Major Toxic Plants Causing Pulmonary Injury in Animals

What are some examples of Plants Known to Cause Pulmonary Toxicity in Animals

 Fog fever

 Perilla frutescens plant toxicity

 Cyanogenic glycoside-containing plants

What is fog fever?.....What causes this?

 Occurs after cattle moved to lush pasture, usually in early fall

 Disease develops 5-10 days after cattle are moved to lush pasture

What animal is affected by Fog Fever or Acute Bovine Pulmonary Edema and Emphysema (ABPEE)

 Respiratory distress syndrome occurs in ruminants, mainly in cattle

What is the first step of Pathogenesis of Fog Fever in Cattle

• lush paster - Lush paster has large amounts of L-tryptophan

What is the second step of Pathogenesis of Fog Fever in Cattle

• rumen metabolism: L-tryptophan is converted to 3- methylindole (3- MI) by rumen microbes

What is the third step of Pathogenesis of Fog Fever in Cattle

• Absorption into bloodstream

• 3-MI is absorbed into the blood from rumen and distributed to lungs

What is the fourth step of Pathogenesis of Fog Fever in Cattle

• pulmonary bioactivation

• 3-MI is conversted to a pneumotoxin by mixed function oxidase, which is highly active in lungs

What is the fifth step of Pathogenesis of Fog Fever in Cattle

• ling injury

• Toxic metabolite causes typical lung injury (ABPEE)

What are the Characteristic Clinical Signs of Fog fever

 Open mouth breathing, drooling, tongue extended

 A loud expiratory grunt is commonly observed

 Any forced exercise can trigger sudden death

What are the Characteristic Lesions Signs of Fog fever

 Lung edema and emphysema are characteristic postmortem findings

 Ruptured alveoli indicating emphysema are seen in histopathology

What is the Diagnosis of Fog Fever

 No specific diagnostic test is available to detect fog fever

 Diagnosis is based on multiple lines of evidence:

• History of recent movement to lush pasture and the season

• Clinical signs indicating respiratory distress

• Presence of characteristic lesions (lung emphysema, edema)

Treatment of Fog Fever are

 There is no antidote or effective treatment

 NSAIDs, corticosteroids, and antihistamines offer little help

 Exercise can worsen the condition- do not chase cattle off pasture

 Keep animals in calm and stress-free environment to speed up recovery

Strategies to Reduce the Risk of Fog Fever Outbreaks are

 Feed ionophore antibiotics (ex- monensin) before moving to pasture

• These suppress bacteria that convert L-tryptophan to 3-MI

 Feed hay before moving to lush pasture

 Gradually increasing grazing time on lush pasture

• It will promote ruminal adaptation

• Reduce toxicity development

What is Perilla Frutescens Plant Toxicity

 Eating several lbs of fresh plant- causes respiratory distress in animals

which animal is susceptible for Perilla Frutescens Plant Toxicity

 Cattle are most susceptible, and horses and sheep are also affected

 Toxicity is most common during late summer when forage is limited

What was the first step of The Mechanism of Toxicity with Perilla Mint

Eating Perilla Mint

What was the second step of The Mechanism of Toxicity with Perilla Mint

Toxic Agents

 Perilla ketone

 4- Ipomeanol

• Toxic Agents Absorbed into Blood

What was the third step of The Mechanism of Toxicity with Perilla Mint

• Metabolic Activation of Toxic Agents in Lungs

• toxic metabolite

What was the fourth step of The Mechanism of Toxicity with Perilla Mint

• Damage to Lung Cells

• induce cell death

What was the fifth step of The Mechanism of Toxicity with Perilla Mint

• Respiratory Distress and Death

Clinical Signs

 Dyspnea

 Open mouth breathing

 Expiratory grunt

 Emphysema under skin

of neck

What is the Diagnosis of Perilla Mint Toxicity

 No specific diagnostic test is available to identify perilla mint toxicity

 Diagnosis is based on multiple lines of evidence:

• History of recent ingestion of perilla mint (several pounds)

• Clinical signs of respiratory distress

• Presence of lung lesions (lung distention, emphysema, and edema)

Treatment of Perilla Mint Toxicity

 There is no antidote or effective treatment for perilla mint toxicity

 The supportive therapies offer little benefit and are not necessary

 Handling and restraining may trigger rapid death

 Those surviving initial toxicity (2-3 days) may fully recover in 7-10 days

What are cyanogenic glycosides?

