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NEU2 > Bovine neurology > Flashcards

Bovine neurology Flashcards

1
Q

Give examples of genetic neurological conditions in cattle

A
  • Hydrocephalus (Holstein, Hereford, Ayrshire, Charolais)
  • Cerebellar hypomyelinogenesis (Shorthorn, Hereford, Angus)
  • Progressive ataxia (Charolais)
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2
Q

What are congenital neurological conditions in cattle commonly associated with?

A

Infectious or toxic insults during pregnancy

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3
Q

Outline the aetiology of cerebellar hypoplasia in cattle

A
  • Genetic condition (rare)
  • congenital condition
  • In utero infection of calves with BVD virus
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4
Q

Describe the epidemiology of cerebellar hypoplasia in cattle

A
  • Infection of naiive cows during pregnancy with BVD
  • Limited effects on dam, virus crosses placental barrier and infects calf
  • Infection between 90-130 days gestation can lead to cerebellar hypoplasia (and other problems e.g. microphthalmia)
  • Single cases, occasionally small storms e.g. batch calving groups
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5
Q

Outline the pathogenesis of cerebellar hypoplasia in cattle

A
  • Cerebellum concerned with fine motor coordination of voluntary movement
  • Hypoplasia leads to dysfunction leading to clumsy, jerky movements
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6
Q

Describe the clinical signs of cerebellar hypoplasia in cattle

A
  • Ataxia and incoordination
  • Wide based stance
  • Hypermetria and intention tremors
  • Lateral recumbency and inability to stand in severe cases
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7
Q

How is cerebellar hypoplasia of cattle diagnosed?

A

Based on clinical signs

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8
Q

Outline the treatment of cerebellar hypoplasia in cattle

A

None, mildly affected often cope if maintained in low stress environments

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9
Q

Outline the prevention of cerebellar hypoplasia in cattle

A
  • Affected calves indicate active circulation of virus in herd so herd level investigation required
  • Control programme for BVD is in place
  • Remove persistently infected individuals
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10
Q

Describe the aetiology of meningitis/meningoencephalitis in cattle

A
  • Inflammation of meninges and/or encephalon
  • Usually bacterial or viral, infection in farm species
  • Streptococcus spp, E coli in young
  • Histophilus somnus in cattle
  • Pasteurella multocida and Mannhemia haemolytica in lambs
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11
Q

Describe the epidemiology of meningitis/meningoencephalitis in cattle

A
  • Most commonly sporadic disease of young (3-10 days) calves/lambs
  • Failure of passive transfer and high environmental bacterial contamination
  • Bacteraemia leads to navel ill/joint ill and less commonly meningitis
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12
Q

Describe the pathogenesis of meningitis/meningoencephalitis in cattle

A
  • Localisation of septic foci in meningeal vessels, occasionally progressing to encephalon
  • Hyperaemia, opacity and accumulation of pus
  • Swelling
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13
Q

Describe the clinical signs of meningitis/meningoencephalitis in cattle

A
  • Initially depression, weakness, lack of suck reflex, low head carriage, neck extension
  • Leads to ataxia, recumbency, lack of menace, episcleral congestion
  • Leads to stupor, hyperaesthesia, opisthotonus and death
  • Other signs: polyarthritis, hypopyon, omphlophlebitis, diarrhoea
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14
Q

Outline the diagnosis of meningitis/meningoencephalitis in cattle

A
  • Clinical signs

- CSF tap (not required for treatment, may show increased protein and WBC count, turbidity and can culture)

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15
Q

Describe the treatment of meningitis/meningoencephalitis in cattle

A
  • Prognosis poor unless early treatment
  • High doses of braod spec, bacteriocidal, BBB crossing antibiotics: 3rd gen cephalosporins, florfenicol, TMPS combinations
  • NSAIDs
  • Supportive treatment e.g. fluids and nursing
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16
Q

Describe the prevention of meningitis/meningoencephalitis in cattle

A
  • Neonatal managment
  • Passive transfer of immunity via colostrum must be ensured
  • Clean environment, disinfect regularly
  • Navel dressing
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17
Q

Describe the aetiology of otitis media in cattle

A
  • Infection usually bacterial
  • Often mixed infection
  • Ascending infection up eustachian tube following pneumonia
  • Haematogenous spread (navel/joint ill in calves)
  • Rarely an extension of otitis externa
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18
Q

What are the common pathogens in otitis media in cattle?

