🐄 Herd Health, Part Two: Worms, Vaccines and the Diseases You Must Report

Ticks you can see. Worms you cannot. A calf carrying a heavy burden of gastrointestinal nematodes does not usually fall over dead. It grows slowly, looks a little rough, eats grass and turns less of it into weight. At weaning it comes in twenty or thirty kilograms lighter than it should have been, and nobody on the farm can point to the day the loss happened. That is what internal parasites cost you: not a dramatic death, but a slow leak out of the weaning weight that is the whole product of your herd.

What does the evidence actually say? A study of traditional West African cattle showed that strategic gastrointestinal nematode control - planned, timed control rather than purely reactive dosing when an animal already looks bad - measurably reduced faecal egg counts. The specific numeric reduction figures from that study could not be retrieved for this course, and no number is supplied here in their place. What the study supports is the principle: planned control works better than waiting until you can see the damage.

Now the part that has changed the advice given to farmers everywhere in the last twenty years. Deworming drugs are losing their power, and in places they have already lost it.

A systematic review and meta-analysis pulled together 28 studies across 9 African countries. The review itself is honest that this covers only about 16.7 percent of the continent, so it is a limited evidence base. Within that evidence base, the efficacy figures are alarming. The conventional threshold for saying a drug still works is 95 percent. Against that:

• Benzimidazole drugs, the group that includes albendazole, measured as low as 0 percent efficacy in Mozambique and 11 to 28.5 percent in Uganda.
• Benzimidazole efficacy in South Africa ranged from 3.8 to 72.1 percent.
• Macrocyclic lactones, the group that includes ivermectin, measured as low as 24 percent in Algeria and 27 percent in South African goats.
• Imidazothiazoles, the group that includes levamisole, measured as low as 7.9 percent in South African sheep.

Read one thing carefully before you carry those numbers into your kraal. That dataset is predominantly sheep and goats, not cattle. It must not be quoted as a cattle-specific resistance figure. It is included here for two honest reasons: it proves that anthelmintic resistance in African livestock is real, measured and in places severe, and the same drug classes are used in cattle. A cattle-specific African resistance dataset of comparable size was not available for this course.

What does resistance mean in practice? Every time you dose, the worms that survive are the ones the drug could not kill. Those survivors breed. Dose the whole herd on a fixed calendar year after year with the same product, and you are running a slow selection programme that breeds a worm population your drug cannot touch. The pattern documented across Africa is of declining, not stable, efficacy for every major class tested.

So the advice has flipped. It used to be: dose everything, every season, on the calendar. The evidence now argues for two changes.

1. Dose when there is a reason to, not simply because it is the month you always dose. A parasite burden worth treating is something you and a veterinarian establish, not something the calendar tells you.
2. Rotate drug classes rather than relying on one. Note the word class, not brand. Two products with different names on the container can contain the same active drug group and give you no rotation at all.

And here is the boundary this course will not cross. Specific dosing rates, which product to choose, and what rotation schedule to run are all set by a national veterinary authority and an animal-health product registration list. They differ by country. This course gives you none of them. Take the container to a veterinary officer and ask what group the active ingredient belongs to and how it should be used here.

The same goes for withholding periods, the time that must pass between the last treatment and slaughter or milk sale. There is no universal number, and this course gives none. It is set by the product label and by your national veterinary authority, without exception.

One last practical link. Correct dosing needs a weight, and most smallholders have no scale. Module 4 gave you the girth tape method, giving an estimate typically within about 10 percent of true liveweight. Underdosing because you guessed the animal's weight low is one of the ways a farm breeds resistance into its own worms.

There is a wrong way to build a vaccination plan and it is very common: copy the list somebody printed in a book or a magazine, buy those products, and inject them. The list came from another country's disease environment. Some of it is irrelevant where you farm, some of it is unavailable, and some of it may be legally required in a form you have not been told about.

There is a right way, and it has two parts. First, structure the plan around the life stage of the animal. Second, fill that structure with the diseases your own district actually has, on the advice of a veterinary authority.

Here is the structure. A South African guideline on building a cattle vaccination plan illustrates it, and it is used here purely as an example of shape, not as your list.