Compounds containing sugar molecule linked to a cyanide-containing aglycone

Cyanogenic glycosides (CGs) = What

protoxins

All CGs have potential to cause what

toxicity

There are over how many GCs in the plant kingdom

100 CGs

Which plants contain Cyanogenic Glycoside-Containing Plants of Veterinary Importance

• black cherry plant

• choke cherry plant

• sorgum plant

• johnsongrass

• bamboo shoots

• Acasia plant

• Apricot

• Lima beans

• Clovers

• Cassava

Factors Contributing to Increased Toxicity with Cyanogenic Plants

Young, rapidly growing plants are rich in cyanogenic glycosides

Environmental stressors that affect plant health can increase toxicity

• Ruminants (Cattle, Sheep, Goat) are highly susceptible to toxicity

What do we mean by Environmental stressors that affect plant health can increase toxicity

- Wilting and drying during drought

- Exposure to frost or freezing

- Crushing or damaging plants

- Application of herbicide and nitrogen fertilizers

Why are ruminants (Cattle, Sheep, Goat) are highly susceptible to toxicity (cyanogenic plants)

- Rumen microbes contain beta-glucosidase and hydroxynitrile lyase

- These enzymes release HCN from cyanogenic glycosides (protoxins)

What are the The Mechanism of Cyanogenic Plant Toxicity

 Inhibits Cytochrome C oxidase in mitochondria

 Impairs aerobic respiration in the cell

Suppresses ATP synthesis

Clinical Presentation of Cyanogenic Plant Toxicity: Acute Cyanide Toxicity (Common)

- Tachypnea followed by dyspnea

- Tachycardia, salivation

- Muscle fasciculation

- Animals eventually collapse (<2 hours)

Clinical Presentation of Cyanogenic Plant Toxicity: Chronic Cyanide Toxicity (Rare)

- Occurs following prolonged ingestion of small amounts of toxic plants

- Suffer neurological disease: Cystitis Ataxia Syndrome (HORSES)

• Posterior paralysis

• Urinary incontinence

• Cystitis

- Goiter (sheep) and teratogenic effects (horses and pigs)

Diagnosis of Cyanogenic Plant Toxicity: Confirmatory Diagnosis are

 Detection of HCN in feed, rumen content, and animal tissues

- Plant material: 200 ppm HCN indicates toxicity potential

- Liver and whole blood: >1 ppm of HCN indicates toxicity

- Brain and myocardium: 1 ppm of HCN indicates toxicity

Diagnosis of Cyanogenic Plant Toxicity: Presumptive Diagnosis are

 History of consuming cyanogenic plants

 Typical clinical signs

 Characteristic lesions

- Pink mucus membrane, which may turn cyanotic after death

- Bright cherry red color of blood (fades rapidly after death)

- Bitter almond smell of rumen content (not reliable or consistent)

Treatment of Cyanogenic Plant Toxicity

 Antidote Therapy (Approach #1):

• Sodium nitrite (10-20 mg/kg)

• Sodium thiosulfate (250-500 mg/kg)

 Antidote Therapy (Approach #2)

- Hydroxocobalamin (70 mg/kg)

- Given slow IV

- Cyanide → Cyanocobalamin (Nontoxic)

 Supportive care

- Remove the plant source

- Provide oxygen

Prevention of Cyanogenic Plant Toxicity

 Reduce access to plants containing high levels of cyanogenic glycosides

- Avoid animals grazing on young, rapidly growing plants- rich in CGs

- Avoid animals grazing on early in the morning, as plants contain >CGs

- Avoid animals foraging on plants that are wilted, frosty, or stressed

 Adopt methods to deplete HCN content in animal fodder

- Preparing hay or silage depletes HCN content significantly

- Feeding hay or silage made from a likely toxic crop is a safe option