Nutritional and Functional Properties of Colostrum in Puppies and Kittens

The review article titled “Nutritional and Functional Properties of Colostrum in Puppies and Kittens” (Rossi et al., 2021) provides an in-depth analysis of the critical role that colostrum plays in the early stages of life for newborn dogs and cats. The neonatal period, generally defined as the first two weeks of life, is a crucial transitional phase during which animals adapt to the extrauterine environment. During this time, puppies and kittens face significant health risks and high mortality rates due to the physiological immaturity of their organ systems, scarce energy reserves, and a weak immune system. Proper nutrition during this phase is paramount, not only for immediate survival but also for its long-term effects on metabolic programming and adult health.

Effective nutritional management of the dam or queen during pregnancy and lactation is the essential first step to ensure correct fetal development and to optimise colostrum and milk production. Canine and feline colostrum is specifically defined as the first secretion of the mammary glands during the first two days postpartum.

Unlike livestock species, colostrum composition in companion animals has historically been less documented. This review synthesises available scientific data to emphasise that colostrum is not merely a source of food, but a complex biological fluid packed with immunoglobulins, growth factors, and essential bioactive compounds vital for neonate survival.

At birth, although the mammalian digestive tract is structurally complete, it remains physiologically immature. During the immediate postnatal period, it undergoes rapid growth and cellular specialisation; for instance, the canine small intestine nearly doubles in weight within the first 24 hours of life.

• Amniotic Fluid: This is the first compound to enter the fetal gastrointestinal system, acting as an important bioactive buffer that stimulates early gut development and serves as an initial barrier.
• Intestinal Functions: The gut modulates selective digestive and absorptive functions while concurrently acting as a physical and immunological barrier against pathogens and toxins through specific and non-specific defenses.
• Impact of Colostrum: Colostrum intake stimulates enterocyte proliferation and long-term intestinal morphological development, exerting a trophic effect that persists well after weaning.

Colostrum supplies water, energy-yielding nutrients, digestive enzymes, and maternal antibodies. Furthermore, it has a mild laxative effect that encourages the elimination of meconium (the first faeces accumulated during fetal life), aiding the excretion of excess bilirubin and preventing neonatal jaundice. It also plays a key role in establishing postnatal circulatory volume.

The recommended guidelines for nutrition and energy calculations in growing puppies, according to FEDIAF standards, are outlined below:

Colostrum energy is primarily derived from proteins (approx. 50% of colostral calories) and lipids (40%). While the energy density (kcal/mL) is comparable to that of mature milk, its pattern during lactation differs between bitches and queens:

• In bitches, the energy value decreases progressively by 20% over the first two weeks postpartum.
• In queens, it drops sharply by 30% during the first 3 days and then steadily rises throughout the remainder of lactation.

Regarding carbohydrates, lactose is the primary sugar source, though its concentration in companion animals is about 30% lower than in cows’ milk. Feline and canine colostrum register lactose levels of 29.9 g/L and 16.6 g/L respectively, rising to 35–42 g/L in mature milk. Lactose serves as the sole digestible glucose source during the first month of life because neonatal pancreatic amylase activity is virtually non-existent. Intestinal lactase activity declines sharply after two months of age, which explains why feeding large amounts of milk to older animals often triggers osmotic diarrhoea.

Colostrum also provides essential micronutrients such as vitamin E (to protect against oxidative stress) and vitamin A (fundamental for cellular differentiation, protein synthesis, vision, and non-specific defenses), with levels up to 80% higher than in mature milk. Additionally, it supplies vitamin D, which is critical for calcium and phosphorus regulation and subsequent bone mineralisation. Puppies and kittens cannot synthesise active vitamin D in their skin from dehydrocholesterol, making them entirely dependent on dietary intake. The calcium-to-phosphorus ratio remains stable at around 1.5 in canine colostrum, whereas it increases significantly from colostrum to milk in queens.

The total protein concentration in colostrum is twice that of milk, and 20–30% of this fraction consists of immunoglobulins (IgG, IgM, IgA), providing systemic and local immunisation.

Carnivores possess an endotheliochorial placenta, whose four cell layers restrict the transplacental transfer of antibodies to only 10–20% of maternal IgG. At birth, a puppy or kitten has only about 5% of an adult’s circulating IgG levels, making them fully reliant on colostrum. Total IgG concentration is 20–30 g/L in bitch colostrum and 50–70 g/L in queen colostrum, but these levels decline drastically within the first 24 hours.