Stage one, the young calf. Vaccination in that guideline begins from around three months of age. There is a biological reason for that timing worth understanding: a calf is born with essentially no immunity of its own and receives antibodies through the dam's first milk, the colostrum. That borrowed immunity fades over the first months of life, and vaccinating too early can be wasted because the maternal antibodies still circulating interfere with the calf's own response. Around three months is when that protection is typically waning and the calf's own immune system can be asked to do the work. In that South African example the first window commonly covers clostridial diseases, a group that includes blackleg and other toxin-producing bacterial diseases, and brucellosis vaccination with the S19 strain is targeted at young heifers around three to eight months.

Stage two, the replacement heifer, in the window between weaning and first breeding. In the same example this stage carries a broader set: lumpy skin disease, three-day stiffsickness, Rift Valley fever, botulism and anthrax. Then, timed to roughly one month before the breeding season because these specifically affect reproduction, vibriosis, bovine viral diarrhoea, infectious bovine rhinotracheitis and leptospirosis. Notice the timing logic. A vaccine against a disease that causes abortion has to be in the animal before she is pregnant, not after you have seen an abortion.

Stage three, mature animals. In the same example these receive annual boosters for botulism, blackleg and anthrax, with anything further added only where that specific herd or region has a documented problem.

Now read the warning that matters more than the list. That entire calendar is a South African commercial-context example. Disease prevalence differs sharply by country and even by district within a country. Rift Valley fever, for instance, is a periodic, rainfall-linked risk in specific regions, not a universal annual concern everywhere. Which vaccines you need, which are available, which are legally required, and when they should be given, is set by your own national or provincial veterinary authority or a private veterinarian. That is the only correct source for your own plan. This course names no vaccine as one you must buy.

So what is genuinely universal, and what should you take away and use? Two things.

The first is the structure. Build around life stage: young calf, weaned and growing replacement, breeding-age female approaching mating, mature adult. Every real plan has these four columns whatever fills them.

The second is documented local disease history. That word documented is doing a lot of work. It means you know what has actually been killing and sickening animals on your farm and around it, and you know it because deaths were investigated, not guessed at. An unexplained death that nobody examined teaches you nothing and may be hiding a disease your vaccination plan should be built around. Post-mortem examination of unexplained deaths, done by someone competent, is part of how a vaccination plan gets built - with the enormous exception you will meet in Lesson 4 of this module, where a suddenly dead animal must never be opened by anyone until a veterinary authority has ruled anthrax out.

There is one more piece of structure worth planning: vaccination is a handling event. Every animal has to come through a crush. That means the vaccination calendar should be planned alongside dipping, dosing, weaning and pregnancy testing, so that you handle animals as few separate times as is safe and sensible. Module 10 covers the facility that makes this possible. Module 11 covers writing down what each animal received, which is what stops you guessing next year whether cow 042 was done.

Across most of this course, ticks have been the main animal-health enemy. Across a very large band of Africa, they are not. There a fly, not a tick, sets the limit on whether cattle can be kept at all.

African animal trypanosomiasis is caused by Trypanosoma protozoan parasites and transmitted by tsetse flies, of the genus Glossina. The area affected is more than 9 million square kilometres, roughly one-third of Africa's total land area, spread across 37 sub-Saharan countries. Around 50 million head of cattle are at risk inside that zone.

The cost is on the same scale as the area. The disease is estimated to cause about 3 million cattle deaths a year. Farmers and veterinary services across the affected zone administer approximately 35 million doses of trypanocidal drugs annually just to hold the ongoing burden in check. Direct production losses are estimated at 1.0 to 1.2 billion US dollars a year, and the wider loss to affected countries' agricultural output, once you count the land and livestock development that the disease forecloses entirely, is estimated at 4.75 billion US dollars a year.

Read that last pair of figures again, because the gap between them is the real lesson. Direct losses are what dead and sick cattle cost. The far larger figure is what never happened: land not used for cattle, herds not built, investment not made, because the fly makes it impossible. Trypanosomiasis does not only kill cattle. It closes territory.

So what does a farmer inside that zone actually do? There are two lines of defence and they are the same two you have already met with ticks.

The first is drugs. Trypanocidal drugs exist and are used at enormous scale, and the 35 million annual doses figure tells you both that they work and that they are a permanent recurring bill. These drugs are regulated exactly as acaricides and dewormers are. Dose, product choice and withholding period are all set by your national veterinary authority and differ by country. This course gives no dose, no product and no withholding period.