A

E coli, Pseudomonas spp., Acinetobacter spp., Mycoplasma bovis

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19
Q

Describe the epidemiology of otitis media in cattle

A
  • Usually younger calves and lambs

- Sporadic single cases, some group outbreaks reported

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20
Q

Describe the clinical signs of otitis media in cattle

A
  • Head tilt, possible ataxia, circling/falling towards affected side
  • Occasionally ear drooping (inflammation of facial nerve)
  • Purulent discharge if tympanic membrane ruptured
  • Pyrexia/anorexia/dull in advanced disease
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21
Q

Outline the diagnosis of otitis media in cattle

A
  • Clincial signs
  • Further investigation possible similar to small animals, but rarely necessary
  • NB trauma may be a differential, higher risk than in small animals
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22
Q

Outline the treatment of otitis media in cattle

A
  • Antibiotics: brad spec, long course 3-4 weeks
  • NSAIDs
  • Irrigation following rupture of tympanic membrane possible
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23
Q

Outline the prevention of otitis media in cattle

A

Difficult, prevent pneumonia and navel/joint ill

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24
Q

Describe the aetiology of hypovitaminosis A in cattle

A
  • Primary deficiency of vit A or carotene in diet

- Secondary deficiency caused by problems with digestion, absorption or metabolism (Less common)

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25
Q

Describe the epidemiology of hypovitaminosis A in cattle

A
  • Usually young housed cattle on diets lacking green plant material i.e. straw and cereals without mineral and vit supplementation
  • May be maternal deficiency leading to congenital deficiencyand disease in young calves
  • Neonates should have high levels of vit A in colostrum
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26
Q

Describe the pathogenesis of hypovitaminosis A in cattle

A

Required for:

  • Rhodopsin photo-receptor
  • Maintenance of epithelial tissue and mucus membranes
  • Normal bone growth
  • Also leads to damage to peripheral nerve roots and increased intracranial pressure
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27
Q

Describe the clinical signs of hypovitaminosis A in growing cattle (not congenital)

A
  • Night blindness leading to complete blindness
  • Rough, dry coat, poor quality hoof horn
  • Paralysis, initially show weakness and incoordination
  • Encephalopathy seen as convulsions and other nervous signs
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28
Q

Describe the clinical signs of hypovitaminosis A as a congenital disease of young calves

A
  • Born blind (optic nerve constriction)
  • Other ocular problems e.g. microphthalmos
  • Tonic-clonic convulsions
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29
Q

Outline the diagnosis of hypovitaminosis A in cattle

A
  • History and clinical signs
  • Vitamin A levels in plasma <10ug/100ml
  • High CSF pressure (theoretical)
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30
Q

Outline the treatment of hypovitaminosis a in cattle

A
  • Parenteral administration of vit A at 400iu/kg BW (rapid response unless chronically affected)
  • Ensure ongoing daily requirements met by diet
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31
Q

Outline the prevention of hypovitaminosis A in cattle

A
  • Daily requirement 40IU/kg BW

- Ensure cattle and sheep of all ages receive green forage or are supplemented with minerals and vitamins

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32
Q

What is cerebrocortical necrosis also known as?

A

Polioencephalomalacia

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33
Q

Describe the aetiology of polioencephalomalacia in cattle

A
  • Deficiency of vit B (thiamin)
  • Normal requirements absorbed from rumen produced by microflora
  • Primary deficiency: inadeuate production/absorption, unclear aetiology
  • Secondary deficiency: presence of thiaminases in rumen of bacterial production of plants
  • High levels of sulphate in diet
  • Brain dependent on carbohydrate in diet, absorbed thiamine converted to thiamine pyrophosphate (TPP), which is coenzyme in TCA and other carb metabolism processes
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34
Q

Give examples of bacterial thiaminases

A
  • Bacillus thiaminolyticus
  • Clostridium sporogenes (Thiaminase type 1)
  • Bacillus anaerinolyticus (thiaminase type II)
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35
Q

Give examples of plant thiaminases

A
  • Bracken fern

- Horsetail

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36
Q

Describe the epidemiology of polioencephalomalacia

A
  • Sporadic, often small clusters of cases
  • Most common vitamin deficiency
  • Usually young, often fast growing/well fed calves (4-18mo) and lambs (4-8mo) on low fibre diets
  • Often associated with chagne in diet
  • Occasionally single cases in adults
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37
Q

Describe the post mortem findings in polioencephalomalacia

A
  • Brain pale, swollen, flattened gyri, sometimes yellow discolouration
  • Necrotic cortical tissues in cerebrum with laminar configuration
  • Affected regions have bright white autofluorescence when viewed with UV light (pathognomic)
  • Histopath shows necrosis esp. in cortex
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38
Q

Describe the clinical signs of polioencephalomalacia in cattle

A
  • Initially dull, diarrhoeic
  • then neuro signs: staggering, high head carriage/star gazing, wandering
  • Blind, no menace response
  • Hyperaesthesia to tactile and auditory stimuli
  • recumbency, muscle tremors, intermitent opisthotonus, convulsion, periods of flaccid and spastic paresis
  • Death in 1-4 days if untreated
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39
Q

What are the pathognomic signs of polioencephalomalacia in cattle?

