
A
Nasitrema globicephalae (Path)
4
Q
Describe the life cycle of Toxoplasma gondii
How does this parasite affect marine mammals?
How prevalent is the disease in marine mammals?
A
Toxoplasma gondii
- Domestic and wild felid definitive host (shed oocysts in feces)
- Infective within 5 days and remain viable for months to years
- All warm-blooded vertebrates serve as intermediate hosts (tissue cysts)
- New hosts infected by consuming intermediate hosts, sporulated oocysts, oocyst contaminated paratenic hosts, contaminated water or transplacental
- Ingestion 🡪 tachyzoites leave intestinal tract 🡪 tachyzoites convert to bradyzoites as host immunity develops 🡪 tissue cysts in CNS, muscle, myocardium (can recrudesce with coinfection – morbillivirus, sepsis, waning immunity).
- T gondii prevalence in marine mammals high in temperate and tropical areas with higher human/cat abundance.
- Transmitted by ingestion of sporulated oocysts from felid feces and paratenic hosts (marine inverts, planktivorous fish)
- Sea otters – high (60% seropositivity)
- Clinical disease reported in phocids, otariids, walrus, odontocete, sirenian, and sea otter.
- In otariids/phocids often associated with concurrent infection/immune suppression
- Affects brain/spinal cord, but can also cause reproductive failure
5
Q
What Neospora species affect marine mammals?
How is it transmitted?
How does it affect marine mammals?
A
Neospora Caninum
- Definitive hosts – canids, and intermediate hosts -birds, dogs, cattle
- Vertical transmission is key route of transmission (not zoonotic)
- Incidental infection in otariids, odontocetes, and river otters.
Neospora Caninum-like
- Incidental in harbor porpoises and California sea lions. Coccidian A and B common in yearlings. Coccidian C pathogens of harbor seals.
6
Q
What Sarcocystis parasites produce disease in marine mammals?
What is the typical life cycle?
Are there geographic areas where marine mammals are more likely to be exposed?
What are the varying clinical presentations of these diseases?
Which parasites produce which type of disease?
A
Sarcocystis neurona and S. neurona-like
- Similar life cycle to T. gondii but new world opossums are the only known definitive hosts and the infective stage (sporocyst) is infectious immediately when defecated.
- Marine mammals act as intermediate hosts or paratenic/transport hosts
- Sporocyst ingested 🡪 asexual reproduction o form merozoites which spread systemically 🡪 enter host cells and form schizonts (brain, lung), then tissue cysts (heart and skeletal muscle)
- Concentrated along the west coast of North America. Exposure decreases as you move mor north (same as T. gondii) – approx. costal human development
- Fatal cases in pacific harbor seals, sea otters, and cetaceans (less common in sea lions). Larger cause of mortality for sea otters than T. gondii.
- PCR required for definitive diagnosis. Can have asymptomatic/resolved infections in sea otters and sea lions.
Sarcocystis spp.
- Associated with fatal necrotizing hepatitis in phocids, otariids, odontocetes, brown, black and polar bears.
- S. arctosi and S. canis – hepatic infections in bears
- S. pinnipedi – innocuous in ringed and bearded seals but causes fatal hepatitis in gray seals.
7
Q
What enteric protozoa produce disease in marine mammals?
What groups of animals are more likely to be affected?
What are the clinical signs?
A
Cystoisospora (Isospora)
- Sporulated oocysts contain two sporocysts, each with 4 sporozoites. Ingest oocysts in food/water.
- Incidental and self-limiting in marine mammals
Eimeria spp
- Host specific infection with 4 sporocysts with 2 sporozoites each.
- Usually younger, immunologically naive animals or high loads (rehab)
- Cx: bloody diarrhea, anorexia, emaciation, dehydration
- Seen in phocids, otariids, sirenians, and ursids
- Phocids: E. phocae, E. weddelli, E. arctowskii
- Sirenians: E. trichechid, E. manatus, E nodulosa
- E. phocae can be pathogenic for harbor seals (and are definitive hosts)
- Oocyst sporulation occurs on land (transmission most efficient in rookeries/haul outs)
Cryptosporidium spp
- Limited to GI tract
- C. parvum, C. muris, and novel cryptospiridum spp
8
Q
What flagellates affect marine mammals?