Intestinal absorption of these intact macromolecules is possible due to the temporary immaturity of enterocyte tight junctions and a low initial production of proteolytic enzymes like trypsin.

• In puppies, the maximum efficiency of immunoglobulin absorption occurs 8 hours after birth, and the intestinal barrier closes completely within 16 to 24 hours.
• In kittens, passive transfer must ideally be completed within 12 hours. Absorption becomes impossible between 16 and 36 hours of life, coinciding with a decrease in colostral trypsin inhibitors and the onset of normal protein digestion.

Transport across the epithelial barrier occurs via selective endocytosis mediated by specific receptors on the apical membrane of the enterocytes, known as neonatal Fc receptors (FcγRn), which safely escort the Fc portion of IgG into the bloodstream, avoiding lysosomal degradation.

Colostrum contains an array of peptides and hormones with potent antimicrobial, immunomodulatory, and trophic properties. Oligosaccharides (both neutral and acidic) act as receptor analogues, preventing pathogenic microorganisms from adhering to the intestinal and urinary tracts, while also serving as prebiotics that stimulate beneficial bacteria such as Bifidobacterium bifidum. It also includes growth factors like EGF (cellular repair and protection), IGF-1 (anabolic muscle mass growth), TGF-α and TGF-β (tissue maturation and IgA production induction), and Hormone of Growth (GH), which altogether promote mucosal development and gut closure.

Colostrum deprivation or poor colostrum quality can stem from maternal factors (stress in primiparous females, dystocia, mastitis, agalactia, or malnutrition) or neonatal factors (weakness, prematurity, or anatomical defects like cleft palate). This triggers severe clinical syndromes known as the Fading Puppy or Fading Kitten Complex, characterised by progressive multiorgan failure.

• Feline Neonatal Isoerythrolysis: This condition occurs primarily in kittens due to naturally occurring alloantibodies in the colostrum of type-B queens nursing type-A or type-AB kittens. These antibodies destroy the neonate’s red blood cells, inducing symptoms that mimic sepsis: persistent hypothermia, rapid weight loss, dyspnoea, apnea, constant vocalization, and eventual death from cardiac arrest.
• Cardiovascular Disorders and Dehydration: Colostrum provides the fluid intake necessary to maintain blood volume in an immature cardiovascular system, whose baroreceptors do not become functional until the fourth day of life. Because water constitutes 80% of a neonate’s body weight and kidney function is immature, their fluid turnover rate is double that of an adult, making them highly susceptible to dehydration. Insufficient colostrum intake leads to dramatic drops in blood pressure, severe bradycardia, and fatal heart failure. Normal maintenance fluid requirements range between 132–220 mL/kg/day.
• Hypothermia: Rectal temperature drops physiologically after birth. Neonates dissipate heat rapidly due to a high surface-area-to-body-volume ratio, an absent shivering reflex, and poor vasoconstriction mechanisms during the first six days, compounded by a lack of subcutaneous fat. During the first week, brown adipose tissue is the main driver of metabolic thermogenesis, a process that requires the carbohydrates and lipids supplied by colostrum to function. If the rectal temperature drops below 35 °C, the metabolic rate is severely compromised.
• Hypoxia, Anoxia, and Acidosis: Parturition is naturally accompanied by transient respiratory and metabolic acidosis. Colostrum deprivation exacerbates this state, predisposing the animal to fatal necrotic enterocolitis induced by tissue hypoxia.
• Hypoglycemia: The fetus relies on a continuous maternal glucose infusion via the placenta. At birth, hepatic glycogen and fat reserves are minimal, and immature gluconeogenic pathways limit the neonate’s ability to maintain glucose homeostasis during fasting. Without colostrum, severe hypoglycemia develops rapidly.