A

Wide based stance and stargazing

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40
Q

Outline the diagnosis of polioencephalomalacia in cattle

A
  • History and clinical signs

- Response to treatment

41
Q

Describe the treatment of polioencephalomalacia in cattle

A
  • Thiamine hydrochloride IV, 10-15mg/kg repeat for 2-3 days
  • Nursing to reverse pathology, reduce other symptoms
  • Maintain hydration and management of whole animal
42
Q

Describe the prevention of polioencephalomalacia in cattle

A
  • If case identified, watch others in group carefully and treat early if any clinical signs
  • Increase fibre/reduce concentrate in diet
  • Ensure no thiaminase plants on pasture
43
Q

What is silage eye?

A

Ocular lesions caused by listeriosis

44
Q

Describe the aetiology of malignant catarrhal fever

A
  • Ovine herpesvirus-2 in UK
  • Do not cause disease in sheep
  • Usually acute or peracute disease, chronic disease seen occasionally
  • Less common vs listeriosis but more severe
45
Q

Describe the epidemiology of malignant catarrhal fever

A
  • Sporadic single cases in yearling/adult cattle, occasionally mini outbreaks
  • Direct or indirect contact with pregnant or lambing sheep
  • Deer can also be affected
  • Cattle to cattle transmission does not occur
  • Incubation period 3-8 weeks
46
Q

Describe the pathogenesis of malignant catarrhal fever

A
  • Lymphoid hyperplasia and infiltration

- Vasculitis

47
Q

Describe the clinical signs of malignant catarrhal fever

A
  • ANorexia and agalactia
  • High pyrexia (41-41.5) and tachycardia
  • Profuse mucopurulent nasal discharge
  • Corneal opactity, eyelid oedema, congestion and discharge, blepharospasm
  • Extensive necrosis of buccal mucosa
  • Occasionally neurological signs weakness, nystagmus, head pressing)
  • Occasionally mild and chronic disease seen
48
Q

How can MCF be differentiated from FMDV?

A
  • MCF will have no coronary band lesions

- FMDV has no ocular signs

49
Q

Describe the clinical pathology results of MCF

A
  • Leukopaenia
  • Virus isolation difficult and problematic
  • Serology may be of value in clinical cases although some do not/have not seroconverted
50
Q

Describe the post mortem findings of MCF

A
  • Lesions (haemorrhagic and erosive) often extensive in GIT, UT and RT
  • Enlarged, oedematous, harmorrhagic lymph nodes
  • Histopath shows necrotising vasculitis, perivascular and mononuclear cell cuffing in most organs
51
Q

Describe the diagnosis of MCF

A
  • History and clinical signs highly suggestive
  • Viral antigen PCR can be attempted
  • Seroconversion (care)
  • PM findings
52
Q

Outline the treatment and prevention of MCF

A
  • Invariably fatal, euthanasia on welfare grounds
  • No vaccine
  • Prevent by preventing sheep to cattle contact
53
Q

Outline the aetiology of Thromboembolic Menincoencephalitis (TEME) in cattle

A

Fulminating bacteraemia caused by Histophilus somnus

54
Q

Describe the epidemiology of TEME in cattle

A
  • Young growing cattle
  • Usually induced by significant stress
  • Uncommon cause of disease in UK, more common in feedlots in US
  • Resp. form most common presentation in Uk
  • Lots of concentrate feeding leading to liver abscesses, which can then seed out and spread around body e.g. to brain
55
Q

Describe the clinical signs of TEME in cattle

A
  • Pyrexia, anorexia, depression
  • Somnolence (aka sleepy calf disease)
  • Ataxia and proprioceptive deficits
  • Occasionally blindness and nystagmus
  • Opisthotonus, convulsions and coma if untreated
  • Pneumonia, pleuritis, myocarditis
  • Joint effusions/swelling leading to lameness
  • Focused lesion e.g. in spinal cord may caused hindlimb ataxia (common in sheep, cattle)
56
Q

Describe the diagnosis of TEME

A
  • Clinical signs
  • Culture from CSF, blood, synovial fluid
  • Acute and convalescent serology
57
Q