How are they transmitted?
A
Flagellates
- 1 flagella, undulating membrane, intracellular kintoplast
- Suspect infected by ingestion, leeches, and arthropods
Trypanosomes (Trypanosoma and Leishmania)
- Undulating membrane, flagella and kinetoplast. Life cycle requires blood feeding arthropods and mammals. In arthropods, trypanosomes infect the GI tract while in mammals they move through the bloodstream and cause systemic infection.
- One case report in a polar bear
- Leishmania – spread via sand flies (cutaneous, mucocutaneous and visceral presentations), reported in a Mediterranean monk seal
Jarellia atramenti – asymptomatic sperm whale blowhole secretion and bottlenose dolphin
Cryptobia – asymptomatic upper respiratory infection of cetaceans
Giardia
- Propensity for GI tract, direct life cycle following ingestion of environmentally resistant infective stages.
- Reported in phocids, otariids, odontocetes, mysticetes, and manatee.
Trichomonads
- Pylorus, fundus, duodenum from sea lions. In severe cases can lead to epithelial cell necrosis (crypt abscesses and gland ectasia). May be a form of dysbiosis.
9
Q
What ciliates affect marine mammals?
What species do they affect?
How are they transmitted adn how pathogenic are they?
A
Ciliates
- External cilia, internal micronucleus, and larger macronucleus
Haematophagus megapterae
- Blood feeding ciliated ectoparasite attaches to baleen plates of mysticetes. Low pathogenicity
Kyaroikeus cetarius, K cetarius-like, Planilamina ovata, P. magna
- Kyaroikeus cetarius, Planilamina ovata, P. magna – direct life cycle requiring physical contact, seen in mucus from blowholes of odontocetes.
- Mucosal colonization in bottlenose, orca, and false killer whales
- Kyaroikeus cetarius - low pathogenicity, however heavy loads my indicate bacterial or Nasitrema spp infection of the URT
- Ciliates reported commonly blowhole and feces of ceteceans
- Can be opportunistic cetacean pathogens in animals with other health conditions – associated with dermatitis, cellulitis, lymphadenitis, and pneumonia.
10
Q
Describe the diagnostics for protozoal diseases in marine mammals?
What is the gold standard for most protozoal parasites?
What samples should be collected?
A
Diagnosis
Clinical signs/Physical exam
- Stranding with CNS, musculoskeletal, cardiac, respiratory, hepatic, and/or female reproductive abnormalities.
- Muscle bx, MRI, PCR of blood/CSF – confirming infection diagnosing clinical disease
- Not possible to diagnose from clinical signs as several parasites can cause severe disease and polyparasitism common.
- Cx: none to death, anorexia, depression, icterus, fever. CNS signs common (lack of fear, tremor, paresis/paralysis, stereotypical behavior
- Fetal malformation/reproductive loss in sea otters, phocids, and ceteceans
- No pathognomonic clinical signs
- Commonly exhibit severe systemic lymphadenopathy
- Sea otter with S. neurona 🡪 chemosis, petechiation, dilated urinary bladder
Chem/Serology
- Hypoglycemia/increased muscle and liver enzymes common in many sick animals. Test for biotoxin exposure to see if primary/contributing factor
- Due to long term tissue cysts, T. gondii and S. neurona seropositivity suggestive of infection, not prior exposure.
- Seropositivity not synonymous with disease
- Immunofluorescence commonly used to screen for T. gondii, S. neurona, and N. caninum
Feces
- Smears and wet mounts of feces, blowhole mucus can facilitate diagnosis. Genus -specific antibodies can help to differentiate.
- Parasite isolation and mouse bioassay – can help confirm infection and provide purified parasites, although can also cause selection bias (T. gondii often outcompete S. neurona in mixed infections)
IHC
- Cannot differentiate between closely related parasites – identification best confirmed through PCR/TEM
- PCR is gold standard for definitive detection (heart, brain, skeletal muscle) – test 2-3 tissues from each animal and repeat testing 3 times due to low parasite burdens. Must correlate PCR results with histopath/IHC to confirm disease
11
Q
What are the recommended treatments for the systemic apicomplexan parasites of marine mammals?