The second is breed, and it is the more interesting one. Certain West African indigenous breeds, most notably N'Dama cattle, carry a genetically based tolerance to trypanosome infection. Trypanotolerant animals can survive and stay productive in tsetse-infested areas where unadapted cattle simply cannot be kept without heavy and continuous drug intervention.

Be honest about the limits of what can be taught here. A specific quantified figure for the N'Dama advantage - how much better they survive or produce than a non-tolerant breed under the same tsetse challenge - could not be retrieved for this course, and no number is supplied in its place. The principle is well established: trypanotolerant indigenous breeds exist and are a real, breed-based alternative to permanent drug dependence. The size of the advantage is a figure you must obtain from a national livestock research institute.

Notice that this is the same trade-off that has run through this whole course, wearing different clothes. Module 2 set it out with ticks and heat: an indigenous animal that survives what would cripple an exotic, against an exotic that grows faster when the stress is removed. Here it is a fly instead of a tick, and the same logic applies. A locally adapted breed can be kept with dramatically lower drug input in a zone that would otherwise be either impossible or permanently drug-dependent.

The practical judgement you must make is which disease constraint dominates where you actually farm. Much of West and Central Africa, and belts of East and southern Africa, sit inside the tsetse zone. If you are in it or near it, trypanosomiasis and not the tick-borne complex may be the dominant limit on your herd, and both your breed choice and your health budget should be built around that fact rather than around the tick advice that suits a different part of the continent.

How do you find out? Not from a book, and not from this course, because the fly's distribution shifts with vegetation, climate and control programmes. Ask a district veterinary officer whether tsetse is present in your area, whether there is an active control programme, and which breeds are recommended locally. That single conversation may reshape your whole herd plan.

This is the most important safety lesson in the whole course. Read it twice, and then teach it to everyone who works with your cattle, including children.

Anthrax is caused by a bacterium called Bacillus anthracis. It kills cattle. It also kills people. It is a zoonosis in the fullest sense, and the main way people get infected is by handling an infected animal or its products - hide, wool, bone, and most dangerously the meat or blood of a carcass that somebody has opened.

Here is the rule, and it has no exceptions.

An animal that dies suddenly and unexpectedly - especially with dark, non-clotting blood oozing from body openings, and without the normal stiffening of the body after death - must be treated as a possible anthrax case. It must not be opened. It must not be skinned. No meat, no hide, no bone and no part of it may be removed, by anyone, under any circumstance, until a veterinary authority has ruled anthrax out.

Not for a post-mortem. Not to save the hide. Not to feed the family. Not because the animal looked healthy yesterday and the meat seems fine. Nothing about that carcass is worth a human life, and the meat and hide of a dead animal are exactly the route by which people are infected.

Why does opening it matter so much? Because of one specific piece of biology that every cattle keeper should know. Bacillus anthracis only forms its resistant spore stage in the presence of oxygen. Inside a closed, unopened carcass there is no oxygen, so there is no sporulation - the bacteria stay in a vegetative form that does not survive long outside the body. The moment the carcass is opened, whether by a knife, by scavengers, or by an unwary post-mortem, the bacteria meet air and can sporulate massively. Those spores contaminate the ground.

That is how one dead cow becomes a piece of land that is dangerous for a long time afterwards. How long? The source consulted describes spore survival in the environment as unpredictable and heavily dependent on climate, particularly temperature. It gives no single duration. This course therefore supplies no figure for how many years anthrax spores survive in soil, because none could be verified. What is certain is that the persistence is long enough to matter and long enough to be documented from old burial sites.

Which brings us to disposal. The preferred method for a confirmed or strongly suspected anthrax carcass is incineration. Burial is explicitly discouraged, because historical evidence shows spores persisting and resurfacing from old burial sites. And who does it? That is set by your national authority. In most countries carcass disposal for a suspected anthrax case is a function the veterinary authority must be involved in, precisely because of the human health risk. It is not a job for an individual farmer acting alone with a shovel. Find out now, before you need to know, who in your district is responsible and what number to call.