Describe the treatment of TEME

A
  • Antibiotics (oxytet - crosses BBB, penicillins, florfenicol)
  • NSAIDs
  • Nursing
  • Need to start treatment quickly, affects prognosis
58
Q

Describe the prevention of TEME

A
  • Prevent/limit stress

- No vaccine in UK

59
Q

Describe the aetiology of lead poisoning in cattle

A

Licking/chewing of lead objects e.g. paint, vehicle batteries, soil from lead mines, engine sump oil, putty, grease

60
Q

Explain the epidemiology of lead poisoning in cattle

A
  • Young more at risk due to lining of intestines having higher number of calcium channels than older
  • These channels can absorb lead due to having the same latency
61
Q

Describe the clinical signs of peracute lead poisoning in cattle

A

Sudden death depending on dose

62
Q

Describe the clinical signs of acute lead poisoning in cattle

A
  • Muscle fasciculations (esp. head and neck)
  • Jaw champing, frothing, bruxism
  • Staggering gait and head pressing
  • Blindness
  • Opisthotonus
  • Tonic-clonic convulsions
  • Bellowing
  • Diarrhoea
63
Q

Describe the clinical signs of lead poisoning in cattle

A
  • Less severe vs acute

- Diarrhoea, depression and poor doing predominate

64
Q

Describe the pathogenesis of lead poisoning in cattle

A
  • Not fully understood
  • Damage to BBB allowing passage of toxins
  • Disturbance of cellular memrbanes
65
Q

Describe the post mortem findings of lead poisoning in cattle

A
  • No gross lesions of acute

- If less acute, abomastitis and enteritis, congestion of the lungs, degeneration of liver and kidney

66
Q

Describe the diagnosis of lead poisoning in cattle

A
  • History and clinical signs
  • LEad in heparinised blood sample >0.4ppm diagnostic
  • Lead in kidney >20ppm diagnostic
67
Q

Describe the treatment of lead poisoning in cattle

A
  • IV chelating agent which is an easily excretable non-ionisable, soluble complex e.g. sodium calcium edetate (Ca-EDTA)
  • Euthanasia as is often unsuccessful
  • Report heavy metal contamination to APHA
  • Oral agents: precipiate soluble Pb into insoluble forms, reduce uptake, e.g. magnesium sulphate
  • Supportive treatments e.g. sedatives, IV fluids, careful nursing
68
Q

Outline the prevention of lead poisoning in cattle

A
  • Search environment for source

- Move all animals from pasture if in doubt

69
Q

Explain the importance of lead poisoning in cattle to human health

A
  • Contaminated milk and meat prevent risk
  • FSA 1990 makes it offence to sell products which could compromise human health
  • All cases of Pb poisoning investigated by VLA on behalf of FSA
  • Need to ensure potentially contaminated produce does not enter food chain
  • Blood sample affected/potentially affected animals before sale
70
Q

Briefly outline other heavy metals that may cause neurological signs

A
  • Arsenic, mercury
  • Much less common vs Pb
  • Arsenic compounds found in herbicides, insecticides, wood preservatives
71
Q

Describe the pathogenesis of organophosphate poisoning in cattle

A
  • Block cholinesterases at cholinergic nerve ends and myoneural junctions
  • Lead to persistence of acetylcholine and continued stimulation
  • stimulation of PSNS, skeletal muscles and CNS
72
Q

How may organophosphates be absorbed?

A

Orally, dermally or by inhalation

73
Q

Describe the clinical signs of organophosphate poisoning

A
  • Profuse salivation, nasal discharge, dyspnoea, cough, excess lacrimation, miosis, diarrhoea, sweating
  • Muscle fasciculation, stiffness leading to paralysis
  • Profound CNS depression
74
Q

Outline the diagnosis of organophosphate poisoning in cattle

A
  • Clinical signs and history

- (reduction in cholinesterase activity in blood or brain tissue)

75
Q

Outline the treatment of organophosphate poisoning in cattle

A
  • Atropine sulphate (blocks acetylcholine): 0.1mg/kg BW slow IV, or 0.4mg/kg BW SC
  • Repeat after 48 hours if necessary
76
Q

How does ionophore poisoning occur?

A
  • Monensin used as growth promotor and coccidiosat

- Excessive feeding or over-supplementation by error

77
Q

Describe the clinical signs of ionophore poisoning

A
  • Diarrhoea
  • Dullness
  • Weakness
  • Tachycardia
  • Neurological signs
  • Heart failure due to myocardial effects
78
Q

Outline the treatment of ionophore poisoning

A

No treatment other than supportive measures

79
Q

What is mycotoxicosis?