When maternal colostrum is poor in immunoglobulins (<20 g/L for bitches and <50 g/L for queens) or unavailable, immediate clinical intervention is required to stabilise vital parameters:

1. Fluid Rehydration: If the neonate is normothermic and has normal gut motility, oral rehydration is preferred. In moderate to severe cases, subcutaneous, intraosseous, or intravenous routes must be utilised with sterile techniques, using balanced solutions like warm Ringer’s lactate (37–38 °C). Dehydrated animals require 60 to 180 mL/kg/day of fluid support. For kittens experiencing cardiovascular collapse, 1.25% to 5% dextrose can be added to a maintenance infusion of 80 to 120 mL/kg/day.
2. Managing Hypoglycemia: For puppies with critical blood glucose levels (<30–40 mg/dL), a slow intravenous administration of 5–10% dextrose in Ringer’s lactate or normal saline is given at 0.5 to 1 g/kg. In kittens (hypoglycemia defined as <50 mg/dL), 5–10% dextrose can be administered via a gastric tube, or a 12.5% dextrose bolus can be delivered intravenously/intraosseously in severe cases, followed by constant-rate infusion to prevent rebound hypoglycemia.
3. Reversing Hypothermia: It is strictly forbidden to feed a puppy or kitten whose body temperature is below 34.4 °C or if bowel sounds are absent. Feeding a hypothermic animal causes gastrointestinal stasis and ileus. Rewarming must be slow and progressive (not exceeding 1 °C per hour) using incubators, oxygen cages, or thermostatic heating pads wrapped in towels that warm the abdomen rather than the back. If the animal is cold, a 10% glucose solution can be given orogastrically every 30 minutes until a rectal temperature of 37 °C is reached, before restoring artificial milk feeding.

For alternative immunisation strategies in cases of failure of passive transfer, establishing a homologous frozen colostrum bank stored at −20 °C is highly effective, as freezing/thawing only slightly affects immunoglobulin viability. Other options include the oral administration of canine blood plasma during the first weeks of life (which improves weight gain and gut microbial diversity) or the use of hyperimmune egg powder derived from hens vaccinated against specific pathogens, which has been shown to increase faecal IgA levels and reduce gastrointestinal stress.

Modern milk replacers are increasingly formulated with specific nutraceuticals to mimic the protective properties of natural colostrum:

• Bovine Colostrum and Lactoferrin: Used as a trans-species treatment to enhance resistance against a wide range of bacterial, viral, fungal, and parasitic pathogens. Added bovine lactoferrin stimulates intestinal cell proliferation and differentiation, improves iron absorption, and exerts direct antiviral activity in the intestinal lumen.
• Polyunsaturated Fatty Acids (PUFAs): Docosahexaenoic acid (DHA, omega-3) is critical for correct retinal and central nervous system development. Although puppies can synthesise DHA from precursors like docosapentaenoic acid (DPA), conversion from alpha-linolenic acid (ALA) is highly inefficient and metabolically competes with omega-6 pathways. Dietary supply of preformed DHA ensures optimal cognitive and electroretinogram responses. Furthermore, DHA competitively inhibits cyclooxygenase, reducing pro-inflammatory mediators and platelet aggregation (thromboxane A2), thus providing systemic anti-inflammatory and cardiovascular protective effects.
• Prebiotics and Probiotics: Symbiotic supplementation supports the transitioning neonatal microbiome. When administered to pregnant dams, they enhance colostrum quality via the entero-mammary immune link, resulting in higher maternal immunoglobulin concentrations transferred to the litter and triggering increased luminal IgA secretions in the puppy’s small intestine.

• The neonatal period (the first two weeks of life) is a high-risk phase of extreme biological vulnerability due to immature metabolic and immune defenses.
• Colostrum provides indispensable caloric support (primarily via proteins and fats) and acts as the primary catalyst for gastrointestinal tract development and mucosal maturation.
• The systemic transfer of passive immunity is entirely dependent on colostrum ingestion within the first 12 to 16 hours of life, before total macromolecular gut closure occurs.
• Colostrum deficiency or deprivation leads to a cascade of fatal systemic failures: circulatory collapse, acute dehydration, severe hypothermia, metabolic acidosis, and clinical hypoglycemia.
• Clinical management of a critical neonate dictates that hypothermia must be corrected and normal core body temperature restored before initiating any artificial bottle-feeding or milk replacer protocols.
• Implementing clinical strategies such as frozen colostrum banks, oral plasma support, bovine colostrum, and essential fatty acids (DHA) in milk replacers serves as an effective means to combat neonatal mortality in veterinary practices and breeding kennels.