Prevention. In anthrax-endemic areas the standard approach is annual livestock vaccination with a live spore vaccine - the Sterne 34F2 strain is the vaccine strain named in the source consulted - giving approximately one year of protection, which is why a booster is needed every year in endemic zones. Whether that vaccine is available where you are, whether vaccination is compulsory, and how the programme is organised are all matters for your national veterinary authority. Because anthrax is a public health matter, it is frequently run as a compulsory or heavily promoted government programme in endemic districts rather than left to individual choice. Ask.

Reporting. Any suspected human case, and any cluster of unexplained sudden cattle deaths, must be reported immediately to both the veterinary authority and the human health authority. Both. This is a One Health disease, and the correct response is never for a farmer or a community to handle it quietly among themselves. Reporting rules, quarantine and movement control around a suspected case are set by your national veterinary authority, and this course states no country's rule as if it were yours.

One last thing. There will be pressure. An animal dies, the meat looks good, a family is short of food or a trader offers money for the hide. This lesson exists so that when that moment comes, the person standing over the carcass already knows the answer and does not have to work it out under pressure. The answer is: leave it closed, keep people and dogs away, and telephone the veterinary office.

Foot-and-mouth disease is the clearest example in this course of a disease whose main cost is not to the animal at all. It is to the market.

Start with the biology, because two things about it are widely misunderstood.

Foot-and-mouth is caused by a virus with multiple serotypes. In an unprotected population, morbidity - the proportion of susceptible animals that become infected - can reach 100 percent. Mortality, however, is generally low in adults, around 1 to 5 percent, though it can exceed 20 percent in young animals. The incubation period is 2 to 14 days. So this is a disease that races through a herd and mostly does not kill the adults it infects.

Africa carries one epidemiological complication that Europe does not: African buffalo are an important wildlife carrier and reservoir of the virus. That means the virus has a home outside your cattle and outside anybody's control, which shapes how control programmes have to be designed on this continent.

The second misunderstanding is a human one, and it matters. Foot-and-mouth disease is not readily transmissible to humans and is not a public health risk. The name confuses people with hand, foot and mouth disease, which is an entirely unrelated human viral illness. Say this clearly when you talk to neighbours and buyers, because panic about a non-existent human risk does real commercial damage on top of the damage the outbreak is already doing.

Now the part that actually costs money. Foot-and-mouth is listed by the World Organisation for Animal Health and is mandatorily reportable to that organisation under the Terrestrial Animal Health Code. Every country's veterinary authority has a formal obligation to report outbreaks internationally, not merely a domestic option to do so. An outbreak triggers quarantine, movement restrictions, and can close export and even domestic markets for a whole region.

Here is the case study that shows exactly what that means to a farmer.

Following a foot-and-mouth outbreak in Botswana, the European Union suspended fresh beef imports from the affected zones for approximately two months. When exports resumed, they resumed from only 7 of Botswana's 19 agricultural and veterinary zones - the remaining 12 zones stayed under restriction. Cattle destined for EU export had to be placed in specifically EU-approved holding facilities for a minimum of 40 days before slaughter. One Botswana farmer with a retail butchery reported a direct ten-day stoppage of sales from the same outbreak. And livestock ownership affects roughly 80 percent of Botswana households.

Work out who lost money there. Not only the owners of infected cattle. Every cattle owner in the 12 restricted zones, whose own animals may never have been within a hundred kilometres of the virus, lost access to the export price for months. A butcher with no infected animals at all lost ten days of trade. That is the shape of a foot-and-mouth loss: it lands on a whole zone, not on a herd.

Two cautions on that case study. It is one real, dated outbreak, presented as an illustration of the general principle. Botswana's export status has moved on since, and you must never take current trade status from a course document. Also, the 40-day holding requirement is that market's rule at that time, not a universal figure.

What about vaccination? Where it is used, the strategy is generally aimed at high coverage - a commonly cited operational target in the literature is around 80 percent - using an inactivated vaccine matched to the circulating serotype. Read both halves of that sentence. Coverage has to be high because the disease spreads so efficiently, and the vaccine has to match the serotype actually circulating, which is why an outbreak strain has to be identified before a vaccine campaign means anything.