A

Umbrella term for toxicosis due to consumption of toxins produced by moulds and fungi

80
Q

How does mycotoxicosis occur?

A

Ingestion of plants or badly stored feed stuffs in wet and warm conditions (where moulds and fungi have grown)

81
Q

Outline the importance of mycotoxicosis to humans

A

Risk to humans via direct consumption or indirectly by consumption of contaminated animal products e.g. milk

82
Q

Describe the clinical signs of mycotoxicosis in cattle

A

More commonly abortion than neurological signs

83
Q

Describe the aetiology of aflatoxicosis in cattle

A
  • Aflatoxins are metabolites produced by range of fungi growing on spoiled/spoiling animal feeds
  • Cattle and sheep affected if ingest affected feed stuffs
  • Toxins include: B1, B2, G1, G2 and second generation metabolites M1 and M2
84
Q

What is the main source of aflatoxins?

A

Aspergillus flavus

85
Q

Describe the epidemiology of aflatoxicosis

A
  • Wet/warm storage conditions of feed
  • Sheep and cattle relatively resistant to effects
  • Can affect any age group
  • Usually all individuals in a group affected
  • Can affect human health via milk
86
Q

Describe the pathogenesis of aflatoxicosis

A
  • Hepatosis and hepatic insufficiency

- Mutagenesis and teratogenesis

87
Q

Describe the clinical signs of aflatoxicosis in cattle

A
  • Dependent on dose consumed
  • Vague signs of ill health/poor performance
  • Blindness, circling, bruxism, frothing, tenesmus and diarrhoea, photosensitivity, abortion
  • Recumbency, convulsions and death
88
Q

Describe the diagnosis of aflatoxicosis in cattle

A
  • CLinical signs (often vague)
  • Sensitive assays for levels in feeds, urine, blood, milk and other tissues (chromatography, ELISA)
  • Elevation go live enzymes in acute case
89
Q

Outline the treatment of aflatoxicosis in cattle

A

None, supportive only

90
Q

Outline the prevention of aflatoxicosis in cattle

A
  • Proper feed storage
  • Do not feed mouldy food
  • Measure levels in feed
  • Commercial products can be mixed with feed which bind toxins and prevent absorption in the gut
91
Q

How does plant poisoning commonly occur in cattle?

A
  • Hunger if kept on sparse pasture
  • Keeping animals on unimproved pasture
  • Curiosity esp. in youngstock
  • Drainage or clearance work
  • Garden clippings thrown over hedges
92
Q

List common plants that may cause neurological signs

A
  • Ragwort
  • Bracken
  • Horsetail
  • Hemlock
  • Hemlock Water dropwort (aka dead man’s fingers)
  • Black nightshade
  • Rhododendron
  • Laburnum
93
Q

List important infectious neurological disease of cattle

A
  • BSE and Scrapie
  • Aujeskys
  • Rabies
  • Gid
94
Q

What are the key aspects for the treatment of ruminant neurological idsease?

A

Antibacterial and anti-inflammatory treatment

95
Q

What are the key criteria for antibacterials to treat neurological conditions in cattle?

A
  • Must cross BBB and achieve high enough concentration
  • Must be bacteriocidal
  • Must be active against causal pathogen
96
Q

List and justify some logical choices of antibacterials for the treatment of neurological conditions in ruminants

A
  • Penicillins: use small animal preparations as can be used IV, large animal preps have limited routes of admin
  • 3rd generation cephalosporins: purely for individual cases, no metaphylaxis, are critically important but may be justified in neuro cases
  • TMPS combinations
  • Florfenicol
97
Q

List and evaluate components of anti-inflammatory teatment for ruminant neurological conditions

A
  • Cerebral oedema and inflammation common, leads to problems
  • Steroids: treat cerebral oedema + inflammation, may interfere with immune response and decrease BBB, dex 1-2mg/kg
  • NSAIDs: broad anti-inflamm and analgesia, no data on efficacy in farm animal neurodisease
  • Frusemide: diuretic, 1-2mg/kg IV but rare due to limited access in pure farm animal practice
  • Dimethyl sulphoxide (DMSO): not licensed for food producing animals
98
Q

Describe the implications of diagnosing a neurological condition for the individual and rest of herd/flock

A
  • Diagnosis of meningitis/meningoencephalitis suggests poor management of herd e.g. poor maternal antibody transfer, dirty environment, need to consider herd welfare and health
  • Listeriosis indicates herd problem as is commonly transmitted via poor silage: consider future protection of bales/batches of food
  • Be aware that initial neuro case of Listeria may mean abortion cases in the future

NEU2 (23 decks)

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