What clinical signs suggest euthanasia may be a better course of action?
How are the enteric and respiratory protozoal parasites of marine mammals treated?
How can protozoal infections be prevented?
A
Treatment and Prognosis
System Apicomplexans (T. gondii, Sarcocystis, Neospora)
- For wild marine mammals, brain, spinal cord, cardiopulmonary and muscular changes often too severe that medical intervention is ineffective – most euthanized
- For managed care – long term therapy and clinical outcome better with milder/acute disease. Often use ponazuril or diclazuril – cross BBB and kill nonencysted protozoa (merozoites and tachyzoites). Often give loading dose first.
- No side effects of ponazuril noted in sea otter/harbor seals but difficult to assess efficacy
- Ponazuril effective in treating S. neurona disease in harbor seals and sea otters, but minimally effective for toxoplasmosis. Treat for 60 days.
- If exhibiting CNS signs – may die during early treatment 🡪 systemic inflammatory or anaphylactic response to rapid death of parasites
- Interferon gamma is key cytokine in protection against S. neurona – immunoglobulin may be beneficial in some cases.
- For muscular sarcocystis 🡪 albendazole, metronidazole and cotrimoxazole
Enteric and Respiratory Protozoa
- Divided into animals without clinical disease and animals with clinical disease suspected/confirmed to be due to protozoal infection
- Reduce load – resistant to most disinfection 🡪 physical removal and filtration. Recommend quarantining and fecal screening incoming animals.
- Oralsulfonamides (sulfaquinoxaline) 🡪 enteric protozoa (cystoisospora and Eimeria). Amprolium for preventative care.
Prevention
- Exclude definitive and intermediate hosts (birds, rodents, arthropods)
- Birds can transmit T. gondii, S. neurona and other parasites if consumed
- UV or chlorination may not inactive oocysts
- Freezing fish helps to reduce protozoa load
- For wild pop 🡪 humane control of introduced/feral animals, limiting relocation of potential animal hosts, and conscientious disposal of pet waste
12
Q
A
13
Q
Describe the pathologic lesions for the following protozoa in marine mammals:
Toxoplasmosis
Sarcocystis
Neospora
Enteric protozoa
Kyaroikeus cetarius
A
Gross and Microscopic Lesions
Systemic Apicomplexa
- Conjunctival chemosis, SQ hemorrhage, lymphadenopathy, splenomegaly, orange-white mottling of myocardium, pericardial effusion, pulmonary edema, muscle atrophy, urine distended/enlarged bladder, multiorgan congestion
- Toxoplasmosis 🡪 nonsuppurative meningoencephalitis (intralesional tachyzoites)
- Nodules throughout brain and spinal cord with necrosis, cavitation and dystrophic mineralization. Cysts and tachyzoites often along outer edges of inflammatory nodules.
- Sea otter 🡪 few parasites outside of CNS (subacute to chronic infection)
- Marine mammals 🡪 extra-CNS lesions – skeletal myositis, myocarditis, interstitial pneumonia, hepatitis, lymphadenitis, splenitis, placentitis
- Endodyogeny – two parasites form by lateral division within the mother cytoplasm. Shorter, stouter and more eosinophilic tachyzoites or bradyzoites.
- Sarcocystis neurona 🡪 more pleocellular and diffuse inflammation than toxoplasma. Endopolygeny – daughter cells bud off the mother cell forming flower like arrangement (rosette form schizonts)
- Cysts are rare in neurophil
- Abortion or neonatal death - transplacental transmission or severe illness in the dam
- Meningoencephalitis less apparent in sea lions, and hepatotropic sarcocystis causes severe fatal necrotizing hepatitis without meningoencephalitis.
- Neospora 🡪 Most cases appear to be incidental. Sea lions appear to serve as definitive hosts for some neospora like spp.