That is stated here as a general principle at the level of international guidance. Actual vaccination policy, zoning, movement permits and compensation schemes for foot-and-mouth are entirely a matter for each country's veterinary authority. South Africa, for example, operates a formal zoning system. This course reproduces no country's zoning map or movement rule, because it is regulatory, it changes with outbreak status, and a wrong answer here could put a learner on the wrong side of the law. Before moving any animal, confirm current zoning and movement-permit requirements with your own veterinary authority.

The last lesson is the uncomfortable one. In a disease-control zone, an unreported sick or suddenly dead animal is not only your private loss. It is a risk to every neighbouring herd's market access. Your own dipping, vaccination compliance and disease reporting help hold the zone status that keeps the price up for everyone around you, including you.

Module 1 of this course was built on a single number: the proportion of cows that fail to produce a calf in a year. Brucellosis is one of the reasons that number is as bad as it is, and it is one of the least suspected, because it does its damage quietly, over years, and looks like bad luck.

Brucellosis in cattle is caused by Brucella bacteria, most commonly Brucella abortus. What it does is characteristic: late-term abortion, retained placenta, and reduced fertility. Set that against the core equation of this course: kilograms weaned equals cows exposed, times calving percentage, times calf survival, times weaning weight. Brucellosis attacks the middle terms directly.

So here is the pattern to watch for. A single abortion in a herd in a year can have many innocent causes. A pattern of unexplained late-term abortions, repeated across seasons and across different cows, is not bad luck and should not be written off as a bad year. It is a herd-level signal, and brucellosis should be specifically investigated rather than assumed away. This is exactly the kind of thing that only shows up if you keep the records taught in Module 11: three abortions in three different years, in three different cows, look like nothing at all in memory and look like a pattern on paper.

Now the part that concerns you and your family, not just your cattle. Brucellosis is a genuine zoonosis. In people it causes a debilitating, often chronic fever - undulant fever - that can drag on for months. There are two main routes by which people catch it.

The first is direct contact with infected reproductive material: an aborted foetus, a retained placenta, birth fluids. Anyone who assists a calving with bare hands and arms is in direct contact with exactly the material that carries the highest risk.

The second is drinking unpasteurised milk, or eating dairy products made from it, from an infected animal.

From those two routes comes a safety rule you can apply today, on any farm, whether or not you know your herd's brucellosis status, and it costs almost nothing.

1. Always handle an aborted foetus, a retained placenta, or birth fluids from an unexplained abortion with gloves.
2. Do not allow children near that material.
3. Do not allow pregnant women near that material.
4. Do not leave an aborted foetus lying where dogs, other cattle or people will come into contact with it, and tell your veterinary officer that it happened.

That rule is worth applying as standard practice regardless of what you know, because the whole point about brucellosis is that a herd can be infected without anyone knowing. Which brings us to the honest gap in this course. Current African cattle brucellosis seroprevalence figures - the percentage of cattle testing positive in South African provinces, Tanzanian pastoral communities, and continent-wide reviews - were identified but could not be retrieved for this course. So this module gives you no percentage for how common brucellosis is in your region, because none could be verified. That is a real loss, because prevalence is exactly the figure that would tell you how seriously to take the risk where you live. Your national veterinary service or a nearby veterinary faculty is where to ask for it.

How is brucellosis controlled? Two tools, used together.

The first is vaccination of young female replacement stock. The S19 strain vaccine, mentioned in the vaccination-plan example in Lesson 2 of this module and targeted there at heifers around three to eight months, is one such product. Note that it targets replacements, not the whole herd - you are protecting the animals that have not yet been exposed and are about to enter the breeding herd.

The second tool is testing and removal of infected adult animals, used in more intensive control programmes. Testing gives you the herd's status; removal is what actually reduces the infection.

What this course cannot tell you is which of those is available, compulsory, subsidised or forbidden where you farm. Whether brucellosis vaccination is available, whether it is compulsory, what strain and product are used, and whether there is a national eradication or certification scheme, are all set by your national veterinary authority. Certification is frequently tied to milk-safety rules and to export access, so the consequences are commercial as well as veterinary. Ask before you buy or test anything.

One last connection. Brucellosis is the third disease in this module handled by an authority rather than by you alone, alongside anthrax and foot-and-mouth. The common thread: the moment a disease can cross to people or cost a district its market, it stops being your private business. Knowing which three those are, and having the telephone number ready, is part of running a cattle enterprise.