Common Diseases: Footrot, Fungal Rusts, and Milk Fever

Overview

These three diseases are explicitly named in the VCAA study design and represent examples of a bacterial animal disease, a fungal plant disease, and a metabolic animal disease respectively. Each has a distinct cause, mode of action, and management approach.

VCAA FOCUS: For each disease, know: the causal agent, classification (microbial/metabolic), affected host, symptoms, conditions that favour its development, and prevention and control strategies.

Disease 1: Footrot

Classification

• Type: Microbial (bacterial)
• Primary pathogen: Dichelobacter nodosus (obligate anaerobe)
• Contributing pathogen: Fusobacterium necrophorum (softens interdigital skin, enabling D. nodosus entry)
• Host: Primarily sheep; also goats and cattle
• Significance: Leading cause of lameness in sheep; major welfare and production issue in Victorian sheep farming

Lifecycle and Disease Development

1. Fusobacterium necrophorum is a common environmental bacterium that causes mild interdigital (between the toes) dermatitis when hoof skin is softened (wet conditions)
2. This creates an entry point for D. nodosus, which can only survive outside the hoof for ~7 days (soil/pasture transmission period)
3. D. nodosus produces proteolytic enzymes that digest the horn of the hoof, separating the outer horn from the sensitive tissue beneath
4. In severe (virulent) strains: progressive destruction of the entire sole of the hoof — virulent footrot
5. In milder (benign) strains: limited to interdigital skin — benign footrot

Symptoms

Conditions favouring spread:
- Wet, muddy paddocks and gateways
- Warm, humid conditions (optimal: >10°C, wet soil)
- High stocking density; congregating animals
- Introduction of infected animals without quarantine

Prevention and Control

KEY TAKEAWAY: Footrot can be eradicated from a property through systematic management — this is unlike many diseases where control (not eradication) is the realistic goal.

Disease 2: Fungal Rusts

Classification

• Type: Microbial (fungal)
• Pathogens: Puccinia species — wheat stem rust (P. graminis f.sp. tritici), wheat leaf rust (P. triticina), stripe rust (P. striiformis), coffee rust (Hemileia vastatrix)
• Host: Primarily cereal crops (wheat, barley, oats); also affects other grasses, ornamentals
• Significance: Wheat rusts are among the most important diseases of cereal crops worldwide; major threat to Australian grain production

Biology and Lifecycle

Rusts are obligate biotrophs — they can only grow and reproduce on living plant tissue. They have a complex lifecycle:

1. Urediniospores (orange-red powdery spores) — produced in uredinia (pustules) on leaves and stems; primary means of spread during the growing season
2. Spores are carried on wind — can travel hundreds to thousands of kilometres
3. Spores germinate in free moisture (dew, rain) and penetrate leaf through stomata
4. Mycelium spreads through intercellular spaces, extracting nutrients
5. New uredinia form within 7–14 days, producing millions more spores
6. Cycle repeats rapidly through the season — polycyclic disease

Symptoms

General symptoms:
- Orange, brown, or yellow powdery pustules on leaf surfaces, stems, or pods
- Ruptured epidermis surrounding pustules
- Severe infections cause: premature leaf death, reduced photosynthesis, shrivelled grain, stem weakening (lodging risk)
- Yield losses of 10–70% in susceptible varieties

Prevention and Control

EXAM TIP: The concept of the “green bridge” — volunteer wheat plants growing in summer between the harvest and next sowing — is critical for understanding how rust survives between seasons. Breaking the green bridge is an important management tool.

Disease 3: Milk Fever (Hypocalcaemia)

Classification

• Type: Metabolic (non-infectious)
• Cause: Sudden drop in blood calcium (Ca²⁺) levels at or after calving
• Host: Primarily high-producing dairy cows; less commonly ewes (in late pregnancy), does, and sows
• Significance: One of the most common metabolic disorders in Australian dairy herds; causes significant welfare, production, and mortality losses

Cause and Pathophysiology

During late pregnancy and early lactation, calcium demand increases dramatically:
- Colostrum and milk production requires large amounts of calcium
- If the cow’s calcium mobilisation from bone and dietary absorption cannot keep pace, blood calcium falls below normal

$$\text{Normal blood Ca}^{2+} \approx 2.2-2.6 \, \text{mmol/L}$$
$$\text{Milk fever} < 1.5 \, \text{mmol/L}$$

Low calcium impairs muscle and nerve function throughout the body.

Risk factors:
- High-yielding cows (greater calcium demand)
- Older cows (reduced ability to mobilise bone calcium quickly)
- Pre-calving diet high in calcium (depresses the cow’s calcium mobilisation system)
- Diets high in potassium and sodium (increase alkalinity, reduce calcium absorption)
- Jersey and Guernsey breeds are more susceptible

Symptoms (Three Stages)

Prevention and Control

REMEMBER: Milk fever is NOT infectious. It cannot be treated with antibiotics. Management focuses entirely on nutrition and calcium supplementation. The distinction between metabolic and microbial disease is critical for selecting the correct management response.

Summary Comparison