Enteric Protozoa
- Often infect with no apparent gross lesions, can cause diarrhea, intestinal mural thickening, mucosal hemorrhage erosions or nodules.
- Clinical disease no reported for Giardia or cryptosporidium
- Infection associated pathology and death more common with Eimeria than cystoisospora
Other Protozoa
- Trypansoma – fatal in a polar bear. Leishmania – fatal in a Mediterranean monk seal.
- Kyaroikeus cetarius tends to be clinically silent when in the URT, but infection has been assoc with dermatitis, pneumonia, and lymphadenitis esp in sick/immunocompromised animals
14
Q
Describe the geographic distribution of systemic apicomplexan parasites in marine mammals.
How is transmission driven? What environmental factors are at play?
What risk factors exist for apicomplexan parasitism in marine mammals?
What coinfections have been documented? Do any make mortality higher?
A
Epidemiology and Epizootiology
- T. gondii distribution mimics distribution of felids, while S. neurona more limited (due to smaller range for opossums). S. neurona primarily west coast of NA.
- With exception of transplacental transmission, most infections result from environmental exposure to oocysts or sporocysts shed by terrestrial definitive hosts, not from marine conspecifics.
- Rainfalls acts as major driver to mobilize parasites into watersheds/coastal waters. Snowmelt can mobilize infective oocysts deposited from previous year.
- Oocysts can persist in shellfish, fish, biofilms on seaweed which are then eaten by snails (high risk prey for sea otters)
- Predominately infected through horizontal transmission – oral ingestion of parasites in water, prey or grooming), vertical transfer can occur.
- T gondii – potential for fetal abortion, hydrocephalus, death
Risk Factors
- Ingestion of protozoa in contaminated food – kelp dwelling snails for T. gondii in sea otters
- T. gondii more common in older animals (chronic, lifelong infection) – sea otters, polar bears, and sea lions.
- Male sea otters higher likelihood of exposure to T. gondii.
- Proximity to freshwater runoff (increased rainfall) and enclosed bays with limited tidal flushing assoc with T gondii and S neurona infections.
- Season – in southern sea otters, higher mortality from S. neurona seen in the spring and summer months. Opossums reproduce during this period and higher rainfall.
Disease Outcome
- Giardia and cryptosporidium reported in normal stool
- Correlations between immunosuppressive factors (morbillivirus, anthropogenic pollutants, bacteria) and clinical toxoplasmosis
- Coinfection with T. gondii and S. neurona linked to increased severity of protozoal encephalitis and higher mortality. Genotype of S. neurona (Type XIII) liked to increased pathogenicity.
Climate change
- Rainfall intensity, warmer artic temperatures, increase storm intensity, and changes in predator/prey dynamics may increase exposure. Wetland degradation, rainfall, and impermeable surface of anthropogenic habitat change increase exposure to contaminated water.
15
Q
Describe the collection of helminths or arthropods from affected marine mammals.
Collection bias is a problem with what groups?
What treatments are used to treat helminth or arthropod infestations?
Toxicity has been reported with what drugs in what species?
A
Collection and Preservation
- Collection bias of stranded animals (often sick) vs hunted animals or bycatch (more are relatively healthy)
- Saline rinses of mucosal surfaces, microscopic examination for parasites is advisable
- Fresher is better, but lightly decomposed (Code 3) may still provide useful specimens
- Acanthocephalans and nematodes tough while digeneans and cestodes may decompose rapidly
- Postmortem migration with cooling - Anisakis sp migrate to esophagus/mouth
- Handle with care - brushes, pipettes, hooked insect pins preferred to forceps
- If working with a parasitologist, consult them about their preferred fixation method and labeling
- Fecals can miss or underestimate infections
Treatment
- Praziquantel: cestodes, digeneans
- Fenbendazole: nematodes
- Ivermectin: Nematodes (lungworms, Uncinaria), some ectoparasites
- Neurologic signs: odontocetes, Guadalupe fur seals (tremors)
- Levamisole: Lethal reactions (2 beluga fatalities), toxicity in sea otters
- Dichlorvos: organophosphate toxicity reported
- Respect clearance intervals for rehab animals
